Neuroscience

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Posts tagged obesity

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Male and female brains aren’t equal when it comes to fatResearchers have found that male and female brains respond in remarkably different ways to high-fat meals. Those differences in the brain lead to greater inflammation and increased health risks in males that indulge on fatty foods in comparison to females, a new study in mice shows. The findings reported in the Cell Press journal Cell Reports on October 16th may help to explain observed differences in obesity outcomes between women and men – premenopausal women carrying extra weight fare better than men do – and suggest that dietary advice should be made more sex-specific.
"Our findings, for the first time, suggest that males and females respond to high-fat diets differently," said Deborah Clegg of the Cedar-Sinai Diabetes And Obesity Research Institute in Los Angeles. "The data would suggest that is probably ‘ok’ for females to occasionally have a high-fat meal, where it is not recommended for males.
"The way we treat patients and provide dietary and nutritional advice should be altered. We might be less concerned about an occasional hamburger for women, but for men, we might more strongly encourage avoidance, especially if they have pre-existing diseases such as heart disease or type 2 diabetes."
Earlier data from Clegg’s team and others had suggested that inflammation in the brain is tied to overeating, blood sugar imbalances, and increased inflammation in other parts of the body, including fat tissue. Those effects can be triggered, in males in particular, by short-term exposure to a high-fat diet.
The researchers say they were initially shocked to discover that male and female brains differ in their fatty acid composition. When they manipulated male mouse brains to have the fatty acid profile of females, they found that those animals were protected from the ill effects of a diet high in fat.
When males with average male brains entered an inflammatory state after eating diets high in fat, they also suffered from reduced cardiac function in a way that female animals in the study did not. Those sex differences in the brain’s response to fat are related to differences between females and males in estrogen and estrogen receptor status.
Clegg says her team is now working out a strategy to confirm whether the findings in mice apply to people too. If they do, there will be some very immediate practical implications for what men and women should put on their plates.
"We have always had ‘one size fits all’ with respect to our nutritional information and our pharmaceutical approach," Clegg said. "Our data begin to suggest that sex should be factored in, and men should be more closely monitored for fat intake and inflammation than women."
(Image: Shutterstock)

Male and female brains aren’t equal when it comes to fat

Researchers have found that male and female brains respond in remarkably different ways to high-fat meals. Those differences in the brain lead to greater inflammation and increased health risks in males that indulge on fatty foods in comparison to females, a new study in mice shows. The findings reported in the Cell Press journal Cell Reports on October 16th may help to explain observed differences in obesity outcomes between women and men – premenopausal women carrying extra weight fare better than men do – and suggest that dietary advice should be made more sex-specific.

"Our findings, for the first time, suggest that males and females respond to high-fat diets differently," said Deborah Clegg of the Cedar-Sinai Diabetes And Obesity Research Institute in Los Angeles. "The data would suggest that is probably ‘ok’ for females to occasionally have a high-fat meal, where it is not recommended for males.

"The way we treat patients and provide dietary and nutritional advice should be altered. We might be less concerned about an occasional hamburger for women, but for men, we might more strongly encourage avoidance, especially if they have pre-existing diseases such as heart disease or type 2 diabetes."

Earlier data from Clegg’s team and others had suggested that inflammation in the brain is tied to overeating, blood sugar imbalances, and increased inflammation in other parts of the body, including fat tissue. Those effects can be triggered, in males in particular, by short-term exposure to a high-fat diet.

The researchers say they were initially shocked to discover that male and female brains differ in their fatty acid composition. When they manipulated male mouse brains to have the fatty acid profile of females, they found that those animals were protected from the ill effects of a diet high in fat.

When males with average male brains entered an inflammatory state after eating diets high in fat, they also suffered from reduced cardiac function in a way that female animals in the study did not. Those sex differences in the brain’s response to fat are related to differences between females and males in estrogen and estrogen receptor status.

Clegg says her team is now working out a strategy to confirm whether the findings in mice apply to people too. If they do, there will be some very immediate practical implications for what men and women should put on their plates.

"We have always had ‘one size fits all’ with respect to our nutritional information and our pharmaceutical approach," Clegg said. "Our data begin to suggest that sex should be factored in, and men should be more closely monitored for fat intake and inflammation than women."

