Archive for the ‘Burn Fat’ Category

Researchers at Albert Einstein College of Medicine of Yeshiva University have discovered a process that controls the amount of fat that cells store for use as a back-up energy source. Disruption of this process allows cellular fat to accumulate — a key factor in age-related metabolic diseases such as obesity and type 2 diabetes. The study is published today in the online version of Nature.

Discovery of this previously unknown fat-fighting pathway could lead to novel drugs for the treatment of metabolic syndrome (characterized by obesity, blood lipid disorders, and insulin resistance) and for a common liver disease known as “fatty liver” or steatohepatitis. Nonalcoholic steatohepatitis (NASH) is a common, often “silent” liver disease. Although NASH resembles alcoholic liver disease, it occurs in people who drink little or no alcohol. NASH affects 2 to 5 percent of Americans, according to the National Institute of Diabetes and Digestive and Kidney Diseases.

All cells store lipids, a type of fat, in the form of small droplets that can be broken down for energy when needed. In situations of excessive food intake or in certain diseases such as diabetes or obesity, these lipid droplets become so large that they interfere with normal cell function.

“In this study, we found that the amount of fat stored in these intracellular lipid droplets is controlled through autophagy, a process until now thought to help primarily in digesting and recycling damaged cellular structures,” says Mark Czaja, M.D., professor of medicine at Einstein whose team worked collaboratively on the research with the laboratory of Ana Maria Cuervo, M.D., Ph.D., associate professor of developmental & molecular biology, medicine, and anatomy & structural biology at Einstein.

Autophagy, or “self-eating,” is carried out by lysosomes, which function as the cell’s recycling center. In studies of liver cells in culture and in live animals, Dr. Czaja and his colleagues discovered that lysosomes do something never before observed: continuously remove portions of lipid droplets and process them for energy production.

“When food is scarce, autophagy becomes a main source of energy for the cells and this process of digesting lipid droplets is accelerated,” says Dr. Cuervo. “If autophagy slows down, as occurs in aging, the lipid droplets stored in cells keep growing and eventually become so big that they can no longer be degraded.”

This slowdown in fat control appears to trigger a vicious cycle in which the enlarging fat droplets impair autophagy, allowing even more fat to accumulate, and so on, which could eventually contribute to diseases such as diabetes. The researchers noted that therapies aimed at helping autophagy operate more efficiently might prevent disease by keeping fat droplets under control.

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Article adapted by MD Sports from original press release.
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Contact: Deirdre Branley
Albert Einstein College of Medicine

Drs. Cuervo and Czaja’s paper, “Autophagy regulates lipid metabolism” is published in the April 1 online version of Nature. Their co-authors at Einstein include Rajat Singh and Susmita Kaushik (primary co-authors), Yongjun Wang, Youqing Xiang, and Inna Novak; as well as Masaaki Komatsu and Keiji Tanaka of the Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku, Tokyo, Japan.

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About Albert Einstein College of Medicine of Yeshiva University

Albert Einstein College of Medicine of Yeshiva University is one of the nation’s premier centers for research, medical education and clinical investigation. It is the home to some 2,000 faculty members, 750 M.D. students, 350 Ph.D. students (including 125 in combined M.D./Ph.D. programs) and 380 postdoctoral investigators. Last year, Einstein received more than $130 million in support from the NIH. This includes the funding of major research centers at Einstein in diabetes, cancer, liver disease, and AIDS. Other areas where the College of Medicine is concentrating its efforts include developmental brain research, neuroscience, cardiac disease, and initiatives to reduce and eliminate ethnic and racial health disparities. Through its extensive affiliation network involving five hospital centers in the Bronx, Manhattan and Long Island – which includes Montefiore Medical Center, The University Hospital and Academic Medical Center for Einstein – the College runs one of the largest post-graduate medical training program in the United States, offering approximately 150 residency programs to more than 2,500 physicians in training. For more information, please visit http://www.aecom.yu.edu.

Lower muscle mass and an increase in body fat are common consequences of growing older.

While exercise is a proven way to prevent the loss of muscle mass, a new study led by McMaster researcher Dr. Mark Tarnopolsky shows that taking a combination of creatine monohydrate (CrM) and conjugated linoleic acid (CLA) in addition to resistance exercise training provides even greater benefits.

