Showing posts with label researchers. Show all posts
Showing posts with label researchers. Show all posts

Thursday, December 16, 2010

Researchers Find Link Between Sugar, Diabetes And Aggression


Main Category: Diabetes
Also Included In: Psychology / Psychiatry
Article Date: 01 Dec 2010 - 3:00 PST window.fbAsyncInit = function() { FB.init({ appId: 'aa16a4bf93f23f07eb33109d5f1134d3', status: true, cookie: true, xfbml: true, channelUrl: 'http://www.medicalnewstoday.com/scripts/facebooklike.html'}); }; (function() { var e = document.createElement('script'); e.async = true; e.src = document.location.protocol + '//connect.facebook.net/en_US/all.js'; document.getElementById('fb-root').appendChild(e); }()); email icon email to a friend ? printer icon printer friendly ? write icon opinions ?
4 and a half stars1 star
A spoonful of sugar may be enough to cool a hot temper, at least for a short time, according to new research.

A study found that people who drank a glass of lemonade sweetened with sugar acted less aggressively toward a stranger a few minutes later than did people who consumed lemonade with a sugar substitute.

Researchers believe it all has to do with the glucose, a simple sugar found in the bloodstream that provides energy for the brain.

"Avoiding aggressive impulses takes self control, and self control takes a lot of energy. Glucose provides that energy in the brain," said Brad Bushman, co-author of the study and professor of communication and psychology at Ohio State University.

"Drinking sweetened lemonade helped provide the short-term energy needed to avoid lashing out at others."

The finding is more than just a medical curiosity, Bushman said. In two published papers, he and his colleagues did several studies showing that people who have trouble metabolizing, or using, glucose in their bodies show more evidence of aggression and less willingness to forgive others.

The problem is that the number of people who have trouble metabolizing glucose -- mainly those with diabetes -- is rising rapidly. From 1980 through 2008, the number of Americans with diabetes has more than tripled (from 5.6 million to 18.1 million).

"Diabetes may not only harm yourself -- it is bad for society," Bushman said. "The healthy metabolism of glucose may contribute to a more peaceful society by providing people with a higher level of energy for self-control."

Bushman conducted the lemonade study with C. Nathan DeWall and Timothy Deckman of the University of Kentucky and Matthew Gailllot of SUNY-Albany. It appears online in the journal Aggressive Behavior and will be published in a future print edition.

In the study, 62 college students fasted for three hours to reduce glucose instability. They were told they were going to participate in a taste-test study, and then have their reaction times evaluated in a computerized test against an opponent.

Half of the participants were given lemonade sweetened with sugar, while the others were given lemonade with a sugar substitute.

After waiting eight minutes to allow the glucose to be absorbed in their bloodstream, the participants took part in the reaction test.

The reaction test has been used and verified in other studies as a way to measure aggression. Participants were told they and an unseen partner would press a button as fast as possible in 25 trials, and whoever was slower would receive a blast of white noise through their headphones.

At the beginning of each trial, participants set the level of noise their partner would receive if they were slower. The noise was rated on a scale of 1 to 10 -- from 60 decibels to 105 decibels (about the same volume as a smoke alarm).

In actuality, each participant won 12 of the 25 trials (randomly determined).

Aggression was measured by the noise intensity participants chose on the first trial -- before they were provoked by their partner.

Results showed that participants who drank the lemonade sweetened with sugar behaved less aggressively than those who drank lemonade with a sugar substitute. Those who drank the sugar-sweetened beverage chose a noise level averaging 4.8 out of 10, while those with the sugar substitute averaged 6.06.

"To our knowledge, this is the first study to find that boosting glucose levels can reduce actual aggressive behavior," Bushman said.

"To be sure, consuming sugar should not be considered a panacea for curbing aggression. But the results do suggest that people who reportedly "snap" with aggression may need some way to boost their mental energy, so they can override their aggressive impulses."

