Junk food as 'addictive as drugs'

"A diet of burgers, chips, sausages and cake will programme your brain into craving even more foods that are high in sugar, salt and fat, according to new research.

Over the years these junk foods can become a substitute for happiness and will lead bingers to become addicted.

Dr Paul Kenny, a neuroscientist, carried out the research which shows how dangerous high fat and high sugar foods can be to our health.

'You lose control. It’s the hallmark of addiction,' he said.

The researchers believe it is one of the first studies to suggest brains may react in the same way to junk food as they do to drugs...

Dr Kenny, who began his research at Guy’s Hospital, London, but now works at Florida’s Scripps Research Institute, divided rats into three groups for his research, due to be published in teh US soon.

One got normal amounts of healthy food to eat. Another lot was given restricted amounts of junk food and the third group was given unlimited amounts of junk, including cheesecake, fatty meat products, and cheap sponge cakes and chocolate snacks.

There were no adverse effects on the first two groups, but the rats who ate as much junk food as they wanted quickly became very fat and started bingeing. (sic)

When researchers electronically stimulated the part of the brain that feels pleasure, they found that the rats on unlimited junk food needed more and more stimulation to register the same level of pleasure as the animals on healthier diets."

Analysis of knockout mice suggests a role for VGF in the control of fat storage and energy expenditure

"Previous studies of mixed background mice have demonstrated that targeted deletion of Vgf produces a lean, hypermetabolic mouse that is resistant to diet-, lesion-, and genetically-induced obesity. To investigate potential mechanism(s) and site(s) of action of VGF, a neuronal and endocrine secreted protein and neuropeptide precursor, we further analyzed the metabolic phenotypes of two independent VGF knockout lines on C57Bl6 backgrounds...

Conclusions: We propose that VGF and/or VGF-derived peptides modulate sympathetic outflow pathways to regulate fat storage and energy expenditure."

Maternal High-Fat Diet Has Serious Implications For Brain Development Of Offspring, Mouse Study Finds

"Feeding high-fat food to pregnant mice can affect their pups' brain development in ways that may cause them to be more vulnerable to obesity and to engage in addictive-like behaviors in adulthood, a new study has found.

The research was presented at Neuroscience 2009, the annual meeting of the Society for Neuroscience and the world's largest source of emerging news about brain science and health.

'We discovered that pups born to mothers fed a high-fat diet during pregnancy and lactation had significant changes in their brain chemistry, with dramatic differences in dopamine- and opioid-related molecules,' said lead author Teresa Reyes, PhD, of the University of Pennsylvania.

These changes may partially explain the differences in behavior observed in these pups compared with ones from normal pregnancies, Reyes added. The pups born to mothers fed a high-fat diet showed a greater preference for a sugar solution and a greater physical response to cocaine than did pups born to mothers fed a standard diet.

The study's findings may have implications for humans. Almost two-thirds of Americans are overweight and one in three is obese, according to government health surveys. Women who are obese currently account for between 20 and 35 percent of all pregnancies in the United States. 'The potential long-term effects of maternal obesity on the brains and behavior of offspring are just beginning to be understood,' Reyes said."

Maternal Mice Fed High-Fat Diet Produce Larger Pups

"Could a woman's food choices during pregnancy affect not only the size and health of her children, but of her grandchildren? Yes, suggests a new study in mice presented at Neuroscience 2009, the annual meeting of the Society for Neuroscience and the world's largest source of emerging news about brain science and health.

University of Pennsylvania researchers found that pregnant mice fed a high-fat diet produce pups that are longer, weigh more, and have reduced insulin sensitivity -- factors that indicate a risk for obesity and diabetes. Interestingly, despite the lack of further high-fat diet exposure, the traits of increased body length and insulin insensitivity persisted into the second generation.

Subsequent investigation found that the changes in gene expression responsible for alterations in body length and insulin insensitivity were sex-dependent. Only female offspring exhibited evidence of altered programming of the growth hormone axis, a gene pathway that controls overall growth and metabolism.