(Image: Shutterstock)

Filed under obesity sex differences fatty acid inflammation diet neuroscience science

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Set of molecules found to link insulin resistance in the brain to diabetes
A key mechanism behind diabetes may start in the brain, with early signs of the disease detectable through rising levels of molecules not previously linked to insulin signaling, according to a study led by researchers at the Icahn School of Medicine at Mount Sinai published today in the journal Cell Metabolism.
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(Image: Shutterstock)

Set of molecules found to link insulin resistance in the brain to diabetes

A key mechanism behind diabetes may start in the brain, with early signs of the disease detectable through rising levels of molecules not previously linked to insulin signaling, according to a study led by researchers at the Icahn School of Medicine at Mount Sinai published today in the journal Cell Metabolism.

Read more

(Image: Shutterstock)

Filed under insulin insulin resistance diabetes obesity Type II diabetes medicine science

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Hunger Games: How the brain ‘browns’ fat to aid weight loss
Researchers at Yale School of Medicine have uncovered a molecular process in the brain known to control eating that transforms white fat into brown fat. This process impacts how much energy we burn and how much weight we can lose. The results are published in the Oct. 9 issue of the journal Cell.
Obesity is a rising global epidemic. Excess fatty tissue is a major risk factor for type 2 diabetes, cardiovascular disease, hypertension, neurological disorders, and cancer. People become overweight and obese when energy intake exceeds energy expenditure, and excess calories are stored in the adipose tissues. The adipose organ is made up of both white and brown fat. While white fat primarily stores energy as triglycerides, brown fat dissipates chemical energy as heat. The more brown fat you have, the more weight you can lose.
It has previously been shown that energy-storing white fat has the capacity to transform into energy-burning “brown-like” fat. In this new study, researchers from the Yale Program in Integrative Cell Signaling and Neurobiology of Metabolism, demonstrate that neurons controlling hunger and appetite in the brain control the “browning” of white fat.
Lead author Xiaoyong Yang, associate professor of comparative medicine and physiology at Yale School of Medicine, conducted the study with Tamas Horvath, professor and chair of comparative medicine, and professor of neurobiology and Obstetrics/gynecology at Yale School of Medicine, and their co-authors.
The team stimulated this browning process from the brain in mice and found that it protected the animals from becoming obese on a high-fat diet. The team then studied the molecular changes in hunger-promoting neurons in the hypothalamus and found that the attachment of a unique sugar called “O-GlcNAc” to potassium ion channels acts as a switch to control brain activity to burn fat.
“Our studies reveal white fat “browning” as a highly dynamic physiological process that the brain controls,” said Yang. “This work indicates that behavioral modifications promoted by the brain could influence how the amount of food we eat and store in fat is burned.”
Yang said hunger and cold exposure are two life-history variables during the development and evolution of mammals. “We observed that food deprivation dominates over cold exposure in neural control of white fat browning. This regulatory system may be evolutionarily important as it can reduce heat production to maintain energy balance when we are hungry. Modulating this brain-to-fat connection represents a potential novel strategy to combat obesity and associated illnesses.”

Hunger Games: How the brain ‘browns’ fat to aid weight loss

Researchers at Yale School of Medicine have uncovered a molecular process in the brain known to control eating that transforms white fat into brown fat. This process impacts how much energy we burn and how much weight we can lose. The results are published in the Oct. 9 issue of the journal Cell.

Obesity is a rising global epidemic. Excess fatty tissue is a major risk factor for type 2 diabetes, cardiovascular disease, hypertension, neurological disorders, and cancer. People become overweight and obese when energy intake exceeds energy expenditure, and excess calories are stored in the adipose tissues. The adipose organ is made up of both white and brown fat. While white fat primarily stores energy as triglycerides, brown fat dissipates chemical energy as heat. The more brown fat you have, the more weight you can lose.

It has previously been shown that energy-storing white fat has the capacity to transform into energy-burning “brown-like” fat. In this new study, researchers from the Yale Program in Integrative Cell Signaling and Neurobiology of Metabolism, demonstrate that neurons controlling hunger and appetite in the brain control the “browning” of white fat.

Lead author Xiaoyong Yang, associate professor of comparative medicine and physiology at Yale School of Medicine, conducted the study with Tamas Horvath, professor and chair of comparative medicine, and professor of neurobiology and Obstetrics/gynecology at Yale School of Medicine, and their co-authors.