In two other studies in the same paper, the researchers showed how problems metabolizing glucose may translate to problems on a societal level. Using 2001 data, the researchers found that the diabetes rates for each of the 50 states were linked to violent crime rates. Those states with higher diabetes rates also tended to have higher rates of murder, assault, rape and robbery, even after controlling for poverty rates in each state.

"This suggests that diabetes did not predict violent crime simply because poverty contributes to both diabetes and violent crime," he said. "There is a real correlation between diabetes and violence."

In a separate analysis, the researchers tested whether another medical problem related to glucose metabolism was linked to violence worldwide.

They examined the prevalence, in the populations of 122 countries around the world, of a deficiency in an enzyme called glucose-6-phosphate dehydrogenase. This enzyme is related to glucose metabolism. It is the most common enzyme deficiency in the world, afflicting more than 400 million people.

Countries with higher levels of the disorder also had more violent killings, even outside of war.

"Taken together, these studies offer different types of evidence linking low glucose and other problems metabolizing glucose with aggression and violence," Bushman said.

The findings were further corroborated in another series of studies, published recently in the journal Personality and Individual Differences.

In that paper, Bushman and DeWall, along with University of Kentucky researcher Richard Pond, had participants complete a commonly used and well-accepted checklist that measures the number and severity of Type 2 diabetes symptoms, such as numbness in the feet, shortness of breath at night, and overall sense of fatigue. In three separate studies, the same participants completed different measures of their willingness to forgive others.

On all three measures, people with higher levels of diabetic symptoms were less likely to forgive others for their transgressions.

In a fourth study, participants took part in a prisoner's dilemma game, which is often used to understand how people deal with conflict. In this version, participants had to choose whether to cooperate or compete against an unseen partner in a computer game.

"We were especially interested in how participants responded when their partner behaved in an uncooperative, antagonizing manner when the game began," Bushman said. "Would they forgive their partner or would they refuse to cooperate?"

Results showed that those who scored higher on diabetic symptoms were less likely to forgive an initially uncooperative partner, when compared to those who scored lower on diabetic symptoms.

"These studies are more evidence that diabetic symptoms may cause difficulty in how people relate to each other on a day-to-day basis," Bushman said.

"It's not an excuse diabetes does not mean people have to act aggressively, but it may shed some light on why these behaviors occur."

"With the rate of diabetes increasing worldwide, it is something that should concern all of us."

Source: Ohio State University

Please rate this article:
(Hover over the stars
then click to rate) Bookmark and Share

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

All opinions are moderated before being added.

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:






View the original article here

Monday, November 22, 2010

Circuit Regulating Anti-Diabetic Actions Of Serotonin Uncovered By Researchers


Main Category: Diabetes
Article Date: 11 Nov 2010 - 3:00 PST window.fbAsyncInit = function() { FB.init({ appId: 'aa16a4bf93f23f07eb33109d5f1134d3', status: true, cookie: true, xfbml: true, channelUrl: 'http://www.medicalnewstoday.com/scripts/facebooklike.html'}); }; (function() { var e = document.createElement('script'); e.async = true; e.src = document.location.protocol + '//connect.facebook.net/en_US/all.js'; document.getElementById('fb-root').appendChild(e); }()); email icon email to a friend ? printer icon printer friendly ? write icon opinions ?
not yet ratednot yet rated
New findings by researchers at UT Southwestern Medical Center suggest that serotonin - a brain chemical known to help regulate emotion, mood and sleep - might also have anti-diabetic properties.

The findings, appearing online this week in Nature Neuroscience, also offer a potential explanation for why individuals prescribed certain kinds of anti-psychotic drugs that affect serotonin signaling sometimes have problems with their metabolism, including weight gain and the development of diabetes.

"In this paper, we describe a circuit in the brain that may explain the anti-diabetic actions of serotonin-receptor signaling," said Dr. Joel Elmquist, professor of internal medicine and pharmacology at UT Southwestern and senior author of the study. "This discovery tells us that drugs that affect serotonin action can have anti-diabetic actions independent of body weight and feeding."