This work adds to the growing body of research in epigenetics, the study of heritable alterations in gene expression that act independently of changes in DNA sequence. Until very recently, scientists believed that our genes were the sole carrier of hereditary information. However, in addition to inheriting genes from our parents, we can also inherit their epigenetic 'switches' that turn our genes on or off. These switches can be flipped by our environments and experiences to help us adapt to challenges put before us, and can be passed from generation to generation."

Halsa Pharmaceuticals Announces ZAG Demonstrates Weight Loss, Rise in Temperature and Reduction of Diabetes Symptoms in Preclinical Studies at Obesity

"Suggests Increase in Energy Expenditure and Potential as Treatment for Obesity and Type 2 Diabetes

HOUSTON--(Business Wire)--

Houston-based Halsa Pharmaceuticals, Inc., a biotechnology company developing therapeutics for the treatment of obesity, diabetes, cachexia and other metabolic diseases, today announced results from preclinical studies demonstrating that recombinant human Zinc-α2-glycoprotein (ZAG) induced a progressive loss of body weight in mice of 3.5g in five days, together with a rise in temperature of 0.4°C, suggesting an increase in energy expenditure. In addition, ZAG produced a normalization of the diabetic glucose tolerance curve after three days of treatment, suggesting that ZAG may have a therapeutic application in the treatment of obesity and Type 2 diabetes. The results from this study were presented at Obesity 2009, the 27th Annual Scientific Meeting of The Obesity Society, one of the largest scientific conferences in the field of obesity, being held in Washington, D.C. October 24-28...

Summary Results:

* ZAG induced a progressive loss of body weight in mice of 3.5g in five days, together with a rise in temperature of 0.4°C."

Study Says Blueberries May Help Maintain Weight, Prevent Diabetes

"The extract from North American lowbush blueberries biotransformed with bacteria from the skin of the fruit has shown promising results in tests against obesity and high blood sugar, according to new research.

Scientists from the Universite de Montreal, the Institut Armand-Frappier and the Universite de Moncton tested the blueberry juice on mice prone to obesity, insulin resistance, diabetes and hypertension, and discovered that the extract reduced their food intake and led to lower body weight.

They concluded that the biotransformed blueberry juice holds great therapeutic promise because it seems to decrease hyperglycemia by up to 35 percent and can protect young pre-diabetic animals from developing these metabolic conditions in the first place."

Scientists seek origins of obesity in the womb

"When Kathy Perusse had weight-loss surgery and shed 120 pounds, she may have done more than make her own life easier.

She went on to have two daughters, and she may have boosted their chances of avoiding becoming obese, like her two older children are.

That's the implication of research suggesting that something in an obese woman's womb can program her fetus toward becoming a fat child and adult. It's not about simply passing along genes that promote obesity; it's some sort of still-mysterious signal.

The idea has only recently entered conversations between doctors and female patients, and scientists are scrambling to track down a biological explanation. That knowledge, in turn, may provide new ways to block obesity from crossing generations.

While there's some disagreement on how important the womb signal is, 'the evidence is building and building that it is a substantial issue,' said Dr. Matthew Gillman of Harvard Medical School, who studies prevention of obesity.

Others agree. 'I think it could be a hugely significant factor,' said Robert Waterland of the Baylor College of Medicine in Houston, who studies the effect in mice."

You are what you eat

"Washington: The popular adage "you are what you eat" is literally true, according to a new research that claims a person's diet has a profound influence on his or her brain.

The findings offer insight into the neurobiological factors behind the obesity epidemic in the world.

In addition, the study exposed changes in brain chemistry due to diet and weight gain.

Obesity has been linked to rises in diabetes, stroke, and heart attacks, among other disorders, but the new research has added another dimension to understanding how obesity rates have more than doubled in the past 30 years.

The new findings show that disruptions in the sleep/wake cycle lead to weight gain, impulsivity, slower thinking, and other physiological and behavioural changes.

