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Fat-generated hormone drives energetic capacity of muscle

The fat-generated hormone adiponectin plays an important role in the energetic capacity of skeletal muscle, according to a new study in the July, 2006, Cell Metabolism, published by Cell Press. Adiponectin is unusual among fat hormones in that its levels generally decline in those who are obese.

The researchers report evidence in people and mice, linking low adiponectin levels to insulin resistance and reductions in the number of "cellular power plants" called mitochondria in skeletal muscle. The findings suggest that therapies designed to boost the adiponectin signal might prove beneficial for the treatment of insulin resistance and diabetes, they said.

"We have discovered a skeletal muscle pathway by which adiponectin increases mitochondrial number and function and exerts antidiabetic effects," said lead author Anthony Civitarese from Pennington Biomedical Research Center in Baton Rouge, Louisiana.

Mitochondria utilize nutrient components, including fats and carbohydrates, to generate usable energy. The number of mitochondria therefore influences the way that muscles function. For example, people who exercise regularly have more mitochondria in their muscles than do those who are sedentary.

Earlier studies found that obese individuals and those with type 2 diabetes have reduced adiponectin concentrations, the researchers said. The new study examined the effects of that reduced adiponectin on skeletal muscle.

The researchers first examined children whose parents had type 2 diabetes and those with no family history of the disease. Muscle taken from individuals prone to diabetes was insulin resistant and had lower than normal concentrations of mitochondrial enzymes, suggesting some dysfunction, they found. The level of adiponectin also correlated with the estimated number of mitochondria in the muscle samples.

Further study of adiponectin-deficient mice similarly found that the animals were resistant to insulin
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Contact: Heidi Hardman
hhardman@cell.com
617-397-2879
Cell Press
5-Jul-2006


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