For the current study, the researchers engineered a mouse model in which the expression of a serotonin receptor called 5-hydroxytryptamine 2C was blocked throughout the entire body. Without functioning receptors, the mice developed insulin resistance in their livers.

Previous research has implicated these receptors in the brain in the regulation of energy balance and glucose metabolism throughout the body. When activated by serotonin, this receptor also is known to suppress appetite. Until now, however, it was unclear which type of neuron in the brain mediated the effects of serotonin to regulate glucose, or blood sugar, levels.

To find out, the study authors engineered another set of mice in which the same serotonin receptor was blocked everywhere except within a group of brain cells called pro-opiomelanocortin, or POMC, neurons. The POMC neurons, which are found in the hypothalamus, are also known to play an important role in suppressing appetite and inducing weight loss.

The researchers found that when they reactivated the serotonin receptor only in the POMC neurons, the mice no longer displayed insulin resistance in the liver. Restoring the receptor essentially protected the mice from developing the metabolic problems usually found in mice which lack the receptor throughout the body.

Dr. Elmquist said that even though the findings are in mice, they do provide potential insight into blood glucose control in humans.

"It also further reinforces our previous findings that specific subsets of POMC neurons within the brain are responsible for the regulation of liver function and blood sugar metabolism," Dr. Elmquist said.

The next step, he said, is to determine what happens to feeding, body weight and liver metabolism in mice engineered to lack this serotonin receptor only in the POMC neurons.

Other UT Southwestern researchers involved in the study included lead author Dr. Yong Xu, instructor of internal medicine; Drs. Eric Berglund, Jen-Chieh Chuang, William Holland and Jong-Woo Sohn, postdoctoral research fellows in internal medicine; Dr. Makoto Fukuda, instructor of internal medicine; Dr. Kevin Williams, assistant instructor of internal medicine; Dr. Jeffrey Zigman, assistant professor of internal medicine and psychiatry; Dr. Philipp Scherer, director of the Touchstone Center for Diabetes Research; and Dr. Jari Rossi, former postdoctoral research fellow in internal medicine. Researchers from Baylor College of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School also contributed to the study.

The study was supported by the American Diabetes Association, American Heart Association, Sigrid Juselius Foundation, the Canadian Institute of Health Research and the National Institutes of Health.

Source:
UT Southwestern Medical Center

Please rate this article:
(Hover over the stars
then click to rate) Bookmark and Share

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

All opinions are moderated before being added.

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:






View the original article here

Wednesday, November 10, 2010

Too much glucosamine can cause the death of pancreatic cells, increase diabetes risk, researchers find

ScienceDaily (Oct. 27, 2010) ? High doses or prolonged use of glucosamine causes the death of pancreatic cells and could increase the risk of developing diabetes, according to a team of researchers at Universite Laval's Faculty of Pharmacy. Details of this discovery were recently published on the website of the Journal of Endocrinology.

In vitro tests conducted by Professor Frederic Picard and his team revealed that glucosamine exposure causes a significant increase in mortality in insulin-producing pancreatic cells, a phenomenon tied to the development of diabetes. Cell death rate increases with glucosamine dose and exposure time. "In our experiments, we used doses five to ten times higher than that recommended by most manufacturers, or 1,500 mg/day," stressed Professor Picard. "Previous studies showed that a significant proportion of glucosamine users up the dose hoping to increase the effects," he explained.

Picard and his team have shown that glucosamine triggers a mechanism intended to lower very high blood sugar levels. However, this reaction negatively affects SIRT1, a protein critical to cell survival. A high concentration of glucosamine diminishes the level of SIRT1, leading to cell death in the tissues where this protein is abundant, such as the pancreas.

Individuals who use large amounts of glucosamine, those who consume it for long periods, and those with little SIRT1 in their cells are therefore believed to be at greater risk of developing diabetes. In a number of mammal species, SIRT1 level diminishes with age. This phenomenon has not been shown in humans but if it were the case, the elderly -- who constitute the target market for glucosamine -- would be even more vulnerable.

