Press Release - New Studies Reveal Hidden Benefits of Exercise for Local Seniors

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Encouraging aging loved ones to take part in autumn activities can provide huge health rewards.

New Studies Reveal Hidden Benefits of Exercise for Local SeniorsOct 19, 2010 This press release is an announcement submitted by Senior Helpers, and was not written by Diabetes Health.

As the weather turns and leaves begin to fall this year, new research shows that local aging seniors are well served to get up and grab a rake themselves - for more reasons than one. A group of four recent studies published in 2010 Harvard University health and medicine journals shows a surprising and strong connection between seniors, exercise, and mental and physical health, especially among aging women.?

"We've known that regular exercise translates to serious health benefits for seniors for years, but connections of this magnitude are incredible," said Peter Ross, senior care expert and CEO of Senior Helpers, the fastest growing in-home care company in the nation. "It's vital to keep mom and dad up and moving as they age, and this is further evidence that proves just how important even the most moderate of exercise efforts can really be."

The four new studies found the following related to seniors, mental health, and physical activity:

Women who exercise regularly(categorized as walking briskly five to six hours per week)?at age 60 were almost twice as likely to live beyond 70 with no cognitive, physical, or mental health limitations; Women age 65-75 who participated in low-level strength training exercises showed significantly improved executive function?(high-order thought processes involved in decision making)?and also improved physical walking speed(a leading predictor of fall and fracture risk)compared to a control group; Men and women over 55 who exercise at a moderate level or higher?(about three times per week)?were half as likely to develop dementia later in life compared to those who did not exercise regularly; and Women, age 70 and up, with mild cognitive impairments?(MCI, a common precursor to dementia)?who engaged in aerobic exercise four times per week showed significant improvements over a control group in all administered cognitive and physiological tests over a six-month trial.

"The successes found by these researchers in improving mental function and physical health can be duplicated in reality, and locally," Ross says. "We work with area seniors living on their own each day, helping them get out of the house, go for a walk, do some light work in the yard or garden or whatever else they can do. It's crucial for elderly individuals to stay active and exercise, but it's also important to have someone there to watch them, assist them, and make sure they are staying safe while being staying active."

Simple Autumn Exercise Ideas for Seniors

Sweeping/Raking leaves: even a quick weekly sweep of the front porch or the stoop offers cardio and strength-building exercise for core muscle groups. Gardening: tending to a small garden or flower box works the hands, forearms, and extremities and is good for the mind. Light Housework: doing the dishes, laundry, dusting, and cleaning offer a great opportunity for an easy everyday exercise routine. Walking: the weeks after the summer heat and before winter chill provide a perfect window for outdoor excursions at any point during the day. Seasonal Activities: pumpkin carving and corn mazes offer physical activity and a chance to interact with family and friends.

"The physical and mental benefits of exercise among seniors are almost endless," Ross says. "Even the simplest of activities can go a long, long way to promoting a healthy, independent lifestyle among aging loved one - and this new research is the proof."

- - - - -

About Senior Helpers:

Senior Helpers connects professional caregivers with seniors who wish to live at home as opposed to a nursing or assisted living facility. The company has 300 franchises in 42 states and one in Canada offering a wide range of personal and companion care services to assist seniors living independently with a strong focus on quality of life for the client and peace of mind for their families. Senior Helpers strives to be the leading companion and personal care provider that offers dependable, consistent and affordable home care. ?For more information, please visit seniorhelpers.com.

Categories: Exercise, Fitness, Geriatrics, Health, Type 2 Issues

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Sensor and insulin pump results in better blood-sugar control in all age groups with diabetes, study finds

ScienceDaily (Sep. 26, 2010) ? Adding a continuous blood sugar level sensor to an insulin pump helps patients with type 1 diabetes achieve better blood sugar control compared to the common standard of care, multiple daily insulin injections, concludes a study published online in the New England Journal of Medicine.

The paper is entitled, Effectiveness of Sensor-Augmented Insulin-Pump therapy in Type 1 Diabetes.

"Combining the best technologies for insulin delivery and blood sugar monitoring really pays off for diabetes control," says Dr. Bruce Perkins, one of the co-authors of the study, endocrinologist at Toronto General Hospital and Assistant Professor at the University of Toronto. "Being aware of continuous blood sugar trends and having the tools to do something about them can help committed patients of all ages self-manage their diabetes very well."

Research conducted at 30 centres across North America, including Toronto General Hospital, found a significant decrease in average blood sugar levels (or A1c levels, which measure the average blood sugar levels over the past two or three months) from a baseline of 8.3% to 7.5% in the group using sensors and insulin pumps, compared to 8.3% to 8.1% in the multiple daily injection group, at one year. The decrease in A1c levels in both adults and children occurred without an increase in the rate of severe hypoglycemia, or low blood sugar, a common problem among patients who are trying to achieve better control of their blood sugar. Symptoms include shakiness, rapid heart beat, confusion and even unconsciousness.

Moreover, the proportion of participants who reached the A1c target of 7% or less was greater in the pump-therapy group than in the injection-therapy group. Adults with diabetes try and maintain A1c levels of seven percent or below in order to reduce the risk of complications from diabetes, such as kidney failure, heart disease and blindness.

The 485 study participants with inadequately controlled type 1 diabetes ranged in ages from seven to 70, and were treated for at least one year, in a randomized, controlled trial.

In the study, patients in the sensor-augmented pump therapy arm used an integrated system which incorporates an insulin pump, continuous glucose monitor and self-management software. A glucose (sugar) sensor reveals fluctuations in glucose levels in real-time, and transmits electric signals wirelessly to the insulin pump, which is about the size and shape of a small cell phone. The pump displays the blood sugar levels, allowing patients to react to either high or low levels before they become dangerous.

The study was sponsored by Medtronic, Inc.; and supported by Novo Nordisk; Lifescan; Bayer Heathcare; and Becton Dickinson.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University Health Network, via EurekAlert!, a service of AAAS.

Note: If no author is given, the source is cited instead.

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New clues to origin of diabetes: Mutant gene protein can derail normal insulin production in animal pancreatic beta cells

ScienceDaily (Oct. 12, 2010) ? University of Michigan scientists have identified events inside insulin-producing pancreatic cells that set the stage for a neonatal form of non-autoimmune type 1 diabetes, and may play a role in type 2 diabetes as well. The results point to a potential target for drugs to protect normally functioning proteins essential for producing insulin.

A study published online in the journal PLoS ONE shows that certain insulin gene mutations involved in neonatal diabetes cause a portion of the proinsulin proteins in the pancreas' beta cells to misfold. Proinsulin proteins are the precursors of insulin, which the body needs to regulate blood sugar levels. Crucially, the misfolded mutant proteins cause normal proinsulin proteins in beta cells to misfold as well, the scientists found in studies of mouse and rat beta cells.

