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Fitness News - January 2007
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Wednesday, 31 January 2007
ANN ARBOR, Mich. - A single protein in brain cells may act as a linchpin in the body's weight-regulating system, playing a key role in the flurry of signals that govern fat storage, sugar use, energy balance and
weight, University of Michigan Medical School researchers report.
And although it's far too early to say how this protein could be useful in new strategies to fight the world's epidemic of obesity, the finding gives scientists an important system to target in future research and the development of anti-obesity medications.
In the February issue of the Journal of Clinical Investigation, U-M researcher Liangyou Rui, Ph.D. and his team report their findings on a protein called SH2B1, and specifically on its activity in brain cells.
Using a variety of genetic, diet and hormone techniques, they were able to show that the action of SH2B1 regulates body weight, the action of the metabolic signaling molecules leptin and insulin, and the use of energy from food. It even moderated the impact of a high-fat diet on body weight.
The experiments were performed in mice, including two types of mice that the team altered genetically so that they only expressed a unique form of the SH2B1 protein in their brain cells. The protein occurs elsewhere in the body, but the researchers were able to zero in on its activity in the hypothalamus: the area of the brain that coordinates signals from the brain and body relating to food, hunger, and the balance of energy and nutrients in the body.
Previously, Rui and his team have shown that mice that lack the gene for SH2B1 - called knockout mice - become obese, diabetic, and unable to stop eating. Their bodies lose the ability to sense the signals sent by leptin and insulin that tell the brain to slow down food intake and fat storage.
For the new paper, they looked at not only normal mice and mice that didn't have the SH2B1 gene, but also at mice that made SH2B1 only in brain cells, either in normal or larger-than-normal amounts. They found that restoring SH2B1 just in the brain completely corrected the metabolic disorders that the knockout mice had developed, but also improved the brain cells' ability to respond to leptin signals and produce further signals that regulate eating.
What's more, the mice that were treated to make extra SH2B1 didn't become obese or lose their ability to respond to leptin signals even after being fed a high-fat diet that caused those effects in other mice.
"Obesity, whether in mice or humans, is the product of an altered balance between energy intake and energy use. The imbalance is linked to alterations in leptin and insulin signaling that lead to excess weight gain and Type 2 diabetes, respectively," says Rui, an assistant professor of molecular and integrative physiology at U-M. "SH2B1 appears to play a key regulatory role in this system, through its direct influence on the processing of leptin and insulin signals in cells of the brain's hypothalamus"
Rui, who first discovered SH2B1's metabolic importance as a graduate student at U-M in the 1990s, worked on the new paper with postdoctoral fellow Decheng Ren, Ph.D., who also collaborated on a paper in the journal Cell Metabolism in 2005 that first indicated SH2B1's key role in obesity.
The team and other researchers have found that SH2B1, which was previously called SH2-B, is a kind of jack-of-all-trades in the world of cell signaling. Able to shuttle between the area just beneath the cell membrane and the nucleus, it can bind to many different molecules and facilitate signaling.
Specifically, it can bind to a variety of molecules called tyrosine kinases, including ones that serve as receptors for insulin and growth factors that circulate in the brain and body. One of its most important binding partners is JAK2, which is activated every time a leptin molecule binds to a cell.
Since leptin is the body's messenger boy to the brain to stop eating, we're full messages, and JAK2 helps receive those messages as they arrive, SH2B1's partnership with JAK2 is an important one. In a previous paper, Rui and his former mentor and current colleague Christin Carter-Su, Ph.D., showed that SH2B1 encourages the action and production of JAK2, unlike two other proteins that have been shown by other teams to reduce its activity. Carter-Su is a professor of molecular and integrative physiology and heads the biomedical research division of the Michigan Diabetes Research and Training Center.
In addition to revealing the importance of SH2B1 activity in the brain, the new paper shows that SH2B1 is expressed in four different forms in many tissues of the body, including fat cells known as adipose tissue, as well as the liver, heart, pancreas and muscle.