"The key point of our work is that glucosamine can have effects that are far from harmless and should be used with great caution," concluded Professor Picard.

The results obtained by Picard and his team coincide with recent studies that cast serious doubt on the effectiveness of glucosamine in treating joint problems.

This study was co-authored by Mathieu Lafontaine-Lacasse and Genevieve Dore.

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 Universite Laval, via EurekAlert!, a service of AAAS.

Journal Reference:

M. Lafontaine-Lacasse, G. Dore, F. Picard. Hexosamines stimulate apoptosis by altering Sirt1 action and levels in rodent pancreatic β-cells. Journal of Endocrinology, 2010; DOI: 10.1677/JOE-10-0243

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


View the original article here

Wednesday, November 3, 2010

Brain Might Be Key To Leptin's Actions Against Type 1 Diabetes, UT Southwestern Researchers Find


Main Category: Diabetes
Also Included In: Clinical Trials / Drug Trials
Article Date: 21 Oct 2010 - 1:00 PDT window.fbAsyncInit = function() { FB.init({ appId: 'aa16a4bf93f23f07eb33109d5f1134d3', status: true, cookie: true, xfbml: true, channelUrl: 'http://www.medicalnewstoday.com/scripts/facebooklike.html'}); }; (function() { var e = document.createElement('script'); e.async = true; e.src = document.location.protocol + '//connect.facebook.net/en_US/all.js'; document.getElementById('fb-root').appendChild(e); }()); email icon email to a friend ? printer icon printer friendly ? write icon opinions ?
5 stars5 stars
New findings by UT Southwestern Medical Center researchers suggest a novel role for the brain in mediating beneficial actions of the hormone leptin in type 1 diabetes.

"Our findings really pave the way for understanding the mechanism by which leptin therapy improves type 1 diabetes," said Dr. Roberto Coppari, assistant professor of internal medicine at UT Southwestern and senior author of the study involving laboratory mice. "Understanding the mechanism is important, because if we can determine how leptin drives these benefits, then we may be able to develop drugs that eliminate the need for insulin."

The findings are available online and will be published in a future issue of the Proceedings of the National Academy of Sciences.

Prior research by Dr. Roger Unger, professor of internal medicine at UT Southwestern, has shown that subcutaneous administration of leptin, a hormone produced by the body's fat cells, can restore terminally ill rodents with type 1 diabetes to full health. The underlying cellular mechanisms that caused that effect, however, have been unclear.

In the current study, the researchers injected leptin continuously into the brains of mice that lacked any naturally produced insulin. Lack of or reduced insulin production is the hallmark of type 1 diabetes in humans.

They found that infusing leptin into the lateral ventricle of the animals' brains reversed the lethal consequences of type 1 diabetes. The results establish the brain as a potentially critical site for mediating the metabolism-improving actions of leptin, Dr. Coppari said.

The team's findings also indicate the smallest amount of leptin required to normalize the animals' food intake, body weight and blood sugar levels.

A human clinical trial currently under way at UT Southwestern aims to determine whether adding leptin to standard insulin therapy might help rein in the tumultuous blood-sugar levels of people with type 1 diabetes.

"It might be that leptin treatment is not going to be effective or well-tolerated or that it might cause unwanted effects," Dr. Coppari said. "However, if we understand the mechanisms and how leptin improves type 1 diabetes, then perhaps we can develop alternatives to harness those mechanisms."

The next step, Dr. Coppari said, is to determine which specific nerve cells in the brain are responsible for the anti-type 1 diabetic actions of leptin.

"Living without insulin was once considered impossible, but our results have shown that it is possible when leptin receptor signaling in the brain is enhanced. If we can identify which neurons are responsible for driving the anti-type 1 diabetic actions of leptin, we may eventually develop better therapies for individuals with type 1 diabetes."

