New insights into relationship between muscle fat accumulation and insulin resistancePress release 3 July 2012
The accumulation of fat in muscle and liver plays an important role in the development of type 2 diabetes. Up till now, the substance diacylglycerol (a by-product of fatty acid oxidation) was thought to be responsible. Researchers at Maastricht University have demonstrated that the relationship between fat accumulation and diacylglycerol is not as unambiguous as once thought, and that the enzyme AMP-activated protein kinase (AMPK) plays an important role. Their research results were published this week in the high-impact journal, Proceedings of the National Academy of Sciences of the USA (PNAS).
Silvie Timmers, a postdoc researcher, stimulated fat accumulation by farmacologically inhibiting fat oxidation in order to study the effects of fat accumulation. Remarkably, it was found that, despite profuse fat accumulation and increased diacylglycerol in the muscles, insulin sensitivity was improved rather than decreased. In additional human, animal and human studies have shown that the activation of AMPK – the enzyme that controls the level of energy in cells – is responsible for this.
These findings shed new light on the relationship between fat accumulation in muscle and insulin sensitivity. Furthermore, the study proves the important role of regular exercise in the treatment of insulin resistance and the prevention of type 2 diabetes, as movement stimulates AMPK activation.
Timmers is a member of the research group of Professor Schrauwen and Professor Hesselink within NUTRIM, which studies the mechanisms that lead to the development of type 2 diabetes.
Note for the press:
Full title of the publication: Silvie Timmers, Miranda Nabben, Madeleen Bosma, Bianca van Bree, Ellen Lenaers, Denis van Beurdena, Gert Schaart, Margriet S. Westerterp-Plantenga, Wolfgang Langhans, Matthijs K. C. Hesselink, Vera B. Schrauwen-Hinderling, and Patrick Schrauwen, Augmenting muscle diacylglycerol and triacylglycerol content by blocking fatty acid oxidation does not impede insulin sensitivity, Proceedings of the National Academy of Sciences of the USA.
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