This could be particularly important for people who do shift work.

The study also showed that pregnant mice fed a high-fat diet produced pups that were longer, weighed more, and had reduced insulin sensitivity - factors that indicate a predisposition toward obesity and diabetes. In addition, despite no further exposure to a high-fat diet, these pups passed on those same traits to their offspring.

Feeding high-fat food to pregnant mice can affect the brain development of their offspring, causing the pups to be more vulnerable to obesity and to engaging in addictive-like behaviours in adulthood, found the researchers."

The Food-Energy Cellular Connection Revealed: Metabolic Master Switch Sets the Biological Clock in Body Tissues

Our body's activity levels fall and rise to the beat of our internal drums-the 24-hour cycles that govern fundamental physiological functions, from sleeping and feeding patterns to the energy available to our cells. Whereas the master clock in the brain is set by light, the pacemakers in peripheral organs are set by food availability. The underlying molecular mechanism was unknown.

Now, researchers at the Salk Institute for Biological Studies shed light on the long missing connection: A metabolic master switch, which, when thrown, allows nutrients to directly alter the rhythm of peripheral clocks.

Since the body's circadian rhythm and its metabolism are closely intertwined, the risk for metabolic disease shoots up, when they are out of sync. "Shift workers face a 100 percent increase in the risk for obesity and its consequences, such as high blood pressure, insulin resistance and an increased risk of heart attacks," says Howard Hughes Medical Investigator Ronald M. Evans, Ph.D., a professor in the Salk Institute's Gene Expression Laboratory...

Genetic inactivation of AMPK in mice blocks these effects, stabilizing CRY1 and severely disrupting peripheral clocks. In contrast, treating mice with AICAR, a synthetic drug that directly activates AMPK, reset the clock in cultured cells as well as in animals, confirming that cryptochromes act as energy sensors that allow to circadian clocks."

Lard Lesson: Why Fat Lubricates Your Appetite

"Researchers have long known that the hormones leptin and insulin play key roles in appetite and food intake. In healthy people leptin, which is secreted by fat tissue, acts as a molecular measuring tape for our waistlines, quashing feelings of hunger. Insulin spikes when the pancreas gets a whiff of the blood sugar increase after a meal; once the brain detects the spike, it knows to tamp down the desire for food.

Certain foods and metabolic disorders, however, can disrupt our ability to respond appropriately to these hormonal signals. In a study published in the September issue of The Journal of Clinical Investigation, scientists report unraveling a central biochemical mechanism behind fat's effect on the mammalian brain . They found that after only three days on a diet high in saturated fat—a common ingredient in beef and cheese—the brains of rats and mice became resistant to leptin and insulin. In contrast, unsaturated fats, such as those found in olive oil, did not trigger resistance."

Hormone Deficiency Linked to Impaired Glucose Metabolism

"Mice deficient in a gastrointestinal hormone implicated in glucose metabolism spontaneously develop impaired glucose tolerance, insulin resistance and visceral obesity, according to a study published online Oct. 9 in Endocrinology...

The researchers found that the mice had normal levels of active glucagon-like peptide 1. By four months, the mice spontaneously developed fasting hyperglycemia, hyperinsulinemia, glucose intolerance, insulin resistance, and visceral obesity."

Obesity Cure May Lie In Converting White Fat Cells Into Their Brown Counterparts

"A recent study has proved that manipulating autophagy - a cellular process which regulates the formation and inter-conversion of white fat cells and brown fat cells in mice - could solve the problem of obesity."

The food-energy cellular connection revealed

"Our body's activity levels fall and rise to the beat of our internal drums—the 24-hour cycles that govern fundamental physiological functions, from sleeping and feeding patterns to the energy available to our cells. Whereas the master clock in the brain is set by light, the pacemakers in peripheral organs are set by food availability. The underlying molecular mechanism was unknown.