The study to be published on Oct. 3 in PLoS One, an international, peer-reviewed online journal of the Public Library of Science, involved 19 men and 20 women who were 65 years or older and took part in a six-month program of regular resistance exercise training.

In the randomized double blind trial, some of the participants were given a daily supplement of creatine (a naturally produced compound that supplies energy to muscles) and linoleic acid (a naturally occurring fatty acid), while others were given a placebo. All participants took part in the same exercise program.

The exercise training resulted in improvements of functional ability and strength in all participants, but those taking the CrM and CLA showed even greater gains in muscle endurance, an increase in fat-free mass and a decrease in the percentage of body fat.

“This data confirms that supervised resistance exercise training is safe and effective for increasing strength and function in older adults and that a combination of CrM and CLA can enhance some of the beneficial effects of training over a six month period,” said Tarnopolsky, a professor of pediatrics and medicine.

This study provides functional outcomes that build on an earlier mechanistic study co-led by Tarnopolsky and Dr. S. Melov at the Buck Institute of Age Research, published in PLoS One this year, which provided evidence that six months of resistance exercise reversed some of the muscle gene expression abnormalities associated with the aging process.
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Article adapted by MD Sports Weblog from original press release.
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Contact: Veronica McGuire
McMaster University

By studying the genes of a German child born with unusually well developed muscles, an international research team has discovered the first evidence that the gene whose loss makes “mighty mice” also controls muscle growth in people.

Writing in the June 24 issue of the New England Journal of Medicine, German neurologist Markus Schuelke, M.D., and the team show that the child’s extra-large muscles are due to an inherited mutation that effectively silences the myostatin gene, proving that its protein normally keeps muscle development in check in people.

People with muscle-wasting conditions such as muscular dystrophy, and others just wanting to “bulk up,” have eagerly followed work on myostatin, hoping for a way to counteract the protein’s effects in order to build or rebuild muscle mass. But while research with mice has continued to reveal myostatin’s role and the effects of interfering with it, no one knew whether any of the results would be relevant to humans.

“This is the first evidence that myostatin regulates muscle mass in people as it does in other animals,” says Se-Jin Lee, M.D., Ph.D., professor of molecular biology and genetics in the Institute for Basic Biomedical Sciences at Johns Hopkins and co-author on the study. “That gives us a great deal of hope that agents already known to block myostatin activity in mice may be able to increase muscle mass in humans, too.”

Lee and his team discovered in 1997 that knocking out the myostatin gene led to mice that were twice as muscular as their normal siblings, lending them the moniker “mighty mice.” Later, others showed that naturally bulky cattle, such as Belgian Blues, got their extra muscles from lack of myostatin, too.

An unusual opportunity to examine myostatin’s role in humans arose when Schuelke examined a newborn baby boy, almost five years ago, and was struck by the visible muscles on the infant’s upper legs and upper arms. When ultrasound proved that the muscles were roughly twice as large as other infants’, but otherwise normal, Schuelke realized that a naturally occurring mutation in the child’s myostatin gene might be the cause.

Sequencing the myostatin gene from the boy and his mother, who had been a professional athlete, revealed a single change in the building blocks of the gene’s DNA. Surprisingly, the change was not in the gene regions that correspond to the resulting protein, but in the intervening regions that are used only to create protein-making instructions, thus changing the gene’s protein-building message.

“The mutation caused the gene’s message, the messenger RNA, to be wrong,” says Hopkins

neurologist Kathryn Wagner, M.D., Ph.D., who tested the genetic mutation’s effect in laboratory studies. “If the message had been used to make a protein, it would be much shorter than it should be. But we think the process doesn’t even get that far; instead the cells just destroy the message.”

Co-authors from Wyeth Research, Cambridge, Mass., analyzed samples of the child’s blood for evidence of the myostatin protein and found none. “Both copies of the child’s myostatin gene have this mutation, so little if any of the myostatin protein is made,” says Schuelke. “As a result, he has about twice the muscle mass of other children.”

Completely lacking myostatin, the boy is stronger than other children his age, and fortunately has no signs of problems with his heart so far, Schuelke says. But he adds that it’s impossible to know whether the lack of myostatin in that crucial muscle might lead to problems as the boy gets older.

