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Reduced mobilization of fat contributes to metabolic health

Obesity and unhealthy diets trigger a variety of health problems, including type 2 Diabetes with more than 60,000,000 Europeans suffering from it. Since many people do not change their unhealthy life styles, pharmaceutical companies have long been seeking for therapeutic interventions to protect from the health problems associated with the metabolic syndrome. Richard Moriggl and his team has now discovered a molecular mechanism that might be suitable as target for such a therapy. The results have been published in Diabetologia, the journal of the European Association for the Study of Diabetes (EASD).

Overweight leads to several comorbidities, including type 2 diabetes. Free image from pixabay

Mice lacking STAT5 in fat cells have a markedly reduced ability to mobilize fat stores. As a result, STAT5-deficient mice have a higher body fat content than normal mice. The researchers were able to demonstrate that STAT5 is involved in the gene regulation of the lipid-cleaving enzyme ATGL. Thereby, a new mechanism that contributes to the regulation of fat depot catabolism was discovered.

Despite the increased body fat content, both young and elderly mice with missing STAT5 are metabolically "healthier" and remain insulin sensitive. This might be attributed to the reduced products of lipolysis in the blood. When fats are mobilized the bloodstream is full of free fatty acids, which are known to contribute to the development of insulin resistance in higher concentrations. The study thus provides a basis for further research into the extent to which the inhibition of STAT5 in adipose tissue might constitute a possible therapeutic intervention for diseases such as diabetes or coronary heart and cardiovascular disease.
 

 

Publication in Diabetologia:
Adipocyte STAT5 deficiency promotes adiposity and impairs lipid mobilisation in mice
D. Kaltenecker, K. M. Mueller, P. Benedikt, U. Feiler, M. Themanns, M. Schlederer, L. Kenner, M. Schweiger, G. Haemmerle and R. Moriggl