Now, researchers at the Salk Institute for Biological Studies shed light on the long missing connection: A metabolic master switch, which, when thrown, allows nutrients to directly alter the rhythm of peripheral clocks.

Since the body's circadian rhythm and its metabolism are closely intertwined, the risk for metabolic disease shoots up, when they are out of sync. 'Shift workers face a 100 percent increase in the risk for obesity and its consequences, such as high blood pressure, insulin resistance and an increased risk of heart attacks,' says Howard Hughes Medical Investigator Ronald M. Evans, Ph.D., a professor in the Salk Institute's Gene Expression Laboratory.

The researchers' findings, which are published in the Oct. 16, 2009, issue of Science, could have far-reaching implications, from providing a better understanding how nutrition and gene expression are linked, to creating new ways to treat obesity, diabetes and other related diseases. 'It is estimated that the activity of up to 15 percent of our genes is under the direct control of biological clocks,' says Evans. 'Our work provides a conceptual way to link nutrition and energy regulation to the genome.'...

Genetic inactivation of AMPK in mice blocks these effects, stabilizing CRY1 and severely disrupting peripheral clocks. In contrast, treating mice with AICAR, a synthetic drug that directly activates AMPK, reset the clock in cultured cells as well as in animals, confirming that cryptochromes act as energy sensors that allow to circadian clocks."

Pain Response To Heat Reduced By Comfort Food

Choose water.

"People often eat food to feel better, but researchers have found that eating chocolate or drinking water can blunt pain, reducing a rat's response to a hot stimulus. This natural form of pain relief may help animals in the wild avoid distraction while eating scarce food, but in modern humans with readily available food, the effect may contribute to overeating and obesity."

Student researches obesity vaccine

"Nathan Freeman was still in high school when he joined a research team investigating possible cures for obesity.
Now a sophomore biochemistry major at USM, Freeman has continued working with the University Medical Center team every Summer for the past four years. Freeman believes that the team has made major progress developing the use of a hormone known as leptin. Secreted by fat cells, leptin is the chemical that tells your brain you are hungry. leptin is also responsible for regulating heart rate, and has effects similar to insulin for alleviating Diabetes...

Recent research by Dr. Alex da Silva of the University Medical Center showed that leptin was able to completely cure Type 2 Diabetes when given to diabetic mice."

Inhibiting the cellular process autophagy makes mice leaner

"Recent data have indicated that the more brown fat cells a person has the lower their body mass. This contrasts with what is known for white fat cells, the more white fat cells a person has the greater their body mass. It has been suggested that manipulating the development of fat cells so that they become brown fat cells rather than white fat cells might be an approach to treat obesity. However, before such an approach can be developed more needs to be learned about the mechanisms regulating the formation, expansion, and interconversion of these two cell types. New research, performed by Mark Czaja and colleagues, at Albert Einstein College of Medicine, New York, has now identified a cellular process that regulates the formation of the distinct fat cell types in mice."

Aging heart can be prevented in mice

"Factors such as high fever, anemia, lung infections, pulmonary embolism, high salt or fluid intake, overexertion, obesity, stress, and rapid heartbeat can worsen or trigger congestive heart failure in people with already weakened hearts."

" Scientists in Japan said they have uncovered evidence, based on mouse studies, that shows it may be possible to delay or prevent heart failure in humans."

Dietary Capsaicin Reduces Obesity-induced Insulin Resistance and Hepatic Steatosis in Obese Mice Fed a High-fat Diet

"Obesity-induced inflammation contributes to the development of obesity-related metabolic disorders such as insulin resistance, type 2 diabetes, fatty liver disease, and cardiovascular disease. In this study, we investigated whether dietary capsaicin can reduce obesity-induced inflammation and metabolic disorders such as insulin resistance and hepatic steatosis. Male C57BL/6 obese mice fed a high-fat diet for 10 weeks received a supplement of 0.015% capsaicin for a further 10 weeks and were compared with unsupplemented controls...