Rui and his team also explored the role of SH2B1 in fat cells, finding that the knockout mice that lacked the SH2B1 gene stored away much more fat than normal mice, and had much larger fat cells - giving them two-and-a-half times more body fat content than normal mice. The mice that had some of their SH2B1 restored in just their brains by genetic alteration did not experience this - and in fact had less fat than normal mice.
Since these mice lacked the ability to make SH2B1 in their fat cells, the authors suspect that fat-cell SH2B1 encourages the storing of fat. When they tested this theory, they found that SH2B1 appeared to help mouse embryonic cells turn into fat cells, a process called adipogenesis. But, they suspect, the action of SH2B1 in the brain trumps its action in fat tissue, leading to the development of obesity in mice that lack SH2B1 in both locations.
Rui and his team now hope to explore SH2B1's role in the brain and body even further, and hope to translate their findings into clinical research involving humans. They hope that their findings will help lead to better tactics for understanding the causes of obesity and its consequences, including Type 2 diabetes, and perhaps better methods for preventing and reversing them.
Monday, 29 January 2007
Do adolescents get enough exercise and eat the right foods? Is there too much fat in their diets? In a study published in the February 2007 issue of the American Journal of Preventive Medicine, researchers analyz
ed the behavior of almost 900 11-to-15 year-olds and found that nearly 80% had multiple physical activity and dietary risk behaviors, almost half had at least three risk behaviors, and only 2% met all four of the health guidelines in the study.
Using both physical measurements and surveying techniques, four behaviors were assessed: physical activity, television viewing time, percent calories from fat, and daily servings of fruits and vegetables. In addition, parental health behaviors were sampled.
Fifty-five percent of adolescents did not meet the physical activity guideline, although significantly more boys (59%) than girls (33.6%) did meet the standard. About 30% exceeded 2 hours of television viewing time and the majority of the sample did not meet dietary standards. Only 32% and 11.9% of the sample met the recommendations for fat consumption and servings of fruits and vegetables, respectively.
There was some evidence that parents' health behaviors were associated with adolescents' health behaviors. For the girls, two parent health behaviors�never smoking and meeting fruit and vegetable guidelines�were associated with fewer adolescent risk behaviors. Parents' number of risk behaviors was weakly but positively associated with a higher number of risk behaviors in boys.
Writing in the article, Alvaro Sanchez, PhD, states, "These findings contribute to the body of evidence that most adolescents fail to meet multiple diet and physical activity guidelines and continue to be in need of interventions that target multiple behaviors. Although health promotion programs frequently target multiple behaviors, little is known about the best approaches to stimulating multiple behavior change. Further research is needed to investigate the feasibility and effectiveness of different strategies for promoting multiple behavior change in adolescence."
Friday, 26 January 2007
California's 'Governator' Arnold Schwarzenegger encourages students in his state to keep fit and stay healthy.
The former action star launched a program that challenges students to exercise for at l east half an hour to an hour thrice a week. In return, the school that gets the highest percentage of participants will be awarded a fitness center. Eleven other schools will get $1,000 to buy fitness equipment.
Schwarzengger gained fame in the 70s when he won the Mr. Olympia bodybuilding competition several times. He later moved into acting and became famous with movies like The Terminator and The Last Action Hero.
Tuesday, 23 January 2007
The researchers found that TRPA1, a protein that helps transmit pain signals, is a direct sensor of reactive chemicals. "While many noxious and pungent compounds were known to activate this pain receptor, we disc
overed that they do so by directly and irreversibly binding to the cysteine amino acids of this protein," said Ardem Patapoutian, a Scripps Research scientist whose laboratory conducted the study. "Our study shows that TRPA1 activation is directly linked to chemical insult."
"Cysteines, one of the twenty building blocks of all proteins, are known to undergo oxidation/reduction reactions," Patapoutian continued. "Somehow the TRPA1 protein is tuned to sense cysteine modifications. In fact, any cysteine reactive agent seems to activate TRPA1, although we don't know exactly how cysteine binding translates into ion channel activation."