"Once the 'good' proinsulin turns 'bad,' it cannot be made into insulin and so the beta cells, and then the whole animal, become insulin deficient. The insulin deficiency causes diabetes and from there, things get worse and worse," says Peter Arvan, M.D., Ph.D., the study's senior author. He directs the Michigan Comprehensive Diabetes Center and is William and Delores Brehm Professor and chief of Metabolism, Endocrinology and Diabetes at the U-M Medical School.

Significance

"We want to see how the mechanism we found in this rare form of neonatal diabetes applies to other forms of diabetes," says Ming Liu, M.D., Ph.D., the study's first author and a research assistant professor of internal medicine at the U-M Medical School.

Diabetes researchers know that protein misfolding in beta cells also occurs on a smaller scale in mice and people without diabetes, and at higher levels in type 2 diabetes, Arvan says. In type 2 diabetes, people develop reduced sensitivity to insulin, causing beta cells to work overtime and eventually fail. In non-autoimmune type 1, diabetes results when genetic mutations cause insufficient production of insulin from pancreatic beta cells.

"In all diabetes, beta cells don't perform to the level needed," says Arvan. "It's possible that the beta cell failure of type 2 diabetes also has a critical protein folding component," he says. "The question is, can you reach a point in ordinary diabetes where misfolding causes the problem we have identified?"

Research details

In lab dish cultures of normal rat and mice beta cells, the scientists introduced single gene mutations known to be involved in various types of neonatal diabetes. They consistently found that misfolding occurred in normal proinsulin protein when mutant proinsulin protein was present. They also observed the same aberrant events in the pancreatic beta cells of Akita mice, a mouse model with the same mutation that occurs in a human family with neonatal diabetes.

Context

Proteins, which are molecules made of amino acids arranged in a certain order determined by genes, normally fold into specific shapes. But sometimes misfolding occurs. Protein folding is a phenomenon that has drawn a lot of recent attention from scientists who believe it plays a role in several common diseases.

Diabetes researchers currently lack a clear picture of why beta cells in the pancreas fail in diabetes. Many researchers look at stress and the stress response from the beta cells' endoplasmic reticulum or ER, a structure that transports materials within the cell. Stress in this structure occurs in diabetes, along with reduced beta cell mass.

Arvan and Liu found in the study that each of the mutations they examined led to ER stress and the ER stress response in beta cells, but that these ER events alone could not block insulin production in normal beta cells and do not appear to be the origin of the insulin deficiency. They hypothesize that protein misfolding events first block insulin production and cause insulin deficiency, leading to diabetes.

What's next

Uncovering the earliest events in the molecular mechanism of the disease may help diabetes researchers discover new therapies, the authors say. New drugs that could emerge would be at least several years away.

"It may be possible to find a way to modulate the environment in the endoplasmic reticulum to let the normal protein fold quickly, before the abnormal protein can act," says Liu.

Additional authors: Leena Haataja, Jordan Wright, U-M Medical School; Nalinda P. Wickramasinghe, Qing-Xin Hua, Nelson F. Phillips, Michael A. Weiss, Case Western Reserve University; Fabrizio Barbetti, University of Tor Vergata, Rome, Italy.

Funding: National Institutes of Health

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Michigan Health System.

Journal Reference:

Matthias G. von Herrath, Ming Liu, Leena Haataja, Jordan Wright, Nalinda P. Wickramasinghe, Qing-Xin Hua, Nelson F. Phillips, Fabrizio Barbetti, Michael A. Weiss, Peter Arvan. Mutant INS-Gene Induced Diabetes of Youth: Proinsulin Cysteine Residues Impose Dominant-Negative Inhibition on Wild-Type Proinsulin Transport. PLoS ONE, 2010; 5 (10): e13333 DOI: 10.1371/journal.pone.0013333

Note: If no author is given, the source is cited instead.

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New study singles out factors linked to cognitive deficits in type 2 diabetes

ScienceDaily (Sep. 11, 2010) ? Older adults with diabetes who have high blood pressure, walk slowly or lose their balance, or believe they're in bad health, are significantly more likely to have weaker memory and slower, more rigid cognitive processing than those without these problems, according to a new study published by the American Psychological Association.

These three health factors stood out from more than a dozen suspected to shape how Type 2 diabetes is frequently shadowed by cognitive impairment, including dementia. An analysis in September's Neuropsychology stresses that although these factors might not actually cause cognitive problems, their presence can warn doctors that such problems may exist or soon develop.

"Awareness of the link between diabetes and cognition could help people realize how important it is to manage this disease--and to motivate them to do so," said co-author Roger Dixon, PhD, of the University of Alberta.

Type 2 diabetes has been found by other researchers to nearly double the risk of dementia and Alzheimer's disease, said Dixon, who studies how health affects cognition in aging. As diabetes becomes more common, this heightened risk could dramatically hike the number of older people with dementia -- a double whammy of serious chronic disease. Among people older than 60, the U.S. prevalence of Type 2 diabetes is more than 23 percent, according to the National Institute of Diabetes and Digestive & Kidney Diseases. The Canadian prevalence is nearly 19 percent, according to the Public Health Agency of Canada.

An analysis of older Canadians living in British Columbia -- 41 with Type 2 diabetes (ages 55-81) and 458 matched healthy controls (ages 53-90) -- found that systolic blood pressure (the top number, or maximum pressure on artery walls during a single heartbeat), a low combination score for gait and balance, and a patient's own reports of poor health all played a statistically significant role in the relationship between diabetes and cognitive impairment relationship.

In other words, higher but still normal blood pressure, slower gait and shakier balance, and/or reporting one's self to be in bad health regardless of actual problems boosted the likelihood that someone with Type 2 diabetes had impaired cognition. The relationships were linear: For example, the worse the balance, the higher the likelihood of cognitive problems, as measured by mental speed (reaction time, switching time and perceptual speed), mental control and flexibility (executive functioning), and recall of recent learning (episodic memory).

The results highlight factors that may work indirectly, gradually and cumulatively to make older diabetics more likely to develop dementia. Researchers tested 13 different variables in all, in the areas of general fitness, emotional health, subjective and functional health, and lifestyle activities.

Mediating Factors

Because diabetes and hypertension often go together, Dixon said he was not surprised that high systolic blood pressure accounted for one-third to one-half of significantly worse scores on four tests. That finding, said the authors, suggests that diabetes and cognition may be connected via diabetics' vascular problems. For example, diabetes and hypertension may both play a role in a larger metabolic syndrome that includes high blood sugar and insulin resistance.