Our data suggest that dietary capsaicin may reduce obesity-induced glucose intolerance by not only suppressing inflammatory responses but also enhancing fatty acid oxidation in adipose tissue and/or liver, both of which are important peripheral tissues affecting insulin resistance. The effects of capsaicin in adipose tissue and liver are related to its dual action on PPAR and TRPV-1 expression/activation."

Diet boosts mitochondrial function, has implications for humans

"Flies fed an 'anti-Atkins' low protein diet live longer because their mitochondria function better. The research, done at the Buck Institute for Age Research, shows that the molecular mechanisms responsible for the lifespan extension in the flies have important implications for human aging and diseases such as obesity, diabetes and cancer...

The study provides a significant advance in understanding the role of 4EBP, a downstream molecular target of TOR, which mediates a switch in metabolism to extend lifespan, Kapahi said. A recent study appearing in the Nature showed that feeding rapamycin (an antibiotic used to prevent the rejection of organ and bone marrow transplants) to mice inhibited TOR and extended their lifespan. The Buck Institute study implies an important role for 4EBP and mitochondrial function as excellent targets to explore their role in lifespan extension in mammals, Kapahi said."

Body Clock, Blood Sugar Control Seem Linked

"A strong link exists between the body's biological clock and blood sugar control, say U.S. researchers who conducted lab experiments on mouse and human stem cells, as well as genetically engineered mice.

'The most surprising part of our findings is that our internal biologic rhythms are embedded directly into another pathway, one that is essential to regulate metabolism,' senior author Dr. Brian Feldman, an assistant professor of pediatric endocrinology at the Stanford University School of Medicine, said in a university news release.

The researchers found that daily fluctuations in hormones called glucocorticoids synchronize the biological clock as part of the mechanism for regulating blood sugar levels. The finding may help lead to new ways to control diabetics' blood sugar levels and may improve understanding of why night-shift workers are at risk for obesity and diabetes."

Timing of meals may affect weight gain

"Mice fed a high-fat diet during their normal sleep and rest period gained significantly more weight than mice fed the same diet during their active hours, a new study shows. The finding suggests that when we eat may influence how we pack on pounds.

Many living organisms-from plants to fruit flies to humans-have internal biological clocks, or circadian rhythms, that govern our daily cycles of sleep and activity. These internal clocks are tied to cycles of light and darkness. Several recent studies have found that circadian clocks can affect metabolism in animals, suggesting that the timing of meals might influence whether incoming calories are burned or stored as fat.

To take a closer look, Dr Fred Turek, Deanna M. Arble and their colleagues at Northwestern University designed a study to search for a direct link between meal times and body weight. Their research is supported by NIH's National Institute on Aging (NIA) and National Heart, Lung and Blood Institute (NHLBI).

For 6 weeks, mice were fed a high-fat diet either during a 12-hour dark phase, when the mice are normally active, or during a 12-hour light phase, when the mice are normally resting. The mice could eat as much as they wanted during their assigned feeding periods, but the food was removed during the remaining 12 hours each day. The study was described in the 3 September 2009 advance online edition of Obesity.

The researchers found that both groups of mice had similar levels of activity and calorie consumption over the 6-week period. However, within the first 2 weeks, the mice who ate during their normal sleeping phase weighed significantly more than the other mice. By the end of the study, the mice who ate when they should be sleeping had a 48% boost to their body weight, on average, compared to a 20% increase in the mice who ate the high-fat diet during their normal waking hours."

Red Wine Chemical May One Day Treat Diabetes

The more common form of diabetes, Type 2, is a disease of fat people.

"Resveratrol, found in red wine, was found to lower blood sugar levels and improve insulin levels when injected directly into the brains of mice fed very high-calorie diets in a study conducted by researchers at the University of Texas Southwestern Medical Center (UTSW).

The finding suggests that the brain plays a key role in resveratrol’s beneficial effect on diabetes and that the benefits may occur independently of diet and body weight."

