Brain Cells : Not Lack of Willpower : Determine Obesity, Study Finds

Brain Cells : Not Lack of Willpower : Determine Obesity, Study Finds

  9:35:00 PM    Science Lover

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An international study has discovered the reason why some people who eat a high-fat diet remain slim, yet others pile on the weight.

The study, led in Australia by the Monash Obesity and Diabetes Institute (MODI) at Monash University, found a high-fat diet causes brain cells to become insulated from the body preventing vital signals, which tell the body to stop eating and to burn energy, from reaching the brain efficiently.

Professor Michael Cowley discovered that a high-fat 
diet caused brain cells to become insulated from the 
body, rendering the cells unable to detect signals of 
fullness to stop eating. (Credit: Image courtesy of 
Monash University)

MODI director and Australian Life Scientist of the Year Professor Michael Cowley said there were two clear outcomes from the findings.

'We discovered that a high-fat diet caused brain cells to become insulated from the body, rendering the cells unable to detect signals of fullness to stop eating," Professor Cowley said.

"Secondly, the insulation also created a further complication in that the body was unable to detect signals to increase energy use and burn off calories/kilojoules."

The research showed that support cells in the brain developed overgrowth in a high-fat diet. This prevented the regular brain cells (the melanocortin system or POMC neurons) from connecting with other neural mechanisms, which determine appetite and energy expenditure.

Professor Cowley said the study findings provide a critical link in addressing the obesity epidemic.

"These neuronal circuits regulate eating behaviours and energy expenditure and are a naturally occurring process in the brain. The circuits begin to form early in life so that people may have a tendency towards obesity even before they eat their first meal," Professor Cowley said.

Eating a high fat diet causes more "insulation" in the nerve cells, and makes it even harder for the brain to help a person lose weight.

"Obese people are not necessarily lacking willpower. Their brains do not know how full or how much fat they have stored, so the brain does not tell the body to stop refuelling. Subsequently, their body's ability to lose weight is significantly reduced."

Professor Cowley and fellow MODI researcher Dr Pablo Enriori collaborated with Research Chair and Professor of Comparative Medicine and Professor of Neurobiology Tamas Horvath and his team at the Yale School of Medicine in the United States, together with teams of scientists in Cincinnati, New Jersey, Mexico and Spain.

For a period of four months, the researchers monitored the eating and body composition of groups of mice and rats and found that those with a neural predisposition to obesity gained 30 per cent more weight compared to six per cent of the group with obesity-resistant cells.

Story Source:
The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Monash University.

Journal Reference:
T. L. Horvath, B. Sarman, C. Garcia-Caceres, P. J. Enriori, P. Sotonyi, M. Shanabrough, E. Borok, J. Argente, J. A. Chowen, D. Perez-Tilve, P. T. Pfluger, H. S. Bronneke, B. E. Levin, S. Diano, M. A. Cowley, M. H. Tschop. Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity. Proceedings of the National Academy of Sciences, 2010; 107 (33): 14875 DOI: 10.1073/pnas.1004282107

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High-Fructose Corn Syrup Prompts Considerably More Weight Gain, Researchers Find

High-Fructose Corn Syrup Prompts Considerably More Weight Gain, Researchers Find

  9:15:00 PM    Science Lover

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A Princeton University research team has demonstrated that all sweeteners are not equal when it comes to weight gain: Rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same.

A Princeton University research team, including (from left) undergraduate Elyse Powell, psychology professor Bart Hoebel, visiting research associate Nicole Avena and graduate student Miriam Bocarsly, has demonstrated that rats with access to high-fructose corn syrup -- a sweetener found in many popular sodas -- gain significantly more weight than those with access to water sweetened with table sugar, even when they consume the same number of calories. The work may have important implications for understanding obesity trends in the United States. (Credit: Princeton University, Office of Communications, Denise Applewhite)

In addition to causing significant weight gain in lab animals, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides. The researchers say the work sheds light on the factors contributing to obesity trends in the United States.

"Some people have claimed that high-fructose corn syrup is no different than other sweeteners when it comes to weight gain and obesity, but our results make it clear that this just isn't true, at least under the conditions of our tests," said psychology professor Bart Hoebel, who specializes in the neuroscience of appetite, weight and sugar addiction. "When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they're becoming obese -- every single one, across the board. Even when rats are fed a high-fat diet, you don't see this; they don't all gain extra weight."

In results published online March 18 by the journal Pharmacology, Biochemistry and Behavior, the researchers from the Department of Psychology and the Princeton Neuroscience Institute reported on two experiments investigating the link between the consumption of high-fructose corn syrup and obesity.

The first study showed that male rats given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas.