However, the other two factors raised new questions. Combined gait and balance had the greatest influence, accounting for between 32 percent and 62 percent of performance on seven cognitive tests. Diabetes might affect the specific nerves that control gait and balance, the authors wrote, or more broadly affect the overlapping brain areas that support both gait-balance and cognition.

Like blood pressure, what people said about their health accounted for about one-third to one-half of performance on five different cognitive tests. Negativity about one's health could reflect related factors such as stress or depression, which did not, in this study, directly mediate between diabetes and cognition. Self-reported health is "an important indicator of ways in which a cluster of health-related beliefs and behaviors can modulate the effect of this disease on cognitive adaptation," Dixon said.

"It's important to pay attention to the health beliefs of older adults, not because they are necessarily accurate or valid indicators of specific health status, but because they might track overall health," Dixon said.

Type 2 diabetes in adults accounts for 90 percent to 95 percent of all diagnosed cases of diabetes, according to the National Institute of Diabetes and Digestive & Kidney Diseases.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Psychological Association, via EurekAlert!, a service of AAAS.

Journal Reference:

McFall et al. Testing covariates of Type 2 diabetes-cognition associations in older adults: Moderating or mediating effects? Neuropsychology, 2010; 24 (5): 547 DOI: 10.1037/a0019246

Note: If no author is given, the source is cited instead.

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Language delays found in siblings of children with autism

ScienceDaily (Oct. 1, 2010) ? Siblings of children with autism have more frequent language delays and other subtle characteristics of the disorder than previously understood. Girls also may be mildly affected more often than recognized in the past.

A new study, led by researchers at Washington University School of Medicine in St. Louis, found mild traits, not strong enough to provoke a diagnosis of autism, seem to be present in the siblings of affected children at significantly higher rates than seen in the general population. The findings appear online and will be published in the November issue of The American Journal of Psychiatry.

"Mild symptoms, called quantitative traits, may be confounding studies that compare children with autism to their siblings," says first author John N. Constantino, MD. "Researchers presume one child is affected, and the other is not, but our findings suggest that although one child may have autism while the other does not, it's very possible both children are affected to some degree by genes that contribute to autism."

Genetic factors exert their influence in different ways. Some families have only a single child with autism and no other affected children. But in other families, more than one child may be affected, or other siblings may have a number of autism characteristics.

The study found that approximately one in five siblings thought to be unaffected experienced language delays or speech problems early in life. The researchers also noticed many female siblings had subtle traits, but few had full-blown autism spectrum disorders. Boys are thought to be affected four times more often than girls. But when the researchers used standardized methods to account for the presence of quantitative traits, the rate looked more like three affected boys for every two affected girls.

"The gender difference may not be as pronounced as we once thought it was," Constantino says. "If we rely only on a professional diagnosis of autism to determine who is affected, then boys vastly outnumber girls. But it may be that many girls are being missed."

The data comes from almost 3,000 U.S. children in 1,235 families who are part of the Interactive Autism Network, a national online research registry. Developed by study co-author Paul Law, MD, director of medical informatics at Kennedy Krieger Institute in Baltimore, the network has more than 35,000 participants who share information to help advance autism research.

For this study, parents provided information about their children using the Social Responsiveness Scale, a survey developed at Washington University that identifies traits associated with autism and autism spectrum disorders such as Asperger Syndrome and Pervasive Developmental Disorder.

About 10 percent of children with autism have genetic mutations believed to directly lead to the disorder. In others, common gene variations create small increases in susceptibility. When a child has an accumulation of quantitative traits, that child will be diagnosed with autism or a related disorder, but siblings can have subtle quantitative traits without reaching the threshold for a diagnosis.

"It's not an all-or-nothing condition," Constantino says. "When we look only at the full syndrome for inherited traits, we miss a lot of individuals who may have genetic susceptibility and subtle aspects of autism. In other words, many siblings of children on the spectrum have significant, subclinical traits of autism, but, for whatever reason, they never actually develop the disorder."

Constantino, the Blanche F. Ittleson Professor of Psychiatry and Pediatrics and director of the William Greenleaf Eliot Division of Child and Adolescent Psychiatry at Washington University, compares it to the difference between insulin resistance and diabetes. Not all people with insulin resistance are diabetic, and some never develop diabetes, but they are at a much higher risk for the disease. The same thing is true for autism, he says.

One striking finding was that among siblings, 20 percent had received a diagnosis of language delay or speech problems early in life. And half of them had particular qualities of speech that are autistic in nature. So the investigators believe that what is aggregating in these families is more than just the full syndrome of autism. In about 11 percent of families, more than one sibling has autism, and in many others, these subtle, quantitative signs and symptoms indicate many undiagnosed children are affected as well.

That's important, Constantino says, because in studies involving DNA tests, brain imaging or biological comparisons between affected children and their unaffected siblings, researchers traditionally assume undiagnosed children are unaffected. But this study would suggest that's not necessarily the case.

The study also found quantitative traits of autism tended to occur more frequently in children from families with more than one fully affected child. In families with only one child with autism, it was much more common for that child's siblings not to have any evidence of quantitative traits. And the study also found that it was less common for siblings to be affected with those traits than for non-identical twins -- a finding suggested by pooling the results of this study with a recent twin study from Law and his colleagues at Kennedy Krieger Institute that used exactly the same methods and the same family registry.

Law and Constantino say their findings provide insight into the inheritance patterns of autism and its associated traits. Although those severely affected with autism spectrum disorders seldom have their own children, those who are affected with quantitative traits of autism usually grow up to be parents themselves, and understanding how best to predict patterns of transmission in families and identifying the specific genetic and environmental factors underlying those patterns could offer hope for new, more effective interventions that could be used early in the lives of affected children, Constantino says.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Washington University School of Medicine.

Journal Reference:

Constantino JN, Zhang Y, Frazier T, Abbacchi AM, Law P. Sibling recurrence and the genetic epidemiology of autism. The American Journal of Psychiatry, Vol. 167 (11), published online Oct. 1, 2010 DOI: 10.1176/appi.ajp.2010.09101470

Note: If no author is given, the source is cited instead.

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Type 2 diabetes and insulin use associated with colorectal cancer in men, study finds

ScienceDaily (Oct. 18, 2010) ? There is an association between type 2 diabetes mellitus and colorectal cancer (CRC) among men, but not women, according to a new study in Gastroenterology, the official journal of the American Gastroenterological Association (AGA) Institute.

In 2000, the prevalence of type 2 diabetes was approximately 171 million worldwide, and 366 million people are projected to have the disease by 2030. Obesity, western-style diet and lack of physical activity are established risk factors for CRC. Hyperglycemia and hyperinsulinemia, which are especially pronounced during the early stages of type 2 diabetes, have been proposed as mediators for the association between CRC and type 2 diabetes. Although it is known that type 2 diabetes is associated with an increased risk of CRC, it is not clear if this association varies by gender or other factors.