The team stimulated this browning process from the brain in mice and found that it protected the animals from becoming obese on a high-fat diet. The team then studied the molecular changes in hunger-promoting neurons in the hypothalamus and found that the attachment of a unique sugar called “O-GlcNAc” to potassium ion channels acts as a switch to control brain activity to burn fat.

“Our studies reveal white fat “browning” as a highly dynamic physiological process that the brain controls,” said Yang. “This work indicates that behavioral modifications promoted by the brain could influence how the amount of food we eat and store in fat is burned.”

Yang said hunger and cold exposure are two life-history variables during the development and evolution of mammals. “We observed that food deprivation dominates over cold exposure in neural control of white fat browning. This regulatory system may be evolutionarily important as it can reduce heat production to maintain energy balance when we are hungry. Modulating this brain-to-fat connection represents a potential novel strategy to combat obesity and associated illnesses.”

Filed under obesity brown fat eating hunger O-GlcNAc ion channels neurons neuroscience science

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Eating is addictive

People can become addicted to eating for its own sake but not to consuming specific foods such as those high in sugar or fat, research suggests.

An international team of scientists has found no strong evidence for people being addicted to the chemical substances in certain foods.

The brain does not respond to nutrients in the same way as it does to addictive drugs such as heroin or cocaine, the researchers say.

Instead, people can develop a psychological compulsion to eat, driven by the positive feelings that the brain associates with eating.

image

"This is a behavioural disorder and could be categorised alongside conditions such as gambling addiction", say scientists at Edinburgh.

They add that the focus on tackling the problem of obesity should be moved from food itself towards the individual’s relationship with eating.

The study, which examined the scientific evidence for food addiction as a substance-based addiction, is published in Neuroscience & Biobehavioral Reviews.

The researchers also say that the current classification of mental disorders, which does not permit a formal diagnosis of eating addiction, could be redrawn.

However, more research would be needed to define a diagnosis, the scientists add.

They add that the focus on tackling the problem of obesity should be moved from food itself towards the individual’s relationship with eating.

(Source: ed.ac.uk)

Filed under eating behavior food addiction obesity reward system addictive disorders neuroscience science

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Eating habits, body fat related to differences in brain chemistry
People who are obese may be more susceptible to environmental food cues than their lean counterparts due to differences in brain chemistry that make eating more habitual and less rewarding, according to a National Institutes of Health study published in Molecular Psychiatry.
Researchers at the NIH Clinical Center found that, when examining 43 men and women with varying amounts of body fat, obese participants tended to have greater dopamine activity in the habit-forming region of the brain than lean counterparts, and less activity in the region controlling reward. Those differences could potentially make the obese people more drawn to overeat in response to food triggers and simultaneously making food less rewarding to them. A chemical messenger in the brain, dopamine influences reward, motivation and habit formation.
"While we cannot say whether obesity is a cause or an effect of these patterns of dopamine activity, eating based on unconscious habits rather than conscious choices could make it harder to achieve and maintain a healthy weight, especially when appetizing food cues are practically everywhere," said Kevin D. Hall, Ph.D., lead author and a senior investigator at National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of NIH. "This means that triggers such as the smell of popcorn at a movie theater or a commercial for a favorite food may have a stronger pull for an obese person – and a stronger reaction from their brain chemistry – than for a lean person exposed to the same trigger."
Study participants followed the same eating, sleeping and activity schedule. Tendency to overeat in response to triggers in the environment was determined from a detailed questionnaire. Positron emission tomography (PET) scans evaluated the sites in the brain where dopamine was able to act.
According to the Centers for Disease Control and Prevention, more than one-third of U.S. adults are obese. Obesity-related conditions include heart disease, type 2 diabetes and certain types of cancer, some of the leading causes of preventable death.
"These findings point to the complexity of obesity and contribute to our understanding of how people with varying amounts of body fat process information about food," said NIDDK Director Griffin P. Rodgers, M.D. "Accounting for differences in brain activity and related behaviors has the potential to inform the design of effective weight-loss programs."
The study did not demonstrate cause and effect among habit formation, reward, dopamine activity, eating behavior and obesity. Future research will examine dopamine activity and eating behavior in people over time as they change their diets, physical activity, and their weight.

