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Induction of cardiac uncoupling protein-2 expression and adenosine 5'-monophosphate-activated protein kinase phosphorylation during early states of diet-induced obesity in mice.

Somoza B, Guzmán R, Cano V, Merino B, Ramos P, Díez-Fernández C, Fernández-Alfonso MS, Ruiz-Gayo M

Departamento de Farmacología, Tecnología y Desarrollo Farmacéutico, Facultad de Farmacia, Universidad San Pablo-Ceu, Urbanización Montepríncipe, Carretera de Boadilla del Monte km 5,3 Boadilla del Monte, 28668 Madrid, Spain.

The objective of this work was to characterize the adaptation of cardiac metabolism to a lipid overload in a model of diet-induced obesity (DIO) in mice. After 8 wk dietary treatment, mice receiving a high-fat diet exhibited an increase in the amount of adipose tissue, accompanied by a surge in plasma leptin concentration (from 5.4-16.0 ng/ml). This was associated with: 1) an induction of uncoupling protein-2 (120%), 2) an increase in the phosphorylated form of AMP-activated protein kinase (120%), and 3) a reduction in lactate concentration and lactate dehydrogenase activity in myocardial tissue (40%). Because DIO induces leptin resistance, we analyzed leptin receptor functionality by measuring phospho-signal transducer and activator of transcription 3 in response to acute leptin (1 mg/kg). We observed that leptin receptor signaling remained unaltered within the heart but was fully impaired within the hypothalamus. Taken together, these data show that during DIO development, there is a metabolic shift in the heart aimed at increasing fatty acid oxidation to the detriment of carbohydrates. This effect seems to be leptin-dependent, suggesting that the increased adiposity observed during the onset of obesity might contribute to impairing ectopic lipidic deposition in the heart.

Published 16 February 2007 in Endocrinology, 148(3): 924-31.
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