"While our study supports an association of type 2 diabetes with colorectal cancer incidence among men, our results also suggest that insulin use is associated with a slight, but not a substantially increased, risk of colorectal cancer among men with type 2 diabetes," said Peter T. Campbell, PhD, of the American Cancer Society and lead author of this study. "Prevention strategies should emphasize adherence to guidelines intended for the general population such as smoking cessation, weight management, exercise and regular early detection exams."

In the final study of 73,312 men and 81,663 women, 1,567 men (227 with type 2 diabetes) and 1,242 women (108 with type 2 diabetes) were diagnosed with colon or rectal cancer by 2007. Among men, type 2 diabetes was associated with increased risk of incident CRC compared to not having type 2 diabetes. CRC risk was higher for those participants with type 2 diabetes regardless of whether or not they used insulin.

Among women, type 2 diabetes and insulin use were not associated with CRC risk. These findings support recent observations that the association may be more prominent in men than in women, and raise the possibility of a stronger association among individuals with a family history of CRC. This finding could have clinical relevance if confirmed by other large studies. The authors speculate that the lack of an association between type 2 diabetes and CRC risk among women might relate to improved glucose control among women with type 2 diabetes in recent years.

Participants were selected from the Cancer Prevention Study II Nutrition Cohort, a prospective study of cancer incidence. In 1992 or 1993, 184,194 adult participants completed a detailed, self-administered questionnaire. Follow-up questionnaires were sent in 1997 and every two years thereafter.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Gastroenterological Association, via EurekAlert!, a service of AAAS.

Note: If no author is given, the source is cited instead.

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Study to determine whether leptin helps type 1 diabetes patients

ScienceDaily (Oct. 11, 2010) ? A clinical trial at UT Southwestern Medical Center aims to determine whether adding the hormone leptin to standard insulin therapy might help rein in the tumultuous blood-sugar levels of people with type 1 (insulin-dependent) diabetes.

This is the first type 1 diabetes treatment trial involving leptin, which is naturally produced by fat cells and involved in body-weight regulation. For this study, UT Southwestern researchers will be using metreleptin, a slightly modified form of the hormone that has been well-tolerated in other clinical trials.

"Leptin has been very effective in improving diabetes in patients with lipodystrophies who have extreme lack of body fat, and recently leptin therapy has helped improve blood sugar control in animal models of type 1 diabetes," said Dr. Abhimanyu Garg, professor of internal medicine and principal investigator of the trial. "Although we have no assurances that this will work in humans, we hope that the addition of leptin will be beneficial to patients with type 1 diabetes."

The phase 1 study also is designed to evaluate the safety and tolerability of adding leptin to a diabetes treatment regimen.

In type 1 diabetes, formerly known as juvenile-onset diabetes, the pancreatic beta cells that produce insulin are destroyed by an autoimmune process. Type 1 diabetics must regiment their diets and take insulin multiple times a day to control blood-sugar levels and prevent diabetic coma. The autoimmune disease, for which there is no cure, affects about 1 million people in the U.S.

Insulin treatment has been the gold standard for type 1 diabetes since its discovery in 1922. The laboratory of Dr. Roger Unger, professor of internal medicine at UT Southwestern, previously found that insulin's benefit resulted from its suppression of glucagon, a hormone produced by the pancreas that raises blood-sugar levels in healthy individuals.

More recently, Dr. Unger's lab, using mouse models of type 1 diabetes, found that administering leptin instead of insulin resulted in better management of blood-sugar variability and lipogenesis, the conversion of simple sugars into fatty acids.

For the clinical study, 12 to 15 participants will add leptin twice a day to their standard insulin therapy over a five-month period. The trial will last a total of seven months and will include 11 visits -- an initial screening, four inpatient visits and six outpatient evaluations -- to UT Southwestern. The first inpatient visit will last a minimum of four days; the others will take two days each.

To be eligible for the initial screening, prospective trial participants must be between 18 and 50 years of age, have a body mass index (BMI) less than 25, and have been diagnosed with type 1 diabetes. BMI is a weight-to-height ratio commonly used in doctors' offices to gauge obesity. A normal BMI is between 18.5 and 25.

Dr. Gregory Clark, assistant professor of internal medicine and a trial investigator, said one incentive to take part in the trial is that participants might lose weight.

"Leptin is known to decrease appetite, so it's likely that participants won't be as hungry," he said. "We hope that the addition of leptin also reduces the blood levels of cholesterol, which increase the risk of coronary heart disease, one of the long-term complications of diabetes."

Dr. Unger emphasized that the goal is not to find a replacement for insulin, but to obtain stable glucose levels, something that has eluded monotherapy with insulin. The theory is that adding leptin might allow a substantial reduction in insulin dose and lower the risk of low blood glucose levels.

"If it works in humans as well as it does in rodents, it will be a major step forward," said Dr. Unger. "In rodents, it eliminated the wide swings in glucose that occur with insulin alone and lowered indices of cholesterol formation. The hope is that it will improve both short- and long-term quality of life for patients with type 1 diabetes."

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by UT Southwestern Medical Center.

Note: If no author is given, the source is cited instead.

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Putting on the pounds after weight loss? Hit the gym to maintain health gains

ScienceDaily (Sep. 23, 2010) ? Although obesity is a major risk factor for disease, much of the threat may be associated with the metabolic (or cardiometabolic) syndrome, a cluster of risk factors related to diabetes and heart disease. Losing weight can improve health and reduce many of these risk factors. However, many people struggle to keep the weight off long-term. Now, researchers at the University of Missouri have found that people who perform resistance training while regaining weight can help maintain strides in reducing their risks for chronic disease.

"Long-term weight loss maintenance is uncommon without regular exercise," said Shana Warner, a doctoral student in the MU Department of Nutrition and Exercise Physiology. "It is very important to address other things that can be done to maintain health as opposed to focusing solely on body weight. Our research indicates that following a consistent exercise program can help maintain certain aspects of metabolic health, even in those who experience weight regain."

The study consisted of two phases, meant to simulate real-life weight loss and regain. In the first phase, overweight and obese participants lost 4 to 6 percent of their initial body weight by following an eight to 12-week regimen of diet and aerobic exercise. In the second phase, participants regained 50 percent of the weight they had lost. During the regain phase, participants performed 45 minutes of supervised resistance training three times each week.

Researchers found that weight training during weight regain has a positive effect on health, which can reduce the risk of diabetes, heart disease and other diseases. Participants maintained improvements acquired through weight loss in cardiorespiratory fitness, body fat percentage, systolic blood pressure and other factors. In addition, participants significantly increased strength and lean body mass. However, they did not maintain reductions in visceral abdominal fat: the fat deposited around internal organs.