While other family members — the boy’s mother and her brother, father and grandfather — were also reported to have been usually strong, only the mother’s DNA was available for analysis along with her son’s. Schuelke discovered that only one copy of the mother’s myostatin gene had the mutation found in both copies of her son’s myostatin gene. (We have two copies of each gene; one inherited from the mother and one inherited from the father.)

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Article adapted by MD Sports Weblog from original press release.
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 Contact: Joanna Downer
Johns Hopkins Medical Institutions

 

The Johns Hopkins researchers were funded by the National Institutes of Health and the Muscular Dystrophy Association. The German researchers were funded by the parents’ self-help group (Helft dem muskelkranken Kind).

Authors on the paper are Schuekle, Christoph Hubner, Thomas Riebel and Wolfgang Komen of Charite, University Medical Center Berlin, Germany; Wagner and Lee of Johns Hopkins; Leslie Stolz and James Tobin of Wyeth Research, Cambridge, Ma.; and Thomas Braun of Martin-Luther-University, Halle-Wittenberg, Germany.

*Under a licensing agreement between MetaMorphix Inc. and The Johns Hopkins University, Lee is entitled to a share of royalty received by the University on sales of products described in this article. Lee also is entitled to a share of sublicensing income from arrangements between MetaMorphix and American Home Products (Wyeth Ayerst Laboratories) and Cape Aquaculture Technologies. Lee and the University own MetaMorphix Inc. stock, which is subject to certain restrictions under University policy. Lee owns Cape Aquaculture Technologies stock, which is subject to certain restrictions under University policy. Lee has served as a paid consultant to MetaMorphix Inc. The terms of these arrangements are being managed by The Johns Hopkins University in accordance with its conflict of interest policies.

And it increases endurance to run a mile and decreases inflammation

The Salk Institute scientist who earlier discovered that enhancing the function of a single protein produced a mouse with an innate resistance to weight gain and the ability to run a mile without stopping has found new evidence that this protein and a related protein play central roles in the body’s complex journey to obesity and offer a new and specific metabolic approach to the treatment of obesity related disease such as Syndrome X (insulin resistance, hyperlipidemia and atherosclerosis).

Dr. Ronald M. Evans, a Howard Hughes Medical Investigator at The Salk Institute’s Gene Expression Laboratory, presented two new studies (date) at Experimental Biology 2005 in the scientific sessions of the American Society for Biochemistry and Molecular Biology. The studies focus on genes for two of the nuclear hormone receptors that control broad aspects of body physiology, including serving as molecular sensors for numerous fat soluble hormones, Vitamins A and D, and dietary lipids.

The first study focuses on the gene for PPARd, a master regulator that controls the ability of cells to burn fat. When the “delta switch” is turned on in adipose tissue, local metabolism is activated resulting in increased calorie burning. Increasing PPARd activity in muscle produces the “marathon mouse,” characterized by super-ability for long distance running. Marathon mice contain altered muscle composition, which doubles its physical endurance, enabling it to run an hour longer than a normal mouse. Marathon mice contain increased levels of slow twitch (type I) muscle fiber, which confers innate resistance to weight gain, even in the absence of exercise.

Additional work to be reported at Experimental Biology looks at another characteristic of PPARd: its role as a major regulator of inflammation. Coronary artery lesions or atherosclerosis are thought to be sites of inflammation. Dr. Evans found that activation of PPARd suppresses the inflammatory response in the artery, dramatically slowing down lesion progression. Combining the results of this new study with the original “marathon mouse” findings suggests that PPARd drugs could be effective in controlling atherosclerosis by limiting inflammation and at the same time promoting improved physical performance.

Dr. Evans says he is very excited about the therapeutic possibilities related to activation of the PPARd gene. He believes athletes, especially marathon runners, naturally change their muscle fibers in the same way as seen in the genetically engineered mice, increasing levels of fat-burning muscle fibers and thus building a type of metabolic ‘shield” that keeps them from gaining weight even when they are not exercising.

But athletes do it through long periods of intensive training, an approach unavailable to patients whose weight or medical problems prevent them from exercise. Dr. Evans believes activating the PPARd pathway with drugs (one such experimental drug already is in development to treat people with lipid metabolism) or genetic engineering would help enhance muscle strength, combat obesity, and protect against diabetes in these patients.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Sarah Goodwin
Federation of American Societies for Experimental Biology

New research on the effects of the female sex hormone estrogen in the brain lend credence to what many women have suspected about the hormonal changes that accompany aging: Menopause can make you fat.Scientists long have sought to understand how changes in hormones during menopause could account for the increase in appetite and accompanying weight gain that often occurs among aging women.