The second experiment -- the first long-term study of the effects of high-fructose corn syrup consumption on obesity in lab animals -- monitored weight gain, body fat and triglyceride levels in rats with access to high-fructose corn syrup over a period of six months. Compared to animals eating only rat chow, rats on a diet rich in high-fructose corn syrup showed characteristic signs of a dangerous condition known in humans as the metabolic syndrome, including abnormal weight gain, significant increases in circulating triglycerides and augmented fat deposition, especially visceral fat around the belly. Male rats in particular ballooned in size: Animals with access to high-fructose corn syrup gained 48 percent more weight than those eating a normal diet. In humans, this would be equivalent to a 200-pound man gaining 96 pounds.

"These rats aren't just getting fat; they're demonstrating characteristics of obesity, including substantial increases in abdominal fat and circulating triglycerides," said Princeton graduate student Miriam Bocarsly. "In humans, these same characteristics are known risk factors for high blood pressure, coronary artery disease, cancer and diabetes." In addition to Hoebel and Bocarsly, the research team included Princeton undergraduate Elyse Powell and visiting research associate Nicole Avena, who was affiliated with Rockefeller University during the study and is now on the faculty at the University of Florida. The Princeton researchers note that they do not know yet why high-fructose corn syrup fed to rats in their study generated more triglycerides, and more body fat that resulted in obesity.

High-fructose corn syrup and sucrose are both compounds that contain the simple sugars fructose and glucose, but there at least two clear differences between them. First, sucrose is composed of equal amounts of the two simple sugars -- it is 50 percent fructose and 50 percent glucose -- but the typical high-fructose corn syrup used in this study features a slightly imbalanced ratio, containing 55 percent fructose and 42 percent glucose. Larger sugar molecules called higher saccharides make up the remaining 3 percent of the sweetener. Second, as a result of the manufacturing process for high-fructose corn syrup, the fructose molecules in the sweetener are free and unbound, ready for absorption and utilization. In contrast, every fructose molecule in sucrose that comes from cane sugar or beet sugar is bound to a corresponding glucose molecule and must go through an extra metabolic step before it can be utilized.

This creates a fascinating puzzle. The rats in the Princeton study became obese by drinking high-fructose corn syrup, but not by drinking sucrose. The critical differences in appetite, metabolism and gene expression that underlie this phenomenon are yet to be discovered, but may relate to the fact that excess fructose is being metabolized to produce fat, while glucose is largely being processed for energy or stored as a carbohydrate, called glycogen, in the liver and muscles.

In the 40 years since the introduction of high-fructose corn syrup as a cost-effective sweetener in the American diet, rates of obesity in the U.S. have skyrocketed, according to the Centers for Disease Control and Prevention. In 1970, around 15 percent of the U.S. population met the definition for obesity; today, roughly one-third of the American adults are considered obese, the CDC reported. High-fructose corn syrup is found in a wide range of foods and beverages, including fruit juice, soda, cereal, bread, yogurt, ketchup and mayonnaise. On average, Americans consume 60 pounds of the sweetener per person every year.

"Our findings lend support to the theory that the excessive consumption of high-fructose corn syrup found in many beverages may be an important factor in the obesity epidemic," Avena said.

The new research complements previous work led by Hoebel and Avena demonstrating that sucrose can be addictive, having effects on the brain similar to some drugs of abuse.

In the future, the team intends to explore how the animals respond to the consumption of high-fructose corn syrup in conjunction with a high-fat diet -- the equivalent of a typical fast-food meal containing a hamburger, fries and soda -- and whether excessive high-fructose corn syrup consumption contributes to the diseases associated with obesity. Another step will be to study how fructose affects brain function in the control of appetite.

The research was supported by the U.S. Public Health Service.

Editor's Note: In response to the above-mentioned study, The Corn Refiners Association issued a statement titled "Gross Errors in Princeton Animal Study on Obesity and High Fructose Corn Syrup: Research in Humans Discredits Princeton Study" (http://www.corn.org/princeton-hfcs-study-errors.html).

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'Fat' Taste Could Hold The Key To Cut Obesity

'Fat' Taste Could Hold The Key To Cut Obesity

  9:48:00 AM    Science Lover

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A newly discovered ability for people to taste fat could hold the key to reducing obesity, Deakin University health researchers believe.

Researchers have discovered that humans can detect a sixth taste: fat. (Credit: iStockphoto/Andrey Stepanov)

Deakin researchers Dr Russell Keast and PhD student Jessica Stewart, working with colleagues at the University of Adelaide, CSIRO, and Massey University (New Zealand), have found that humans can detect a sixth taste -- fat. They also found that people with a high sensitivity to the taste of fat tended to eat less fatty foods and were less likely to be overweight. The results of their research are published in the latest issue of the British Journal of Nutrition.

"Our findings build on previous research in the United States that used animal models to discover fat taste," Dr Keast said.

"We know that the human tongue can detect five tastes -- sweet, salt, sour, bitter and umami (a taste for identifying protein rich foods). Through our study we can conclude that humans have a sixth taste -- fat."