Eating habits, body fat related to differences in brain chemistry

People who are obese may be more susceptible to environmental food cues than their lean counterparts due to differences in brain chemistry that make eating more habitual and less rewarding, according to a National Institutes of Health study published in Molecular Psychiatry.

Researchers at the NIH Clinical Center found that, when examining 43 men and women with varying amounts of body fat, obese participants tended to have greater dopamine activity in the habit-forming region of the brain than lean counterparts, and less activity in the region controlling reward. Those differences could potentially make the obese people more drawn to overeat in response to food triggers and simultaneously making food less rewarding to them. A chemical messenger in the brain, dopamine influences reward, motivation and habit formation.

"While we cannot say whether obesity is a cause or an effect of these patterns of dopamine activity, eating based on unconscious habits rather than conscious choices could make it harder to achieve and maintain a healthy weight, especially when appetizing food cues are practically everywhere," said Kevin D. Hall, Ph.D., lead author and a senior investigator at National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of NIH. "This means that triggers such as the smell of popcorn at a movie theater or a commercial for a favorite food may have a stronger pull for an obese person – and a stronger reaction from their brain chemistry – than for a lean person exposed to the same trigger."

Study participants followed the same eating, sleeping and activity schedule. Tendency to overeat in response to triggers in the environment was determined from a detailed questionnaire. Positron emission tomography (PET) scans evaluated the sites in the brain where dopamine was able to act.

According to the Centers for Disease Control and Prevention, more than one-third of U.S. adults are obese. Obesity-related conditions include heart disease, type 2 diabetes and certain types of cancer, some of the leading causes of preventable death.

"These findings point to the complexity of obesity and contribute to our understanding of how people with varying amounts of body fat process information about food," said NIDDK Director Griffin P. Rodgers, M.D. "Accounting for differences in brain activity and related behaviors has the potential to inform the design of effective weight-loss programs."

The study did not demonstrate cause and effect among habit formation, reward, dopamine activity, eating behavior and obesity. Future research will examine dopamine activity and eating behavior in people over time as they change their diets, physical activity, and their weight.

Filed under obesity eating behavior dopamine brain chemistry striatum neuroscience science

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Training Your Brain to Prefer Healthy Foods
It may be possible to train the brain to prefer healthy low-calorie foods over unhealthy higher-calorie foods, according to new research by scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University and at Massachusetts General Hospital. Published online today in the journal Nutrition & Diabetes, a brain scan study in adult men and women suggests that it is possible to reverse the addictive power of unhealthy food while also increasing preference for healthy foods.
“We don’t start out in life loving French fries and hating, for example, whole wheat pasta,” said senior and co-corresponding author Susan B. Roberts, Ph.D., director of the Energy Metabolism Laboratory at the USDA HNRCA, who is also a professor at the Friedman School of Nutrition Science and Policy at Tufts University and an adjunct professor of psychiatry at Tufts University School of Medicine. “This conditioning happens over time in response to eating – repeatedly! - what is out there in the toxic food environment.”
Scientists have suspected that, once unhealthy food addiction circuits are established, they may be hard or impossible to reverse, subjecting people who have gained weight to a lifetime of unhealthy food cravings and temptation. To find out whether the brain can be re-trained to support healthy food choices, Roberts and colleagues studied the reward system in thirteen overweight and obese men and women, eight of whom were participants in a new weight loss program designed by Tufts University researchers and five who were in a control group and were not enrolled in the program.
Both groups underwent magnetic resonance imaging (MRI) brain scans at the beginning and end of a six-month period. Among those who participated in the weight loss program, the brain scans revealed changes in areas of the brain reward center associated with learning and addiction. After six months, this area had increased sensitivity to healthy, lower-calorie foods, indicating an increased reward and enjoyment of healthier food cues. The area also showed decreased sensitivity to the unhealthy higher-calorie foods.
“The weight loss program is specifically designed to change how people react to different foods, and our study shows those who participated in it had an increased desire for healthier foods along with a decreased preference for unhealthy foods, the combined effects of which are probably critical for sustainable weight control,” said co-author Sai Krupa Das, Ph.D., a scientist in the Energy Metabolism Laboratory at the USDA HNRCA and an assistant professor at the Friedman School. “To the best of our knowledge this is the first demonstration of this important switch.” The authors hypothesize that several features of the weight loss program were important, including behavior change education and high-fiber, low glycemic menu plans.
“Although other studies have shown that surgical procedures like gastric bypass surgery can decrease how much people enjoy food generally, this is not very satisfactory because it takes away food enjoyment generally rather than making healthier foods more appealing,” said first author and co-corresponding author Thilo Deckersbach, Ph.D., a psychologist at Massachusetts General Hospital. “We show here that it is possible to shift preferences from unhealthy food to healthy food without surgery, and that MRI is an important technique for exploring the brain’s role in food cues.”
“There is much more research to be done here, involving many more participants, long-term follow-up and investigating more areas of the brain,” Roberts added. “But we are very encouraged that, the weight loss program appears to change what foods are tempting to people.”