This study furthers research completed earlier this year, in which MU researchers found that participation in aerobic exercise while regaining weight counters many of the risk factors associated with chronic diseases. These studies are some of the first to consider the effects of exercise on people's health who regain weight they recently lost.

The study, "The Effects of Resistance Training on Metabolic Health with Weight Regain," was published this year in The Journal of Clinical Hypertension. Researchers from the Department of Nutrition and Exercise Physiology (part of the College of Human Environmental Sciences, the School of Medicine and the College of Agriculture, Food and Natural Resources) completed the study in conjunction with MU scientists in the Department of Internal Medicine, the Department of Medical Pharmacology and Physiology, and the Harry S. Truman VA Memorial Hospital.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Missouri-Columbia.

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Key action of a gene linked to both Alzheimer's disease and type 2 diabetes identified

ScienceDaily (Sep. 29, 2010) ? A research team led by Mount Sinai School of Medicine has identified the mechanism behind a single gene linked to the causes of both Alzheimer's disease and Type 2 diabetes. The data show that a gene for a protein called SorCS1, which can cause Type 2 diabetes, impacts the accumulation of amyloid-beta (Abeta) in the brain. Abeta plays a key role in the development of Alzheimer's disease.

The study is published in the September 29th issue of the Journal of Neuroscience.

Sam Gandy, MD, PhD, the Mount Sinai Professor in Alzheimer's Disease Research, Professor of Neurology and Psychiatry, and Associate Director of the Alzheimer's Disease Research Center at Mount Sinai School of Medicine, led the study, together with first author Rachel Lane, PhD, a postdoctoral researcher in Gandy's Lab. Lane and Gandy analyzed both the brains of mice genetically engineered to be deficient in SorCS1 as well as cells engineered to express high levels of SorCS1. They found an increased level of Abeta in SorCS1-deficient mice, and low levels of Abeta in the cells overexpressing SorCS1.

"We knew that Type 2 diabetes could increase the risk for Alzheimer's disease, but we were not sure how that risk was caused or whether that diabetes risk would impact Abeta levels in the brain," said Dr. Gandy. "These results elucidate a common mechanism between diabetes and Alzheimer's and will bring us a step closer to identifying effective treatments for both diseases."

The researchers were also interested to find that the SorCS1-deficient mice had decreased levels of the protein Vps35, which was linked to Alzheimer's by Scott Small, MD, Associate Professor of Neurology, Columbia University College of Physicians and Surgeons, who co-authored the new study with Gandy. They propose that depleted SorCS1 may cause Vps35 levels to also decrease, leading to further accumulation of Abeta in mice. Further studies are required to better understand the impact of SorCS1 on Vps35 levels.

SorCS1 deficiency has been linked to Type 2 diabetes by geneticist Alan Attie, PhD, Professor of Biochemistry, University of Wisconsin, who also co-authored the new study. Rudolph E. Tanzi, PhD, Joseph P. and Rose F. Kennedy Professor of Neurology and Director of Genetics and Aging Research Unit at Harvard Medical School also contributed genetic data to the new study. Now that Dr. Gandy and his team have connected the same protein to increased Abeta levels, they can evaluate this protein and the family of proteins of which it is a member as drug targets for the treatment of both diseases.

"Alzheimer's and Type 2 diabetes are reaching epidemic levels, afflicting millions of Americans," said Dr. Gandy. "Their risk factors overlap and include high cholesterol, obesity, vascular disease, and inflammation. Now that we have a better understanding of where the connection between these two diseases originates on a molecular level, the next step is to develop drugs that will help reduce their devastating impact. Such drugs will require much more research, but having this new target helps put us on the right track."

The study was supported by the Cure Alzheimer's Fund, the National Institute on Aging, and the National Institute of Diabetes and Digestive and Kidney Diseases.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by The Mount Sinai Hospital / Mount Sinai School of Medicine, via EurekAlert!, a service of AAAS.

Journal Reference:

R. F. Lane, S. M. Raines, J. W. Steele, M. E. Ehrlich, J. A. Lah, S. A. Small, R. E. Tanzi, A. D. Attie, S. Gandy. Diabetes-Associated SorCS1 Regulates Alzheimer's Amyloid-β? Metabolism: Evidence for Involvement of SorL1 and the Retromer Complex. Journal of Neuroscience, 2010; 30 (39): 13110 DOI: 10.1523/JNEUROSCI.3872-10.2010

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T cell discovery shows promise for Type 1 diabetes treatment

ScienceDaily (Oct. 7, 2010) ? A research team from the University of British Columbia and the Child & Family Research Institute (CFRI) at BC Children's Hospital has identified the role of a type of T cell in type 1 diabetes that may lead to new treatment options for young patients.

Also known as juvenile diabetes, type 1 diabetes is an autoimmune disease primarily affecting children and young adults. In patients with type 1 diabetes, the body attacks itself by destroying insulin-producing cells in the pancreas that regulate glucose, or blood sugar.

Led by Rusung Tan, a Pathology professor in the UBC Faculty of Medicine and co-head of the Immunity in Health and Disease research cluster at CFRI, the research team has identified the increased presence of Th17 cells, a type of T cell discovered in 2005, in children newly diagnosed with type 1 diabetes.

"T cells are white blood cells and key members of the immune system that control infections," says Tan, who is also a member of the Department of Pathology & Laboratory Medicine at BC Children's Hospital and a senior scholar of the Michael Smith Foundation for Health Research. "In healthy individuals, Th17 cells provide a strong defence against bacteria and viruses by guiding the immune system to strongly attack infected targets within our bodies."

However, Th17 has been associated with other autoimmune diseases such as Crohn's disease, which suggests they can play a harmful role. Treatments designed to block Th17 cells are in clinical trials for these diseases.

"The elevated levels of Th17 cells in type 1 diabetes patients suggest that these cells may also play a key role in the early development of this disease in young patients," says Tan. "This discovery opens the door to new treatments for childhood diabetes that target Th17 cells."

The findings are published in the current issue of the Journal of Immunology. The team consists of researchers from UBC, CFRI and the Vancouver Coastal Health Research Institute. At the time of the study, lead author Dr. Ashish Marwaha was a master's student at UBC and CFRI. The study was supported by grants from the Canadian Institutes of Health Research and the Juvenile Diabetes Research Foundation.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of British Columbia.