The research team developed a screening procedure to test the ability of people to taste a range of fatty acids commonly found in foods.

They found that people have a taste threshold for fat and that these thresholds vary from person to person; some people have a high sensitivity to the taste while others do not.

"Interestingly, we also found that those with a high sensitivity to the taste of fat consumed less fatty foods and had lower BMIs than those with lower sensitivity," Dr Keast said.

"With fats being easily accessible and commonly consumed in diets today, this suggests that our taste system may become desensitised to the taste of fat over time, leaving some people more susceptible to overeating fatty foods.

"We are now interested in understanding why some people are sensitive and others are not, which we believe will lead to ways of helping people lower their fat intakes and aide development of new low fat foods and diets."

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Food Emits Anti-Hunger Aromas During Chewing

Food Emits Anti-Hunger Aromas During Chewing

  10:13:00 AM    Science Lover

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A real possibility does exist for developing a new generation of foods that make people feel full by releasing anti-hunger aromas during chewing, scientists in the Netherlands are reporting after a review of research on that topic. Such foods would fight the global epidemic of obesity with aromas that quench hunger and prevent people from overeating. Their article appears in ACS' Journal of Agricultural and Food Chemistry.

A real possibility does exist for developing a new generation of foods that make people feel full by releasing anti-hunger aromas during chewing. (Credit: iStockphoto/Jan Couver)

Rianne Ruijschop and colleagues note that scientists long have tried to develop tasty foods that trigger or boost the feeling of fullness. Until recently, that research focused on food's effects in stomach after people swallow it. Efforts now have expanded to include foods that release hunger-quenching aromas during chewing. Molecules that make up a food's aroma apparently do so by activating areas of the brain that signal fullness.

Their analysis found that aroma release during chewing does contribute to the feeling of fullness and possibly to consumers' decisions to stop eating. The report cites several possible applications, including developing foods that release more aroma during chewing or developing aromas that have a more powerful effect in triggering feelings of fullness.

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Large People Prone To Enlarged Hearts: Obesity Leading Risk Factor Of Left Atrial Enlargement During Aging

Large People Prone To Enlarged Hearts: Obesity Leading Risk Factor Of Left Atrial Enlargement During Aging

  9:52:00 AM    Science Lover

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Image via Wikipedia

Aside from aging itself, obesity appears to be the most powerful predictor of left atrial enlargement (LAE), upping one's risk of atrial fibrillation (the most common type of arrhythmia), stroke and death, according to findings published in the November 17, 2009, issue of the Journal of the American College of Cardiology.

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That Late-night Snack: Worse Than You Think

That Late-night Snack: Worse Than You Think

  9:12:00 PM    Science Lover

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Eat less, exercise more. Now there is new evidence to support adding another "must" to the weight-loss mantra: eat at the right time of day.

Eating at irregular times -- the equivalent of the middle of the night for humans,
when the body wants to sleep -- influences weight gain, a new study has found.
(Credit: iStockphoto/Curt Pickens)

A Northwestern University study has found that eating at irregular times -- the equivalent of the middle of the night for humans, when the body wants to sleep -- influences weight gain. The regulation of energy by the body's circadian rhythms may play a significant role. The study is the first causal evidence linking meal timing and increased weight gain.

"How or why a person gains weight is very complicated, but it clearly is not just calories in and calories out," said Fred Turek, professor of neurobiology and physiology in the Weinberg College of Arts and Sciences and director of the Center for Sleep and Circadian Biology. "We think some factors are under circadian control. Better timing of meals, which would require a change in behavior, could be a critical element in slowing the ever-increasing incidence of obesity."

The findings could have implications for developing strategies to combat obesity in humans, as the United States and the world battle what has been called an "obesity epidemic." More than 300 million adults worldwide are obese, including more than a third of American adults.

Details of the obesity study, which was led by Turek, will be published online Sept. 3 by the journal Obesity.

"One of our research interests is shift workers, who tend to be overweight," said lead author Deanna M. Arble, a doctoral student in Turek's lab. "Their schedules force them to eat at times that conflict with their natural body rhythms. This was one piece of evidence that got us thinking -- eating at the wrong time of day might be contributing to weight gain. So we started our investigation with this experiment."

Simply modifying the time of feeding alone can greatly affect body weight, the researchers found. Mice that were fed a high-fat diet during normal sleeping hours gained significantly more weight (a 48 percent weight increase over their baseline) than mice eating the same type and amount of food during naturally wakeful hours (a 20 percent increase over their baseline). There was no statistical difference between the two groups regarding caloric intake or the amount of activity.

Over a period of six weeks, both groups of mice were allowed to eat as much high-fat diet as they wanted during their daily 12-hour feeding phase. (Much like many humans, mice have a preference for high-fat food.) Since mice are nocturnal, the 12-hour feeding phase was during the day for those fed during normal sleeping hours and during the night for those fed during naturally wakeful hours. Food was not provided during the other 12 hours of their day.