Training Your Brain to Prefer Healthy Foods

It may be possible to train the brain to prefer healthy low-calorie foods over unhealthy higher-calorie foods, according to new research by scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University and at Massachusetts General Hospital. Published online today in the journal Nutrition & Diabetes, a brain scan study in adult men and women suggests that it is possible to reverse the addictive power of unhealthy food while also increasing preference for healthy foods.

“We don’t start out in life loving French fries and hating, for example, whole wheat pasta,” said senior and co-corresponding author Susan B. Roberts, Ph.D., director of the Energy Metabolism Laboratory at the USDA HNRCA, who is also a professor at the Friedman School of Nutrition Science and Policy at Tufts University and an adjunct professor of psychiatry at Tufts University School of Medicine. “This conditioning happens over time in response to eating – repeatedly! - what is out there in the toxic food environment.”

Scientists have suspected that, once unhealthy food addiction circuits are established, they may be hard or impossible to reverse, subjecting people who have gained weight to a lifetime of unhealthy food cravings and temptation. To find out whether the brain can be re-trained to support healthy food choices, Roberts and colleagues studied the reward system in thirteen overweight and obese men and women, eight of whom were participants in a new weight loss program designed by Tufts University researchers and five who were in a control group and were not enrolled in the program.

Both groups underwent magnetic resonance imaging (MRI) brain scans at the beginning and end of a six-month period. Among those who participated in the weight loss program, the brain scans revealed changes in areas of the brain reward center associated with learning and addiction. After six months, this area had increased sensitivity to healthy, lower-calorie foods, indicating an increased reward and enjoyment of healthier food cues. The area also showed decreased sensitivity to the unhealthy higher-calorie foods.

“The weight loss program is specifically designed to change how people react to different foods, and our study shows those who participated in it had an increased desire for healthier foods along with a decreased preference for unhealthy foods, the combined effects of which are probably critical for sustainable weight control,” said co-author Sai Krupa Das, Ph.D., a scientist in the Energy Metabolism Laboratory at the USDA HNRCA and an assistant professor at the Friedman School. “To the best of our knowledge this is the first demonstration of this important switch.” The authors hypothesize that several features of the weight loss program were important, including behavior change education and high-fiber, low glycemic menu plans.

“Although other studies have shown that surgical procedures like gastric bypass surgery can decrease how much people enjoy food generally, this is not very satisfactory because it takes away food enjoyment generally rather than making healthier foods more appealing,” said first author and co-corresponding author Thilo Deckersbach, Ph.D., a psychologist at Massachusetts General Hospital. “We show here that it is possible to shift preferences from unhealthy food to healthy food without surgery, and that MRI is an important technique for exploring the brain’s role in food cues.”

“There is much more research to be done here, involving many more participants, long-term follow-up and investigating more areas of the brain,” Roberts added. “But we are very encouraged that, the weight loss program appears to change what foods are tempting to people.”