Other UT Southwestern researchers involved in the study were Dr. Teppei Fujikawa, lead author and postdoctoral researcher in internal medicine; and Drs. Jen-Chieh Chuang, Giorgio Ramadori and Ichiro Sakata, postdoctoral researchers in internal medicine.

The National Institutes of Health and the American Heart Association funded the study.

Source:
Kristen Holland Shear
UT Southwestern Medical Center

Please rate this article:
(Hover over the stars
then click to rate) Bookmark and Share

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

All opinions are moderated before being added.

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:






View the original article here

Million Euro Starting Grants From ERC For 2 Researchers From MDC And Charite


Main Category: Diabetes
Also Included In: Neurology / Neuroscience;??Genetics
Article Date: 25 Oct 2010 - 3:00 PDT window.fbAsyncInit = function() { FB.init({ appId: 'aa16a4bf93f23f07eb33109d5f1134d3', status: true, cookie: true, xfbml: true, channelUrl: 'http://www.medicalnewstoday.com/scripts/facebooklike.html'}); }; (function() { var e = document.createElement('script'); e.async = true; e.src = document.location.protocol + '//connect.facebook.net/en_US/all.js'; document.getElementById('fb-root').appendChild(e); }()); email icon email to a friend ? printer icon printer friendly ? write icon opinions ?
4 starsnot yet rated
Two European Research Council (ERC) Starting Grants worth almost one and a half million euros each over the next five years have been awarded to two researchers from the Max Delbruck Center for Molecular Medicine (MDC) Berlin-Buch and the Charite - Universitatsmedizin, Berlin in Germany. American Diabetes researcher Dr. Matthew Poy and British neuroscientist Dr. James Poulet, belong to the 427 researchers the ERC has chosen from more than 2873 applicants this year.

With his research project Dr. Poy wants to improve the treatment of diabetes, especially the transplantation of pancreatic islets, and to facilitate the development of therapeutic strategies for this disease. Dr. Poulet, who is located at the excellence cluster NeuroCure and who is financed from the MDC, wants to shed light on the function of specific neurons in the cortex. This part of the brain plays a key role for example in sensory perception, control of movement, memory and attention.

MicroRNAs and Diabetes

Dr. Poy investigates a group of genes, called microRNAs, and their role in metabolic diseases such as diabetes. Using a multidisciplinary approach, his work will focus on elucidating how microRNAs within the insulin producing cells of the pancreas, the pancreatic beta cells, regulate their interaction to neighbouring endothelial cells.

The researcher believes that developing an understanding of how these interactions change during the pathogenesis of disease will provide insight into how islet growth and insulin release is dependent upon signals received from adjacent cell types. With this strategy, emphasis will be placed on genetic mouse models to identify relevant genes that can help improve the transplantation of beta cells.

Recently, the World Health Organization (WHO) gives an estimate of more than 220 million people worldwide suffering from this disease. "Both type 1 and type 2 diabetes are characterized by the deterioration and impaired function of beta cells of the pancreatic islet", Dr. Poy points out. Beta cells produce the hormone insulin which regulates the blood glucose levels, the body's main source of energy.

In patients with type 1 diabetes the beta cells have been destroyed due to a misguided response of the immune system, and blood glucose levels are elevated. These patients must self-inject insulin throughout their whole life.

Even in patients with type 2 diabetes, who initially can be treated with a special diet and pills, the beta cells can decline and fail over time, so that these patients, too, must self-inject insulin.

The development of more efficient and accurate insulin replacement therapies, however, has long proved to be a difficult task. This is why physicians have been trying for a long time to transplant intact beta cells or whole pancreas organs, but with little success.

For nearly two years Dr. Poy has been leading a Helmholtz junior research group at MDC, an institution of the Helmholtz Association, and at Charite - Universitatsmedizin Berlin. He came from the Swiss Federal Institute of Technology (ETH), Zurich. There he was able to show that microRNAs play a crucial role in the regulation of metabolic processes.