Our circadian clock, or biological timing system, governs our daily cycles of feeding, activity and sleep, with respect to external dark and light cycles. Recent studies have found the body's internal clock also regulates energy use, suggesting the timing of meals may matter in the balance between caloric intake and expenditure.

The researchers next plan to investigate the molecular mechanisms behind their observation that eating at the "wrong" time can lead to weight gain.

In addition to Turek and Arble, other authors of the paper are Joseph Bass, Aaron D. Laposky and Martha H. Vitaterna, all from Northwestern.

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Mice Can Eat 'Junk' And Not Get Fat: Researchers Find Gene That Protects High-fat-diet Mice From Obesity

Mice Can Eat 'Junk' And Not Get Fat: Researchers Find Gene That Protects High-fat-diet Mice From Obesity

  10:47:00 AM    Science Lover

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University of Michigan researchers have identified a gene that acts as a master switch to control obesity in mice. When the switch is turned off, even high-fat-diet mice remain thin.

Both mice were fed high-fat diets for several months.
Deleting the IKKE gene in the mouse on the left protected it
against the weight gain apparent in the mouse on the right.
(Credit: Photo by Scott Galvin, U-M Photo Services)

Deleting the gene, called IKKE, also appears to protect mice against conditions that, in humans, lead to Type 2 diabetes, which is associated with obesity and is on the rise among Americans, including children and adolescents.

If follow-up studies show that IKKE is tied to obesity in humans, the gene and the protein it makes will be prime targets for the development of drugs to treat obesity, diabetes and complications associated with those disorders, said Alan Saltiel, the Mary Sue Coleman Director of the U-M Life Sciences Institute.

"We've studied other genes associated with obesity – we call them 'obesogenes' – but this is the first one we've found that, when deleted, stops the animal from gaining weight," said Saltiel, senior author of a paper to be published in the Sept. 4 edition of the journal Cell.

"The fact that you can disrupt all the effects of a high-fat diet by deleting this one gene in mice is pretty interesting and surprising," he said.

Obesity is associated with a state of chronic, low-grade inflammation that leads to insulin resistance, which is usually the first step in the development of Type 2 diabetes. In the Cell paper, Saltiel and his colleagues show that deleting, or "knocking out," the IKKE gene not only protected high-fat-diet mice from obesity, it prevented chronic inflammation, a fatty liver and insulin resistance, as well.

The high-fat-diet mice were fed a lard-like substance with 45 percent of its calories from fat. Control mice were fed standard chow with 4.5 percent of its calories from fat. The dietary regimen began when the mice were 8 weeks old and continued for 14 to 16 weeks.

The gene IKKE produces a protein kinase also known as IKKE. Protein kinases are enzymes that turn other proteins on or off. The IKKE protein kinase appears to target proteins which, in turn, control genes that regulate the mouse metabolism.

When the high-fat diet is fed to a normal mouse, IKKE protein-kinase levels rise, the metabolic rate slows, and the animal gains weight. In that situation, the IKKE protein kinase acts as a brake on the metabolism.

Knockout mice placed on the high-fat diet did not gain weight, apparently because deleting the IKKE gene releases the metabolic brake, allowing it to speed up and burn more calories, instead of storing those calories as fat.

"The knockout mice are not exercising any more than the control mice used in the study. They're just burning more energy," Saltiel said. "And in the process, they're generating a little heat, as well – their body temperature actually increases a bit."

Saltiel's team is now searching for small molecules that block IKKE protein-kinase activity. IKKE inhibitors could become candidates for drug development.

"If you find an inhibitor of this protein kinase, you should be able to obtain the same effect as knocking out the gene. And that's the goal," Saltiel said. If successful candidates are identified and drug development is pursued, a new treatment for obesity and diabetes is likely a decade away, he said.

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First author of the Cell paper is Shian-Huey Chiang of the Life Sciences Institute. Co-authors are U-M researchers Merlijn Bazuine, Carey Lumeng, Lynn Geletka, Jonathan Mowers, Nicole White, Jing-Tyan Ma, Jie Zhou, Nathan Qi, Dan Westcott and Jennifer Delproposto. Timothy Blackwell and Fiona Yull of the Vanderbilt University School of Medicine also are co-authors.

The research was funded by the National Institutes of Health and the American Diabetes Association. All animal use was conducted in compliance with the Institute of Laboratory Animal Research's Guide for the Care and Use of Laboratory Animals and was approved by the University Committee on Use and Care of Animals at the University of Michigan.

Related links:

Life Sciences Institute:

http://www.lsi.umich.edu

Saltiel Lab:

http://www.lsi.umich.edu/facultyresearch/labs/saltiel

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