Fat Hormone Leptin May Control Diabetes

Leptin May Control Gene in Liver That Reverses Diabetes

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Jan. 5, 2010 -- The so-called fat hormone leptin may play a key role in controlling and potentially reversing diabetes, a role that has nothing to do with its link to weight loss.

The hormone leptin has been nicknamed the fat hormone after numerous studies have shown it promotes weight loss, which in turn has a beneficial effect on diabetes control.

But a new study suggests that small amounts of leptin -- too small to promote weight loss -- are enough to control the activity of a gene known as IGFBP2 in the liver that improves diabetes in animals and may have the same effect in people.

"It was surprising to me how potent leptin was in treating diabetes," researcher Jeffrey Friedman of Rockefeller University says in a news release. "It had a highly significant impact at plasma levels that were undetectable."

Researchers say the findings confirm that leptin’s beneficial effects on diabetes control are independent of the hormone’s weight loss effects. Previous studies have shown that treatment with hormone leptin corrects high blood sugar and insulin levels in mice and people with low levels of the hormone.

To examine leptin’s effects on diabetes control, researchers first identified the lowest dose of leptin that improved insulin resistance and diabetes without causing animals to eat less or lose weight.

They then looked at the effects of these low doses of leptin on activity of genes in the animals’ livers.

The results, published in Cell Metabolism, showed leptin increased IGFBP2 in obese and diabetic mice and reversed their diabetes. Researchers also found mice treated with the fat hormone responded to insulin three times better than untreated mice.

Further studies will be needed to determine if leptin treatment in people has the same positive effects on diabetes control.

WebMD Health News Reviewed by Louise Chang, MD on January 05, 2010

Sources

SOURCES:

Hedbacker, K. Cell Metabolism, January 2010; vol 11: pp 11-22.

News release, Cell Press.

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