But this activation mechanism comes with an interesting property.
"Generally, compounds that activate ion channels bind in a lock-and-key mechanism that is readily reversible," said Lindsey Macpherson, another author of the study and a Ph.D. candidate in the Scripps Research Kellogg School of Science and Technology. "The mechanism by which noxious compounds activate TRPA1 is unique. For example, compounds that activate an ion channels through a lock-and-key mechanism have structural similarity. TRPA1 activators have no structural similarity; instead, they share a common potential for chemical reactivity, and their binding is long-lasting."
TRPA1 is not unique among proteins to be activated by cysteine modifying agents, the study noted. Another signaling protein known as Kelch-like ECH-associated protein 1 (KEAP1) is activated by many of the same compounds that activate TRPA1; KEAP1 is a sensor for oxidative damage from free radicals and upregulates expression of antioxidant enzymes. Apparently, reactive compounds can activate at least two pathways through cysteine modification as a warning against cell damage, the study concluded.
"Our findings, which are the result of a successful collaboration with the Ben Cravatt and Peter Schultz labs at Scripps Research, show that modification of reactive cysteines within TRPA1 can cause channel activation," Macpherson said. "Our research efforts are now aimed at further understanding how binding of these compounds activate the channel, and identifying the physiological role of TRPA1 in sensing oxidative stress." The protein is currently being investigated by several pharmaceutical companies as a potential target for chronic pain, Patapoutian noted.
The study was published January 21, 2007 in an advanced online edition of the journal Nature.
Friday, 19 January 2007
Given that around half of the world's burden of cardiovascular disease is carried by low and middle income countries in the region, these findings, published by the Asia-Pacific Cohort Studies Collaboration (APCS
C) in the Journal of Hypertension, highlight the immense impact that blood pressure-lowering strategies could have in the area.
Dr Alexandra Martiniuk, author and Senior Research Fellow at The George Institute for International Health (part of the APCSC Secretariat) said, "We aimed to identify the role of hypertension (high blood pressure) in cardiovascular diseases in the Asia-Pacific region and found that hypertension was the key factor in more than half of cases. This shows the potential reduction in deaths from heart disease and stroke that could have been achieved if high blood pressure were controlled in this region."
APCSC Researchers found that the fraction of deaths caused by stroke, as a result of hypertension, reaches up to over 60% in certain countries (Indonesia and Mongolia). High levels were also found in Malaysia, China, Philippines and Hong Kong (over 50%). The study also identified high blood pressure causes a high percentage of deaths caused by heart disease in Mongolia and China at around 30%.
Researchers used recent data on hypertension from more than half a million adult participants to determine the risks for heart disease and stroke attributable to hypertension. The research was also able to attain precise estimates for women in the region, confirming that hypertension is as risky for women as men.
Hypertension is the third leading modifiable risk factor for global burden of disease after tobacco and alcohol. Priority needs in this area include population-based strategies to prevent or reduce high blood pressure, as well as prevention and treatment of high blood pressure in individuals.
Dr Martiniuk added that "There is little doubt that salt is the leading cause of high blood pressure in the area. Salt consumption in China, particularly Northern China, is among the highest in the world. Efforts to restrict its addition to food and as a storage medium in parts of Asia would help in reducing its role in increasing hypertension."
Low and middle income countries such as China and India account for 80% of global cardiovascular-related deaths and 87% of cardiovascular related disabilities.
Priority needs in this area include population-based prevention strategies to prevent or reduce high blood pressure as well as individual-level prevention and treatment of high blood pressure.
The APCSC is the largest-ever partnership and study of cardiovascular disease in the Asian region. Project partners included many medical institutions across the Asia Pacific region.
The collaboration's primary goal is to provide direct, reliable evidence about the determinants of stroke, coronary heart disease, and other common causes of death in Asia-Pacific populations. It aims to produce region-, age- and gender-specific estimates of the cardiovascular disease risks associated with blood pressure, cholesterol, diabetes and other major risk factors.
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