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An answer to obesity: weight control protein

Sometimes the answers to complex problems lies at hand but that is the place no one looks. Same is the case with a new anti obesity drug. A weight control protein with a key role in the brain's ability to monitor body fat content may

Sometimes the answers to complex problems lies at hand but that is the place no one looks. Same is the case with a new anti obesity drug. A weight control protein with a key role in the brain's ability to monitor body fat content may yield new approaches for treating obesity and type 2 diabetes. The findings in mice further suggest that particular variants of the protein SH2-B might underlie obesity in humans, the researchers said. SH2-B, which has multiple functions in cells throughout the body, keeps the brain sensitive to the fat hormone leptin, found researchers from the University of Michigan Medical School. Produced by fat tissue, the leptin hormone sends signals to the brain about the body's fat content. That signal, in turn, elicits adjustments in appetite and energy expenditure to maintain normal body weight.

"Our findings reveal SH2-B as an important positive regulator of leptin sensitivity inside cells of the brain region known as the hypothalamus," said senior author of the study, Liangyou Rui. The hypothalamus is a key area in the central nervous system that integrates neuronal, hormonal, and nutrient-related signals to maintain body weight, he explained. Leptin is a hormone produced by fat that normally decreases food intake and increases energy expenditure. In many species, including humans, the hormone acts to stabilize weight and glucose balance through activating its receptors in the hypothalamus.

The current study shows that SH2-B also regulates energy balance and body weight by enhancing leptin sensitivity in animals, Rui said.

Further examination found that the animals lacking SH2-B ate nearly twice as much as normal. Surprisingly, Rui said, the animals burned more calories; however, the animals still have a net positive energy imbalance of more than 60% higher than normal animals at 18–19 weeks of age, owing to voracious feeding. The mice also exhibited defects in the leptin signaling pathway in brain cells of the hypothalamus, they report.

The new findings reveal SH2-B as a critical component in maintaining leptin sensitivity, Rui said. Therefore, SH2-B and signaling events regulated by SH2-B may serve as potential therapeutic targets for the treatment of obesity and type 2 diabetes.

"Because SH2-B sensitizes both leptin and insulin, action drugs that mimic or enhance SH2-B action may improve insulin and leptin sensitivity and have potential value in treatment of obesity and type 2 diabetes," he added

This could be a giant step in the leap for anti- obesity drugs.

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Source: University of Michigan


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