Journal Reference:

A. K. Marwaha, S. Q. Crome, C. Panagiotopoulos, K. B. Berg, H. Qin, Q. Ouyang, L. Xu, J. J. Priatel, M. K. Levings, R. Tan. Cutting Edge: Increased IL-17-Secreting T Cells in Children with New-Onset Type 1 Diabetes. The Journal of Immunology, 2010; 185 (7): 3814 DOI: 10.4049/jimmunol.1001860

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Epigenomics discovery yields new information about fat cells

ScienceDaily (Sep. 30, 2010) ? By creating a "map" of histone modifications in fat cells, investigators have discovered two new factors that regulate fat formation, a key step on the road to better understanding obesity, diabetes and other metabolic disorders. Led by investigators at Beth Israel Deaconess Medical Center (BIDMC) and the Broad Institute, the study appears in the October 1 issue of the journal Cell.

"These findings help to demonstrate the power of epigenomic mapping when it comes to gleaning key insights into fat cell formation," explains senior author Evan Rosen, MD, PhD, an investigator in the Department of Endocrinology, Diabetes and Metabolism at BIDMC and Associate Professor of Medicine at Harvard Medical School. Fat cells, also called adipocytes, play an integral role in regulating metabolism by controlling lipid and glucose balance.

To better understand how adipocytes control the genes that impart the specialized functions of these cells, the researchers turned to epigenomics, and specifically the arm of epigenomics known as histone modifications.

"Deoxyribonucleic acid [DNA] is tightly wound around proteins called histones, which, over time, can accumulate chemical modifications or 'marks,'" explains Rosen. "These marks instruct the cell which genes to turn on and off, and by mapping these modifications, we can gain important insights that would be unattainable through traditional means."

Unlike previous investigations, which examined fat cells at a single static time point, this new study mapped several histone modifications throughout the course of the fat cell development, using a technique called chromatin immunoprecipitation followed by massively parallel sequencing or ChIP-Seq. This method relies on the ability to sequence tens of millions of short stretches of DNA (in this case DNA bound to modified histones) and then to reassemble results into a coherent genome. In addition to following these histone markers across time, the scientists also mapped the markers across species.

"Our study looked at both mouse cells and human cells," explains Rosen. "This is key because each cell type can accumulate histone marks that actually have nothing to do with fat cell differentiation. Consequently, by comparing two different cell models, we were able to sift through and focus on the epigenetic marks that appeared in both cell types."

What emerged was a "core" set of histone modifications that formed the basis of a "road map" for the scientists to follow. And, by using this new map, the investigators discovered two transcription factors (proteins that control the copying of DNA into RNA) that regulate fat cell formation.

"We found two new transcription factors -- SRF and PLZF -- involved in fat cell development," explains Rosen. "We have essentially demonstrated how an epigenomic 'road map' can be used to identify biology that could not have been predicted through any other means." Subsequent experiments confirmed the proteins' roles in fat cell development: When either the SRF or the PLZF protein was decreased, fat cells generated at a faster rate and, conversely, when the amount of either protein was increased, fat cell development ceased.

"Although these particular studies were focused on the development of fat cells, we have reason to think that SRF and PLZF may be involved in the workings of mature fat cells as well," notes Rosen, adding that these new findings, therefore, have the potential to impact metabolic diseases such as obesity and Type 2 diabetes.

"The huge costs of obesity and metabolic disease, both in terms of health and from a financial standpoint, are making adipocyte biology increasingly important," he adds. "With these new findings we now have a better understanding of normal fat cell development, and going forward, we can compare normal fat cells to fat cells in disease states. If we can better understand why fat cells behave as they do, then we can work to develop therapies for obesity or diabetes."

This study was funded by grants from the National Institutes of Health and the American Diabetes Association.

Co-first authors of the study are Zhao Xu of BIDMC and Tarjei Mikkelsen of the Broad Institute. Coauthors include Broad Institute investigators Xiaolan Zhang, Li Wang and Eric Lander; and Jeffrey Gimble of the Pennington Biomedical Research Center, Louisiana University System.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Beth Israel Deaconess Medical Center.

Journal Reference:

Tarjei S. Mikkelsen, Zhao Xu, Xiaolan Zhang, Li Wang, Jeffrey M. Gimble, Eric S. Lander, Evan D. Rosen. Comparative Epigenomic Analysis of Murine and Human Adipogenesis. Cell, Volume 143, Issue 1, 156-169, 1 October 2010 DOI: 10.1016/j.cell.2010.09.006

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Eating mostly whole grains, few refined grains linked to lower body fat

ScienceDaily (Oct. 20, 2010) ? People who consume several servings of whole grains per day while limiting daily intake of refined grains appear to have less of a type of fat tissue thought to play a key role in triggering cardiovascular disease and type 2 diabetes, a new study suggests.

Researchers at the Jean Mayer USDA Human Nutrition Researcher Center on Aging (USDA HNRCA) at Tufts University observed lower volumes of Visceral Adipose Tissue (VAT) in people who chose to eat mostly whole grains instead of refined grains.

"VAT volume was approximately 10 % lower in adults who reported eating three or more daily servings of whole grains and who limited their intake of refined grains to less than one serving per day," says first author Nicola McKeown, PhD, a scientist with the Nutritional Epidemiology Program at the USDA HNRCA. "For example, a slice of 100% whole wheat bread or a half cup of oatmeal constituted one serving of whole grains and a slice of white bread or a half cup of white rice represented a serving of refined grains."

McKeown and colleagues, including senior author Caroline S. Fox, MD, MPH, medical officer at The Framingham Heart Study of the National Heart Lung and Blood Institute (NHLBI), examined diet questionnaires submitted by 2,834 men and women enrolled in The Framingham Heart Offspring and Third Generation study cohorts. The participants, ages 32 to 83, underwent multidetector-computed tomography (MDCT) scans, to determine VAT and subcutaneous adipose tissue (SAT) volumes.

Visceral fat surrounds the intra-abdominal organs while subcutaneous fat is found just beneath the skin. "Prior research suggests visceral fat is more closely tied to the development of metabolic syndrome, a cluster of risk factors including hypertension, unhealthy cholesterol levels and insulin resistance that can develop into cardiovascular disease or type 2 diabetes," explains co-author Paul Jacques, DSc, director of the Nutritional Epidemiology Program at the USDA HNRCA and a professor at the Friedman School of Nutrition Science and Policy at Tufts. "Not surprisingly, when we compared the relationship of both visceral fat tissue and subcutaneous fat tissue to whole and refined grain intake, we saw a more striking association with visceral fat. The association persisted after we accounted for other lifestyle factors such as smoking, alcohol intake, fruit and vegetable intake, percentage of calories from fat and physical activity."

Published online Sept. 29 by The American Journal of Clinical Nutrition, the present study builds on prior research that associates greater whole grain intake with reduced risk of metabolic syndrome and insulin resistance. "However, because these studies are observational, future research that specifically investigates whole grain intake and body fat distribution in a larger, more diverse study population is needed to identify the mechanism that is driving this relationship," Jacques adds.