In a series of animal experiments described today at the 234th national meeting of the American Chemical Society, the world’s largest scientific society, researchers showed how estrogen receptors located in the hypothalamus serve as a master switch to control food intake, energy expenditure and body fat distribution. When these receptors are destroyed, the animals immediately begin to eat more food, burn less energy and pack on pounds.

This research seems to support a link between estrogen and regulation of obesity, especially the dangerous accumulation of abdominal fat linked to heart disease, diabetes, and cancer, says Deborah J. Clegg, Ph. D., assistant professor of psychiatry at the University of Cincinnati Academic Health Center, who is directing the studies.

The findings may also help scientists develop more targeted hormone replacement therapies, capable of stimulating estrogen receptors in one part of the brain or body while dampening it in the next, Clegg says.

Estrogen receptors are located on cells throughout a woman’s body. Previous studies have shown that one type of estrogen receptor, known as estrogen receptor alpha or ER-alpha, plays a role in regulating food intake and energy expenditure. But scientists have been unable to pinpoint exactly where these fat-regulating receptors reside or how they work to govern these behaviors.

To determine the effect of dwindling estrogen levels in the brain, Clegg and her colleagues are focusing on two ER-alpha rich regions located in the hypothalamus, an area of the brain that controls body temperature, hunger and thirst. The first region, called the ventromedial nucleus or VMN, is a key center for energy regulation.

Using a relatively new gene-silencing technique called RNA interference, the researchers in earlier research deactivated the alpha-receptors in the VMN. The estrogen receptors in other regions of the brain maintained their normal capacity.

When estrogen levels in the VMN dipped, the animals’ metabolic rate and energy levels also plummeted. The findings show the animals quickly developed an impaired tolerance to glucose and a sizable weight gain, even when their caloric intake remained the same. What’s more, the excess weight went straight to their middle sections, creating an increase in visceral fat.

The findings suggested that the ER-alpha in this region plays an essential role in controlling energy balance, body fat distribution and normal body weight.

Clegg now plans to perform a similar experiment to deactivate ER-alpha in the arcuate nucleus region of the hypothalamus. This region contains two populations of neurons: one puts the brake on food intake and the other stimulates food intake. Clegg anticipates that a loss of estrogen in this region may create an increase in the animals’ appetites as well as their weight.

Clegg says her studies address an area that is sorely needed given the incidence and impact of gender differences in obesity and its complications.

“The accumulation of abdominal fat puts both men and women at a heightened risk of cardiovascular disease, diabetes, and insulin resistance,” she says. “Women are protected from these negative consequences as long as they carry their weight in their hips and saddlebags. But when they go through menopause and the body fat shifts to the abdomen, they have to start battling all of these medical complications.”

By identifying the critical brain regions that determine where body fat is distributed, Clegg says her findings may help scientists design hormone replacement therapies to better manage and manipulate estrogen levels.

“If we could target those critical regions and estrogen receptors associated with weight gain and energy expenditure, we could perhaps design therapies that help women sidestep many of the complications brought on by the onset of menopause,” she says.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Charmayne Marsh
American Chemical Society

 The American Chemical Society — the world’s largest scientific society — is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.

Deborah J. Clegg, Ph.D., is assistant professor of psychiatry at the University of Cincinnati Academic Health Center in Cincinnati, Ohio.

Taking a break in the middle of your workout may metabolize more fat than exercising without stopping, according to a recent study in Japan. Researchers conducted the first known study to compare these two exercise methods—exercising continually in one long bout versus breaking up the same workout with a rest period. The findings could change the way we approach exercise. Who wouldn’t want to take a breather for that”“Many people believe prolonged exercise will be optimal in order to reduce body fat, but our study has shown that repetitions of shorter exercise may cause enhancements of fat mobilization and utilization during and after the exercise. These findings will be informative about the design of [future] exercise regimens,” said lead researcher Kazushige Goto, Ph.D. “Most people are reluctant to perform a single bout of prolonged exercise. The repeated exercise with shorter bouts of exercise will be a great help [in keeping up with fitness].”