Albany Medical College enters agreement with Aegis

"Albany Medical College has entered into an agreement with Aegis Therapeutics LLC that could speed the development and commercialization of an anti-obesity peptide that could also benefit people with Type 2 diabetes.

The pact authorizes San Diego-based Aegis to develop a partnership with a pharmaceutical company, with the goal of beginning human clinical trials of the OB-3 peptide. The peptide was discovered by researchers at the Albany, N.Y., medical college.

If successful, the trials could result in the new drug becoming commercially available.

Dr. Patricia Grasso, associate professor of medicine at Albany Med, said the school’s researchers have developed a synthetic fragment of leptin, a protein hormone, that decreases appetite and increases metabolism. This has resulted in significant weight loss and lower blood glucose levels in the mice and rats.

'Now we hope to demonstrate that the OB-3 peptide can be similarly effective in humans,' she said."

The Calorie-Restriction Experiment

"Going back more than a half century to an experiment at Cornell University in the mid-1930s, calorie restriction has been shown again and again to extend the lives of mice, rats and other animals."

Body's Circadian Rhythm Tightly Entwined With Blood Sugar Control

"Scientists have long struggled to understand the body's biological clock. Its tick-tock wakes us up, reminds us to eat and tells us when to go to bed. But what sets that circadian rhythm?

New research now shows that daily fluctuations in powerful hormones called glucocorticoids directly synchronize the biological clock as an integral part of our mechanism for regulating blood sugar.

'The most surprising part of our findings is that our internal biologic rhythms are embedded directly into another pathway, one that is essential to regulate metabolism,' said senior study author Brian Feldman, MD, PhD, assistant professor of pediatric endocrinology at the Stanford University School of Medicine. Feldman also practices at Lucile Packard Children's Hospital.

The new findings give the first in vivo evidence of a direct link between glucocorticoid hormones and genes that regulate our biological clock. The research may eventually help doctors reduce disabling side effects of glucocorticoid drugs such as prednisone, Feldman said. The work could also help diabetics control their blood sugar levels and may shed light on why night-shift workers are at risk for obesity and diabetes.

The study will be published online Oct. 5 in Proceedings of the National Academy of Sciences. Feldman worked previously at the University of California-San Francisco, where much of the research was conducted.

Feldman's team began their experiments by applying a synthetic glucocorticoid to dishes of mouse and human stem cells to see which genes responded. To the team's surprise, three genes known to control the biological clock changed their activity in a direct response to the hormone."

Polyphenol found in turmeric reduces weight gain in animal studies

"According to a Tufts University, Boston, MA study funded by a grant from the United States Department of Agriculture and released to the media on May 18, 2009, curcumin, the major polyphenol found in turmeric, appears to reduce weight gain in mice and suppress the growth of fat tissue in mice and cell models. Can it also stop humans from gaining weight?"

Gene transfer can help ailing heart heal itself

"[C]oronary artery disease, hypertension or high blood pressure, and diabetes" are all related to overweight/obesity.

"In a major breakthrough, scientists jump-started a failing heart by transferring a gene, which could help the heart heal itself.

The breakthrough also offers a tantalizing glimpse of a day when “closed heart surgery” via gene therapy is as commonly prescribed as today’s cocktail of drugs.

Five million people in the US have heart failure, about 550,000 new cases are diagnosed each year, and more than 287,000 people die each year of heart failure, according to the US Center for Disease Control and Prevention.

The most common causes of heart failure are coronary artery disease, hypertension or high blood pressure, and diabetes.

Heart failure is a condition where the heart cannot pump enough blood and oxygen to meet the needs of other body organs.

'We hope that our study will lead some day to the development of new genetic-based therapies for heart failure patients,' said Todd J. Herron, study co-author and professor at the University of Michigan (U-M).

Herron and colleagues treated heart muscle cells from the failing hearts of rabbits and humans with a virus modified to carry a gene which produces a protein that enables heart cells to contract normally."

I know that rabbits are not rodents.

"...Rodentia does not include rabbits; rabbits differ from rodents in having an extra pair of incisors and in other skeletal features."