Filed under obesity nutrition neuroimaging weight loss reward system neuroscience science

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Brain Benefits From Weight Loss Following Bariatric Surgery
Weight loss surgery can curb alterations in brain activity associated with obesity and improve cognitive function involved in planning, strategizing and organizing, according to a new study published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism (JCEM).
Obesity can tax the brain as well as other organs. Obese individuals face a 35 percent higher risk of developing Alzheimer’s disease compared to normal weight people.
Bariatric surgery is used to help people who are dangerously obese lose weight. Bariatric surgery procedures are designed to restrict the amount of food you can eat before you feel full by reducing the stomach’s size or limit the absorption of nutrients by removing part of the small intestine from the path food takes through the digestive tract. Some procedures, such as Roux-en-Y gastric bypass (RYBG) surgery, use a combination of these methods. This study was the first to assess brain activity in women before and after bariatric surgery.
“When we studied obese women prior to bariatric surgery, we found some areas of their brains metabolized sugars at a higher rate than normal weight women,” said one of the study’s authors, Cintia Cercato, MD, PhD, of the University of São Paolo in São Paolo, Brazil. “In particular, obesity led to altered activity in a part of the brain linked to the development of Alzheimer’s disease – the posterior cingulate gyrus. Since bariatric surgery reversed this activity, we suspect the procedure may contribute to a reduced risk of Alzheimer’s disease and other forms of dementia.”
The longitudinal study examined the effect of RYBG surgery on the brain function of 17 obese women. Researchers used positron emission tomography (PET) scans and neuropsychological tests to assess brain function and activity in the participants prior to surgery and six months after the procedure. The same tests also were run once on a control group of 16 lean women.
Before they underwent surgery, the obese women had higher rates of metabolism in certain areas of the brain, including the posterior cingulate gyrus. Following surgery, there was no evidence of this exacerbated brain activity. Their brain metabolism rates were comparable to the activity seen in normal weight women.
After surgery, the obese women also performed better on a test measuring executive function – the brain’s ability to connect past experience and present action – than they did before the procedures. Executive function is used in planning, organizing and strategizing. Five other neuropsychological tests measuring various aspects of memory and cognitive function showed no change following the surgery.
“Our findings suggest the brain is another organ that benefits from weight loss induced by surgery,” Cercato said. “The increased brain activity the obese women exhibited before undergoing surgery did not result in improved cognitive performance, which suggests obesity may force the brain to work harder to achieve the same level of cognition.”
(Image: Getty)

Brain Benefits From Weight Loss Following Bariatric Surgery

Weight loss surgery can curb alterations in brain activity associated with obesity and improve cognitive function involved in planning, strategizing and organizing, according to a new study published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism (JCEM).

Obesity can tax the brain as well as other organs. Obese individuals face a 35 percent higher risk of developing Alzheimer’s disease compared to normal weight people.

Bariatric surgery is used to help people who are dangerously obese lose weight. Bariatric surgery procedures are designed to restrict the amount of food you can eat before you feel full by reducing the stomach’s size or limit the absorption of nutrients by removing part of the small intestine from the path food takes through the digestive tract. Some procedures, such as Roux-en-Y gastric bypass (RYBG) surgery, use a combination of these methods. This study was the first to assess brain activity in women before and after bariatric surgery.

“When we studied obese women prior to bariatric surgery, we found some areas of their brains metabolized sugars at a higher rate than normal weight women,” said one of the study’s authors, Cintia Cercato, MD, PhD, of the University of São Paolo in São Paolo, Brazil. “In particular, obesity led to altered activity in a part of the brain linked to the development of Alzheimer’s disease – the posterior cingulate gyrus. Since bariatric surgery reversed this activity, we suspect the procedure may contribute to a reduced risk of Alzheimer’s disease and other forms of dementia.”

The longitudinal study examined the effect of RYBG surgery on the brain function of 17 obese women. Researchers used positron emission tomography (PET) scans and neuropsychological tests to assess brain function and activity in the participants prior to surgery and six months after the procedure. The same tests also were run once on a control group of 16 lean women.

Before they underwent surgery, the obese women had higher rates of metabolism in certain areas of the brain, including the posterior cingulate gyrus. Following surgery, there was no evidence of this exacerbated brain activity. Their brain metabolism rates were comparable to the activity seen in normal weight women.

After surgery, the obese women also performed better on a test measuring executive function – the brain’s ability to connect past experience and present action – than they did before the procedures. Executive function is used in planning, organizing and strategizing. Five other neuropsychological tests measuring various aspects of memory and cognitive function showed no change following the surgery.

“Our findings suggest the brain is another organ that benefits from weight loss induced by surgery,” Cercato said. “The increased brain activity the obese women exhibited before undergoing surgery did not result in improved cognitive performance, which suggests obesity may force the brain to work harder to achieve the same level of cognition.”