This finding is part of a study entitled Enhancement of fat metabolism by repeated bouts of moderate endurance exercise, found in the June 2007 edition of the Journal of Applied Physiology, which is published by the American Physiological Society. It was conducted by Kazushige Goto, of both the Department of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, Komaba, Tokyo, Japan and the Institute of Sports Medicine, Bispebjerg Hospital, Copenhagen, Denmark; Naokata Ishii, of the Department of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, Komaba, Tokyo, Japan; and Ayuko Mizuno and Kaoru Takamatsu, both of the Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan.

Summary of Methodology

The researchers used seven healthy (avg. body mass: 66.1, percentage fat: 17.6) men with an average age of 25 who were physically active and familiar with exercise and had them perform three separate trials:

  • one single bout of 60-min exercise followed with a 60-min recovery period (Single)
  • two bouts of 30-min exercise with a 20-min rest after the first 30-min bout, along with a 60-min recovery period at the end (Repeated)
  • one 60-min rest period (Control)

The men performed each trial at the same time of day after fasting overnight. They exercised on a single ergometer (cycling machine) at the commonly recommended exercise prescription of 60% maximum oxygen intake. The recovery and rest periods were conducted while the subjects sat in chairs. Blood samples were taken every 15 minutes during the exercise and every 30 minutes during the recovery period. Their respiratory gas and heart rates were monitored continuously throughout the trial.

Summary of Results

The Repeated trial showed a greater amount of lipolysis (fat breakdown) than did the Single trial. This Repeated trial also had a pronounced increase in free fatty acids and glycerol (chemical compounds that are released when stored fat is used) concentrations in the final 15 minutes of exercise, whereas these concentrations only progressively increased throughout the Single trial. Also, the second half of the Repeated trial showed a significantly greater epinephrine response while also having a rapid decrease in insulin concentration as a result of lower plasma glucose. This combination of high epinephrine and low insulin concentration may have also increased the lipolysis. There was also enhanced fat oxidation in the recovery period of the Repeated trial than in the Single trial, but this result may be because the free fatty acids concentration was already high before the recovery period.

Conclusions

The American College of Sports Medicine recommends moderate exercise for the duration of 45 to 60 minutes to ensure a sufficient amount of energy is depleted in obese individuals. This has caused a greater focus on extending exercise sessions in order to burn more fat. However, this study shows that this method may not be the most effective way to enhance fat metabolism, as splitting up a long bout of exercise with a rest period burns more fat than a continuous bout of exercise. This study could help with the practical application of implementing new exercise methods in order to better manage and control weight in individuals in the future. However, Goto and his team of researchers plan on conducting further studies in order to explore the results in a variety of exercise durations as well as in different types of individuals.

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Article adapted by MD Only Weblog from original press release.
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Contact: Celia Lee
American Physiological Society

It actually takes approximately twice as much time to take the elevator when ascending or descending one floor.  To test this, researchers at the University of South Carolina recorded the time required to ascend and descend one floor by taking the stairs and elevator over several days.  A small group of participants were instructed to alternate between elevator and stair use and to take the stairs at a self-selected “normal” pace during the course of their daily routine.

The time required to take the elevator was significantly greater than the time required to use the stairs going both up and down one floor. The excess time required when taking the elevator was attributed to the wait, not the travel time, since the actual elevator ride was measured at approximately 10 seconds.  The time required to ascend the stairs was greater than the time to descend the stairs, while there was no significant difference between taking the elevator up and elevator down one floor.

The study team hopes this information can be used as part of an intervention to increase stair use, where specific and relevant messages have been shown to be effective in encouraging physical activity.

“If climbing the stairs a few floors saves you time and adds to the physical activity you can accumulate throughout the day, it’s a win-win,” said researcher Joshua Westmeier-Shuh, lead author of the study.  “Let’s look first at shifting the perception that the elevator is a better choice when rushing to work or thinking about how to incorporate activity into the day, and then think about the implications this can have for worksite wellness.  Bottom line: stairs win.”

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Article adapted by MD Sports Weblog from original press release.
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Contact: Communications and Public Information
American College of Sports Medicine

The conclusions outlined in this news release are those of the researchers only, and should not be construed as an official statement of the American College of Sports Medicine.