Close enough.

Whatever it takes to help the overfat.

In Mouse Model Scientists Find Obesity Alone Does Not Cause Arthritis

"The link between obesity and osteoarthritis may be more than just the wear and tear on the skeleton caused by added weight.

A Duke University study has found that the absence of the appetite hormone leptin can determine whether obese mice experience arthritis, no matter how heavy they are.

'We were completely surprised to find that mice that became extremely obese had no arthritis if their bodies didn't have leptin,' said Farshid Guilak, Ph.D., director of orthopaedic research in the Duke Department of Surgery. 'Although there was some earlier evidence that leptin might be involved in the arthritis disease process, we didn't think that there would be no arthritis at all.'"

Study offers clues on diet benefits without the diet

"Experiments which mimicked a low-calorie diet by tinkering with genes in mice extended their lives and prevented disease, and a drug that has the same effect could give people longer, healthier lives, scientists said on Thursday...

Deleting S6K1 meant the mice's bodies behaved in a similar way to mammals whose calorie intake is restricted, they said.

'These mice were resistant to type 2 diabetes... and they also appeared to have reduced incidence of the mouse-equivalent of osteoporosis -- so they had stronger bones,' Withers said.

Balance, strength and coordination all improved in the knockout mice, and they were more inquisitive, suggesting their brains were healthier...

Most calorie restriction studies have found that a lifetime of deprivation is needed to achieve the longer-life benefits, and many researchers are working on ways to replicate the findings with drugs."

Discovery Of Gene That Protects High-Fat-Diet Mice From Obesity

"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.

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."

Leptin-Serotonin Pathway Offers New Clues For Obesity And Osteoporosis Prevention

"New research from Columbia University Medical Center has illuminated a previously unknown leptin-serotonin pathway in the brain that simultaneously promotes appetite and bone mass accrual. The research, which explains how leptin - well-known appetite-suppressing hormone - acts in the brain, is published in the Sept. 4 issue of Cell.

When the leptin-serotonin pathway is turned on in mice, the researchers found, appetite increases, the animals eat more, gain weight, and their bone mass increases. When the pathway is turned off, mice eat less, lose weight, and their bones weaken. Furthermore, leptin was found to not act in the hypothalamus as previously thought, but in the brain stem acting on serotonin, a hormone that in the brain acts to control appetite, mood and anger."

Caloric Restriction Only Benefits Obese Mice: The Journal Of Nutrition

"If you are a mouse on the chubby side, then eating less may help you live longer.

For lean mice - and possibly for lean humans, the authors of a new study predict - the anti-aging strategy known as caloric restriction may be a pointless, frustrating and even dangerous exercise...

He and Michael Forster, of the University of North Texas Health Science Center, compared the life span and caloric intake of two genetically engineered strains of mice.

The 'fat' strain, known as C57BL/6, roughly doubles in weight over its adult life. That strain benefited from caloric restriction, Sohal said.

The 'lean' strain, DBA/2, does not become obese. Caloric restriction did not extend the life of these mice, confirming previous work by Forster and Sohal...

By measuring the animals' metabolic rate, Sohal and his colleagues came to a deceptively simple conclusion: Caloric restriction is only useful when, as in the case of the obese mice, an animal eats more than it can burn off.

'Your energy expenditure and your energy intake should be in balance,' Sohal said.
'It's as simple as that. And how do you know that? By gain or loss of weight. (sic)

'The whole thing is very commonsensical.'

For humans of normal weight, Sohal strongly cautions against caloric restriction. In a 2003 study, he and Forster found that caloric restriction begun in older mice - both in DBA and leaner C57 individuals - actually shortened life span...

Sohal's study is not the first to question the allegedly universal benefits of caloric restriction. A study by Ross et al. published in Nature in 1976 ('Dietary practices and growth responses as predictors of longevity') found that caloric restriction works best in mice that gain weight rapidly in early adulthood, Sohal said."