(Image: Getty)

Filed under brain activity cognitive function obesity weight loss neuroscience science

125 notes

Clues to curbing obesity found in neuronal ‘sweet spot’
Preventing weight gain, obesity, and ultimately diabetes could be as simple as keeping a nuclear receptor from being activated in a small part of the brain, according to a new study by Yale School of Medicine researchers.
Published in the Aug. 1 issue of The Journal of Clinical Investigation (JCI), the study showed that when the researchers blocked the effects of the nuclear receptor PPARgamma in a small number of brain cells in mice, the animals ate less and became resistant to a high-fat diet.
“These animals ate fat and sugar, and did not gain weight, while their control littermates did,” said lead author Sabrina Diano, professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale School of Medicine. “We showed that the PPARgamma receptor in neurons that produce POMC could control responses to a high-fat diet without resulting in obesity.”
POMC neurons are found in the hypothalamus and regulate food intake. They are the neurons that when activated make you feel full and curb appetite. PPARgamma regulates the activation of these neurons.
Diano and her team studied transgenic mice that were genetically engineered to delete the PPARgamma receptor from POMC neurons. They wanted to see if they could prevent the obesity associated with a high-fat, high-sugar diet.
“When we blocked PPARgamma in these hypothalamic cells, we found an increased level of free radical formation in POMC neurons, and they were more active,” said Diano, who is also professor of comparative medicine and neurobiology at Yale and director of the Reproductive Neurosciences Group.
The findings also have key implications in diabetes. PPARgamma is a target of thiazolidinedione (TZD), a class of drugs used to treat type 2 diabetes. They lower blood-glucose levels, however, patients gain weight on these medications.
“Our study suggests that the increased weight gain in diabetic patients treated with TZD could be due to the effect of this drug in the brain, therefore, targeting peripheral PPARgamma to treat type 2 diabetes should be done by developing TZD compounds that can’t penetrate the brain,” said Diano. “We could keep the benefits of TZD without the side-effects of weight gain. Our next steps in this research are to test this theory in diabetes mouse models.”

Clues to curbing obesity found in neuronal ‘sweet spot’

Preventing weight gain, obesity, and ultimately diabetes could be as simple as keeping a nuclear receptor from being activated in a small part of the brain, according to a new study by Yale School of Medicine researchers.

Published in the Aug. 1 issue of The Journal of Clinical Investigation (JCI), the study showed that when the researchers blocked the effects of the nuclear receptor PPARgamma in a small number of brain cells in mice, the animals ate less and became resistant to a high-fat diet.

“These animals ate fat and sugar, and did not gain weight, while their control littermates did,” said lead author Sabrina Diano, professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale School of Medicine. “We showed that the PPARgamma receptor in neurons that produce POMC could control responses to a high-fat diet without resulting in obesity.”

POMC neurons are found in the hypothalamus and regulate food intake. They are the neurons that when activated make you feel full and curb appetite. PPARgamma regulates the activation of these neurons.

Diano and her team studied transgenic mice that were genetically engineered to delete the PPARgamma receptor from POMC neurons. They wanted to see if they could prevent the obesity associated with a high-fat, high-sugar diet.

“When we blocked PPARgamma in these hypothalamic cells, we found an increased level of free radical formation in POMC neurons, and they were more active,” said Diano, who is also professor of comparative medicine and neurobiology at Yale and director of the Reproductive Neurosciences Group.

The findings also have key implications in diabetes. PPARgamma is a target of thiazolidinedione (TZD), a class of drugs used to treat type 2 diabetes. They lower blood-glucose levels, however, patients gain weight on these medications.

“Our study suggests that the increased weight gain in diabetic patients treated with TZD could be due to the effect of this drug in the brain, therefore, targeting peripheral PPARgamma to treat type 2 diabetes should be done by developing TZD compounds that can’t penetrate the brain,” said Diano. “We could keep the benefits of TZD without the side-effects of weight gain. Our next steps in this research are to test this theory in diabetes mouse models.”

Filed under obesity neurons PPARgamma receptor diabetes hypothalamus medicine science

51 notes

Striatal dopamine transporter binding correlates with body composition and visual attention bias for food cues in healthy young men

Research to be presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, describes a way that brain chemistry may make some people notice food more easily, which can tempt overeating even in people who are not overweight. Dopamine activity in the striatum, an area of the brain sensitive to food reward, was linked to how quickly men noticed a food picture hidden among neutral pictures. In turn, the men who quickly noticed food pictures also ate more.