Additionally, in the present study, the authors observed that participants who consumed, on average, three daily servings of whole grains but continued to eat many refined grains did not demonstrate lower VAT volume. "Whole grain consumption did not appear to improve VAT volume if refined grain intake exceeded four or more servings per day," says McKeown, who is also an assistant professor at the Friedman School. "This result implies that it is important to make substitutions in the diet, rather than simply adding whole grain foods. For example, choosing to cook with brown rice instead of white or making a sandwich with whole grain bread instead of white bread."

This study is funded by the National Heart Lung and Blood Institute (NHLBI), the USDA, and a research grant from the General Mills Bell Institute of Health and Nutrition.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Tufts University, Health Sciences.

Journal Reference:

N. M. McKeown, L. M. Troy, P. F. Jacques, U. Hoffmann, C. J. O'Donnell, C. S. Fox. Whole- and refined-grain intakes are differentially associated with abdominal visceral and subcutaneous adiposity in healthy adults: the Framingham Heart Study. American Journal of Clinical Nutrition, 2010; DOI: 10.3945/ajcn.2009.29106

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Got fish? Nutrition studies explore health benefits

ScienceDaily (Oct. 18, 2010) ? Some of America's most popular fish--salmon and albacore tuna, for example--are rich in healthful natural compounds known as omega-3 fatty acids. Ongoing studies by U.S. Department of Agriculture (USDA) chemist Darshan S. Kelley and co-investigators are helping uncover new details about how these fish-oil components help protect us from chronic diseases.

Kelley is with the USDA Agricultural Research Service (ARS) Western Human Nutrition Research Center at the University of California-Davis. ARS is the USDA's principal intramural scientific research agency.

In an early study with laboratory mice, Kelley and colleagues investigated the interplay of two omega-3 fatty acids from fish oil-DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid)-and a third fatty acid, CLA (as trans-10, cis-12 CLA) found in some dietary supplements.

Kelley's 8-week test with 50 laboratory mice indicated that DHA protected the animals against two harmful side effects of CLA: CLA-induced insulin resistance and CLA-induced non-alcoholic fatty-liver disease. In contrast, EPA offered only partial protection against CLA-induced non-alcoholic fatty liver disease and provided no protection against insulin resistance.

If untreated, insulin resistance can lead to diabetes. An estimated 36 million to 57 million Americans are insulin-resistant. Non-alcoholic fatty liver disease can result in cirrhosis of the liver or liver cancer. The study appeared in a 2007 issue of Metabolic Syndrome and Related Disorders.

In related work, published in a 2009 article in Current Opinion in Clinical Nutrition and Metabolic Care, Kelley and University of California-Davis graduate student Dawn Fedor reviewed results from several dozen EPA and DHA studies. In their review, the scientists indicate that findings reported in the past decade have been inconsistent in regard to the effects of EPA and DHA on insulin resistance in human volunteers.

Their review underscores the need for new investigations, with larger numbers of volunteers. Kelley, for example, would like to determine whether DHA can improve the ability of adult, pre-diabetic volunteers to use insulin efficiently, and thus help delay onset of diabetes. Such research might reveal more about the mechanisms of action that DHA and EPA use, the sites upon which they act in the human body, and the genes that control these mechanisms.

Read more about the research in the October 2010 issue of Agricultural Research magazine, available online at: http://www.ars.usda.gov/is/AR/archive/oct10/nutrition1010.htm.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by USDA/Agricultural Research Service.

Note: If no author is given, the source is cited instead.

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Pilot study demonstrates safety of diabetes medication for patients with Alzheimer's disease

ScienceDaily (Sep. 14, 2010) ? A pilot study suggests the diabetes medication pioglitazone is generally well tolerated and may warrant further study as a treatment for patients with Alzheimer's disease, according to a report posted online that will appear in the January 2011 print issue of Archives of Neurology, one of the JAMA/Archives journals.

"Alzheimer's disease is an immense and growing public health problem," the authors write as background information in the article. "Although prescription drug therapy for the symptoms of Alzheimer's disease has been available since 1993, these agents do not fundamentally alter the pathological expression of the disease or its progressive course. The failure of several recent treatment trials directed at the beta-amyloid peptide, a key pathological correlate of Alzheimer's disease, suggests a need to explore alternative approaches to Alzheimer's disease treatment that are not focused on beta-amyloid metabolism."

Another potential therapeutic target for the treatment of Alzheimer's disease is the nuclear receptor peroxisome proliferator-activated receptor gamma, PPAR-gamma, which acts to regulate glucose and lipid metabolism. A class of drugs known as thiazolidinediones, originally developed to reduce insulin resistance in patients with type 2 diabetes, are potent agonists (trigger a response) of PPAR-gamma. To evaluate the safety of one of these medications, pioglitazone, in patients without diabetes but with Alzheimer's disease, David S. Geldmacher, M.D., of the University of Virginia Health System, Charlottesville, and colleagues conducted an 18-month, double-blind, placebo-controlled randomized controlled trial. Twenty-nine patients without diabetes but with probable Alzheimer's disease were randomly assigned to receive either pioglitazone (titrated to 45 milligrams daily) or matching placebo, along with 200 international units of vitamin E.

A total of 25 patients (12 taking pioglitazone and 13 taking placebo) completed 18 months of therapy. Two of the patients who discontinued participation in the study early had a change in caregivers status, and two withdrew their consent; no discontinuations were attributed to adverse events.

Peripheral edema, swelling of the legs and feet, was the main adverse event, affecting four patients in the pioglitazone group (28.6 percent) compared with none in the placebo group. "This is consistent with the known adverse event profile of pioglitazone," the authors write. "No group differences in laboratory measures were identified."

"No significant treatment effect was observed on exploratory analysis of clinical efficacy," they continue, noting that the study was not intended to determine treatment efficacy. Based on the results of sample size analyses, the researchers estimate that a study would need to enroll between 155 and 340 participants randomly assigned to placebo or pioglitazone to find treatment effects for patients with Alzheimer's disease. Given that trials leading to Food and Drug Administration approval of current drugs typically enrolled 250 to 500 patients, and that several ongoing trials will enroll more than 1,000, further studies to assess the clinical efficacy of pioglitazone would be feasible.

"Disappointing results of treatment trials based on the amyloid hypothesis, and the reasonable degree of safety identified in this trial, suggest that exploratory studies of thiazolidinediones remain warranted," the authors conclude. "Future studies of this class should focus on earlier stages of disease progression and be augmented by biomarkers, such as nuclear imaging techniques, to measure changes in microglial activation associated with treatment."