Matthew Poy studied biology at the Medical College of Ohio in Toledo, USA, where he also received his PhD in biomedical sciences. Prior to coming to Europe, he was working at Rockefeller University in New York City in the USA.

Brain States and Behaviour

Dr. Poulet is interested in studying changes in patterns of neuronal activity or "brain state". This phenomen was first recorded in 1929 in the awake human brain. Today recordings about these changes exist from mouse to man.

It is thought, that changes in brain state are fundamental to normal brain function and neuronal computation. "However, very little is known about the underlying neuronal mechanisms that generate these changes or their precise impact on neuronal processing and behaviour", Dr. Poulet explains.

Therefore in his new project Dr. Poulet wants to record the activity of neurons in the awake, behaving mouse to investigate the network and cellular mechanisms involved in generating brain state, using high resolution electrophysiology, neural imaging and molecular and behavioural techniques.

In previous work he had already characterized changes in brain state in the mouse during whisker movements, which he will now investigate further. With his research he hopes to be able to open new perspectives in the treatment of neurological diseases such as stroke or epilepsy.

During his PhD the neuroscientist played a key role in detecting a phenomenon researchers call "corollary discharge". It prevents crickets from deafening themselves while generating extremely loud mating songs.

Furthermore, due to "corollary discharge" it is also impossible to tickle oneself. A corollary discharge is a signal in the brain that filters out the perception of sounds or touch generated by ones own behaviour.

Until the summer of 2009 James Poulet was a postdoc at Ecole Poly-technique Federale de Lausanne, Switzerland, where he succeeded in recording the intracellular activity of two nerve cells in the cerebral cortex of a conscious, behaving animal for the first time.

Dr. Poulet is originally from London, England. He studied biology at the University of Bristol, went on to graduate studies at the University of Cambridge (UK), where he received his PhD in 2002 and was a postdoc between 2002 and 2005.

Dr. Poy and Dr. Poulet are the second and third recipients of an ERC-grant at the MDC. In 2009, developmental biologist Dr. Francesca Spagnoli, received a one million ERC-grant. The ERC, established in 2007 by the European Commission, is funded through the 7th Research Framework Programme of the European Union.

Source:
Barbara Bachtler
Helmholtz Association of German Research Centres

Please rate this article:
(Hover over the stars
then click to rate) Bookmark and Share

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

All opinions are moderated before being added.

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:






View the original article here

Monday, November 1, 2010

Brain might be key to leptin's actions against type 1 diabetes, researchers find

ScienceDaily (Oct. 19, 2010) ? New findings by UT Southwestern Medical Center researchers suggest a novel role for the brain in mediating beneficial actions of the hormone leptin in type 1 diabetes.

"Our findings really pave the way for understanding the mechanism by which leptin therapy improves type 1 diabetes," said Dr. Roberto Coppari, assistant professor of internal medicine at UT Southwestern and senior author of the study involving laboratory mice. "Understanding the mechanism is important, because if we can determine how leptin drives these benefits, then we may be able to develop drugs that eliminate the need for insulin."

The findings are available online and will be published in a future issue of the Proceedings of the National Academy of Sciences.

Prior research by Dr. Roger Unger, professor of internal medicine at UT Southwestern, has shown that subcutaneous administration of leptin, a hormone produced by the body's fat cells, can restore terminally ill rodents with type 1 diabetes to full health. The underlying cellular mechanisms that caused that effect, however, have been unclear.

In the current study, the researchers injected leptin continuously into the brains of mice that lacked any naturally produced insulin. Lack of or reduced insulin production is the hallmark of type 1 diabetes in humans.

They found that infusing leptin into the lateral ventricle of the animals' brains reversed the lethal consequences of type 1 diabetes. The results establish the brain as a potentially critical site for mediating the metabolism-improving actions of leptin, Dr. Coppari said.

The team's findings also indicate the smallest amount of leptin required to normalize the animals' food intake, body weight and blood sugar levels.

