4.4 Article

PPAR- agonist elicits metabolically active brown adipocytes and weight loss in diet-induced obese mice

Journal

CELL BIOCHEMISTRY AND FUNCTION
Volume 33, Issue 4, Pages 249-256

Publisher

WILEY
DOI: 10.1002/cbf.3111

Keywords

PPAR-; brown adipocytes; thermogenesis; UCP-1; NRF-1; obesity

Funding

  1. Brazilian Council of Science and Technology (CNPq) [443014/2014-0]

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Obesity is considered a public health problem worldwide. Fenofibrate, a selective peroxisome proliferator-activated receptor (PPAR-) agonist, elicits weight loss in animal models. This study aimed to examine the effects of fenofibrate on energy expenditure, body mass (BM) and gene expression of thermogenic factors in brown adipose tissue of diet-induced obese mice. Male C57BL/6 mice were fed a standard chow (SC; 10% lipids) diet or a high-fat (HF; 50% lipids) diet for 10weeks. Afterwards, groups were subdivided as SC, SC-F, HF and HF-F (n=10, each). Treatment with fenofibrate (100mgkg(-1) BM mixed into the diet) lasted 5weeks. Treated groups had reduced final BM compared with their counterparts (p<005), explained by the increase in energy expenditure, CO2 production and O-2 consumption after treatment with fenofibrate (p<005). Similarly, genes involved in thermogenesis as PPAR-, PPAR- coactivator 1, nuclear respiratory factor 1, mitochondrial transcription factor A (Tfam), PR domain containing 16 (PRDM16), -3 adrenergic receptor (3-AR), bone morphogenetic protein 8B and uncoupling protein 1 were significantly expressed in brown adipocytes after the treatment (p<005). All observations ensure that selective PPAR- agonist can induce thermogenesis by increasing energy expenditure and enhancing the expression of genes involved in the thermogenic pathway. These results suggest fenofibrate as a coadjutant drug for the treatment of obesity. Copyright (c) 2015 John Wiley & Sons, Ltd.

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