Washington, Jan 6 (ANI): A new study has found that fat hormone leptin might help control diabetes.

The researchers found that the hormone controls the activity of a gene known as IGFBP2 in the liver, which has antidiabetic effects in animals and could have similar therapeutic effect in humans.

“It was surprising to me how potent leptin was in treating diabetes,” said Jeffrey Friedman of Rockefeller University.

“It had a highly significant impact at plasma levels that were undetectable,” Friedman added.

Earlier studies have shown that leptin treatment effectively corrects high blood sugar and insulin levels in leptin-deficient mice and humans.

Leptin’s usefulness as a therapy has also been shown in some clinical settings, in people with rare metabolic disorders. But it wasn’t clear exactly how the hormone produced in fat tissue acts to improve diabetes.

During the study, Friedman and his colleagues first identified the lowest dose of leptin that could correct insulin resistance and diabetes without leading animals to eat less or lose weight.

They then looked to see how that very low-level infusion of leptin changes the activity of genes in the animals’ livers. That survey led them to IGFBP2.

Treatments designed to increase IGFBP2 expression in obese and diabetic mice reversed their diabetes.

The researchers found that animals treated with the protein responded to insulin three times better than untreated ones.

They also found that leptin-deficient patients do indeed have lower blood levels of IGFBP2 at baseline and that those levels can be raised with low-dose leptin treatment.

“In summary, we have developed a set of conditions in which leptin treatment potently improves diabetes independent of its ability to correct weight and food intake,” said the researchers.

“This protocol was used to identify IGFBP2 as a leptin-regulated gene whose expression is correlated with leptin’s antidiabetic effect…Further studies will reveal whether IGFBP2 shows similar antidiabetic effects in clinical settings,” they added. (ANI)