A human clinical trial currently under way at UT Southwestern aims to determine whether adding leptin to standard insulin therapy might help rein in the tumultuous blood-sugar levels of people with type 1 diabetes.

"It might be that leptin treatment is not going to be effective or well-tolerated or that it might cause unwanted effects," Dr. Coppari said. "However, if we understand the mechanisms and how leptin improves type 1 diabetes, then perhaps we can develop alternatives to harness those mechanisms."

The next step, Dr. Coppari said, is to determine which specific nerve cells in the brain are responsible for the anti-type 1 diabetic actions of leptin.

"Living without insulin was once considered impossible, but our results have shown that it is possible when leptin receptor signaling in the brain is enhanced. If we can identify which neurons are responsible for driving the anti-type 1 diabetic actions of leptin, we may eventually develop better therapies for individuals with type 1 diabetes."

Other UT Southwestern researchers involved in the study were Dr. Teppei Fujikawa, lead author and postdoctoral researcher in internal medicine; and Drs. Jen-Chieh Chuang, Giorgio Ramadori and Ichiro Sakata, postdoctoral researchers in internal medicine.

The National Institutes of Health and the American Heart Association funded the study.

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, via EurekAlert!, a service of AAAS.

Journal Reference:

T. Fujikawa, J.-C. Chuang, I. Sakata, G. Ramadori, R. Coppari. Leptin therapy improves insulin-deficient type 1 diabetes by CNS-dependent mechanisms in mice. Proceedings of the National Academy of Sciences, 2010; 107 (40): 17391 DOI: 10.1073/pnas.1008025107

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


View the original article here

Tuesday, October 26, 2010

Chronic diseases a global problem requiring global solutions, researchers say

ScienceDaily (Sep. 15, 2010) ? Policymakers should increase their sense of urgency to stop the global spread of chronic diseases such as heart disease, cancer and diabetes that threaten the health and economies of industrialized and developing nations alike, Emory University global health researchers say.

Writing in the current issue of The New England Journal of Medicine, authors K. M. Venkat Narayan, MD, Mohammed Ali, MBChB, MSc, and Jeffrey Koplan, MD, MPH, assert that the worldwide spread of chronic conditions, also known as noncommunicable diseases, offers a unique opportunity for low-, middle- and high-income countries around the globe to unite in their efforts to find tangible solutions for reducing the health and economic burdens of these diseases.

Chronic diseases account for 60 percent of all deaths worldwide. Trends also suggest that the major risk factors for these diseases -- hypertension, high glucose levels, obesity, and inactivity -- are all on the rise, especially in developing countries. Six out of the 10 risk factors for mortality worldwide are related to chronic noncommunicable diseases, and not infections or lack of nutrition, as was previously the case.

In addition to the health consequences, the long-term costs of treatment of chronic ailments and the negative effects on productivity take devastating tolls on the economic situations of individuals, families and countries. According to estimates, China, India and Britain will lose $558 billion, $237 billion, and $33 billion, respectively, in national income over the next decade as a result of largely preventable heart disease, strokes and diabetes. In the U.S., cardiovascular disease and diabetes together cost the country $750 billion annually.

"There is a unique opportunity now for global cooperation to tackle noncommunicable diseases," says Narayan, professor of global health and epidemiology at Emory's Rollins School of Public Health and professor of medicine in the Emory School of Medicine. "In fact, unless noncommunicable diseases are tackled, goals relating to child health and infectious diseases cannot be achieved nor can economic development be sustained."

Narayan and his co-authors also cite examples of how global cooperation and connections have benefited the movement to reduce chronic disease, including the development and testing of a new screening test for cervical cancer in India that could result in a lower cost screening test for millions of women worldwide.

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 Emory University, via EurekAlert!, a service of AAAS.

Journal Reference:

Narayan KV, Ali MK, Koplan JP. Global Noncommunicable Diseases ? Where Worlds Meet. New England Journal of Medicine, 2010; DOI: 10.1056/NEJMp1002024

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


View the original article here