From rodent research it is clear that dopamine action in the striatum motivates eating, and this goes awry in obesity. “We do know that in human obesity the striatal dopamine system is affected, but interesting enough we know little about the striatal dopamine system of young, healthy individuals and how it relates to the motivation to eat” says Susanne la Fleur from the Academic Medical Center in Amsterdam, who directed the study linking dopamine, attention to food, and eating.

Ordinarily the burst of dopamine during a rewarding activity is eventually stopped when it is re-absorbed into the cells it came from. That re-uptake process requires a brain chemical called “dopamine transporter” (DAT). Lower DAT means dopamine is reabsorbed more slowly, causing it to keep acting on the brain. The researchers scanned brains of healthy, non-obese young men to determine available DAT. The men completed a computerized visual attention task to see how quickly they could detect food pictures among neutral pictures. Subjects were also asked to report food intake during 7 days.

The researchers found that the men with lower DAT, which means higher dopamine activity, showed a stronger visual attention bias towards food, detecting food pictures more quickly. “We could speculate that in healthy humans dopamine does motivate eating, however although we did observe a correlation between striatal dopamine transporter binding and the visual attention bias for food; and between visual attention bias for food and actual food intake, we did not observe a correlation between striatal dopamine transporter binding and actual food intake. Thus, a factor in addition to dopamine must be involved in going from being motivated to actual eating”, la Fleur concluded.

(Source: eurekalert.org)

Filed under striatum dopamine dopamine transporter obesity visual attention neuroscience science

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Brain Response to Appetizing Food Cues Varies Among Obese People

People who have the most common genetic mutation linked to obesity respond differently to pictures of appetizing foods than overweight or obese people who do not have the genetic mutation, according to a new study published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism (JCEM).

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More than one-third of adults are obese. Obesity typically results from a combination of eating too much, getting too little physical activity and genetics. In particular, consumption of appetizing foods that are high in calories can lead to weight gain. Highly palatable foods such as chocolate trigger signals in the brain that give a feeling of pleasure and reward. These cravings can contribute to overeating. Reward signals are processed in specific areas of the brain, where sets of neurons release chemicals such as dopamine. However, very little is known about whether the reward centers of the brain work differently in some people who are overweight or obese.

The most common genetic cause of obesity involves mutations in the melanocortin 4 receptor (MC4R), which occur in about 1 percent of obese people and contribute to weight gain from an early age. The researchers compared three groups of people: eight people who were obese due to a problem in the MC4R gene, 10 people who were overweight or obese without the gene mutation and eight people who were normal weight. They performed functional Magnetic Resonance Imaging (fMRI) scans to look at how the reward centers in the brain were activated by pictures of appetizing food such as chocolate cake compared to bland food such as rice or broccoli and non-food items such as staplers.

“In our study, we found that people with the MC4R mutation responded in the same way as normal weight people, while the overweight people without the gene problem had a lower response,” said lead researcher Agatha van der Klaauw, MD, PhD, of the Wellcome Trust-MRC Institute of Metabolic Science at Addenbrooke’s Hospital in Cambridge, U.K. “In fact, the brain’s reward centers light up when people with the mutation and normal weight people viewed pictures of appetizing foods. But overweight people without the mutation did not have the same level of response.”

The scans revealed that obese people with the MC4R mutation had similar activity in the reward centers of the brain when shown a picture of a dessert like cake or chocolate as normal weight people. The researchers found that, in contrast, the reward centers were underactive in overweight and obese volunteers who did not have the gene mutation. This finding is intriguing as it shows a completely different response in two groups of people of the same age and weight.

“For the first time, we are seeing that the MC4R pathway is involved in the brain’s response to food cues and its underactivity in some overweight people,” van der Klaauw said. “Understanding this pathway may help in developing interventions to limit the overconsumption of highly palatable foods that can lead to weight gain.”

To address the obesity epidemic, the Cambridge team is continuing to study the pathways in the brain that coordinate the need to eat and the reward and pleasure of eating

(Source: endocrine.org)

Filed under obesity MC4R melanocortin gene mutations brain activity neuroscience science

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