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by JAMA and Archives Journals.

Journal Reference:

David S. Geldmacher; Thomas Fritsch; McKee J. McClendon; Gary Landreth. A Randomized Pilot Clinical Trial of the Safety of Pioglitazone in Treatment of Patients With Alzheimer Disease. Arch Neurol, 2010; 0 (2010): archneurol. 2010. 229 [link]

Note: If no author is given, the source is cited instead.

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Biologists discover biochemical link between biological clock and diabetes

ScienceDaily (Sep. 20, 2010) ? Biologists have found that a key protein that regulates the biological clocks of mammals also regulates glucose production in the liver and that altering the levels of this protein can improve the health of diabetic mice.

Their discovery, detailed in this week's advanced online publication of the journal Nature Medicine, provides an entirely new biochemical approach for scientists to develop treatments for obesity and type 2 diabetes. It also raises the interesting possibility that some of the rise in diabetes in the U.S. and other major industrialized countries could be a consequence of disturbances in sleep-wake cycles from our increasingly around-the-clock lifestyles.

"We know that mice that don't have good biological clocks tend to develop diabetes and obesity," said Steve Kay, Dean of the Division of Biological Sciences at UC San Diego and one of the lead authors of the research study. "And we know that mice that have developed diabetes and obesity tend not to have very good biological clocks. This reciprocal relationship between circadian rhythm and the maintenance of a constant supply of glucose in the body had been known for some time. But what we found that's so significant is that a particular biological clock protein, cryptochrome, is actually regulating how the hormone that regulates glucose production in the liver works in a very specific way."

"We used to think that our metabolism was regulated primarily by hormones that are released from the pancreas during fasting or feeding. This work shows that the biological clock determines how well these hormones work to regulate metabolism," says Marc Montminy, a professor in the Clayton Foundation Laboratories for Peptide Biology at the Salk Institute for Biological Studies. "The study may explain why shift workers, whose biological clocks are often out of kilter, also have a greater risk of developing obesity and insulin resistance."

Cryptochrome was first discovered by scientists as a key protein regulating the biological clocks of plants. It was later found to have the same function in fruit flies and mammals. But its role in regulating glucose production in the liver came as a complete surprise to the UCSD and Salk team, which included scientists from the Genomics Institute of the Novartis Research Foundation in San Diego, the University of Memphis and the Chinese Academy of Sciences in Shanghai.

"What was incredibly surprising is that cryptochrome has a new function that nobody had predicted," said Eric Zhang, the first author of the study and a researcher in Kay's UCSD laboratory. "Until now, cryptochrome had been known as a protein inside the nucleus of mammalian cells that switches genes on and off in a rhythmic way. What we showed was that cryptochrome has a role outside the nucleus as well."

That additional function of cryptochrome in mammalian cells, the scientists discovered, is to regulate a process known as "gluconeogenesis," in which our bodies supply a constant stream of glucose to keep our brain and the rest of our organs and cells functioning. When we're awake and eating, sufficient glucose is supplied to our bloodstream. But when we're asleep or fasting, glucose needs to be synthesized from the glycogen stored in our liver to keep our glucose levels up.

"That is how our energy metabolism evolved to function in concert with our diurnal activity, or in the case of the mice, their nocturnal activity," said Kay. "This molecular mechanism involving cryptochrome presumably evolved to coordinate our energy metabolism with our daily activity and feeding levels. So could some instances of diabetes be the result of a faulty circadian clock? And if that's the case, can we find ways of fixing the clock to treat this disease? Such an approach would be a whole new way of thinking about how to develop new treatments for diabetes."

In their study, the scientists found evidence that such an approach would be feasible. "Our experiments show very nicely that modulating cryptochrome levels in the liver of mice can actually give diabetic animals a benefit," Kay added.

The researchers discovered cryptochrome's role in gluconeogenesis while studying how a signaling molecule known as cyclic AMP interacted with the biological clock.

"It had been known for some time now that there was a connection between cyclic AMP signaling and circadian rhythm regulation and that's where we started," said Kay, "by asking the question: How are those two connected?"

Zhang and his UCSD colleagues conducted a series of experiments that found that the production of the next step after cyclic AMP, a protein called Creb, ebbed and flowed rhythmically in the livers of mice. That led the scientists to their initial discovery that cryptochrome was regulating the production of Creb in the liver.

In their studies with fasting and insulin-resistant mice at the Salk Institute, the scientists found that cryptochrome was regulating how the hormone glucagon, which controls gluconeogenesis, works in a very specific way. By controlling the production of cyclic AMP, crytochrome regulates the activity of Creb in the liver. In this way, the production of glucose in the liver is tied through our daily eating, sleeping and fasting activities through the biological clock.

The scientists say their discovery may open up a whole new area of research into how cryptochrome may be regulating other cell functions outside the nucleus.

"There's a wide role that the biological clock may be playing in influencing other hormones, not just glucagon, that are important for metabolism," said Kay.

In addition, studies on human populations have found links between disturbances in the biological clock, such as shift work and chronic jet lag, and the propensity to develop certain kinds of cancers as well as diabetes. Because of this, the scientists plan to continue their research into cryptochrome, looking for compounds that may enhance or diminish the activity of this critical biological clock protein.

The research was funded by grants from the National Institutes of Health. Other co-authors of the paper include Tsuyoshi Hirota, Dmitri A Nusinow, Pagkapol Pongsawakul and Andrew Liu of UCSD's Division of Biological Sciences; David Brenner and Yuzo Kodama of the UCSD School of Medicine; Yi Liu, Renaud Dentin and Severine Landais of The Salk Institute; and Xiujie Sun of the Chinese Academy of Sciences.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of California -- San Diego. The original article was written by Kim McDonald.

Journal Reference:

Eric E Zhang, Yi Liu, Renaud Dentin, Pagkapol Y Pongsawakul, Andrew C Liu, Tsuyoshi Hirota, Dmitri A Nusinow, Xiujie Sun, Severine Landais, Yuzo Kodama, David A Brenner, Marc Montminy, Steve A Kay. Cryptochrome mediates circadian regulation of cAMP signaling and hepatic gluconeogenesis. Nature Medicine, 2010; DOI: 10.1038/nm.2214

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Press Release - 2010 Guidelines for CPR and Emergency Cardiovascular Care

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Your Name:Your Email:Recipient's Name:Recipient's Email:Close2010 Guidelines for CPR and Emergency Cardiovascular CareOct 18, 2010 This press release is an announcement submitted by American Heart Assoiciation, and was not written by Diabetes Health.

The 2010 Guidelines for CPR and Emergency Cardiovascular Care are here! What are the new changes? Watch the YouTube video and learn more.

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