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Effects of IL‐15 on Rat Brown Adipose Tissue: Uncoupling Proteins and PPARs
Author(s) -
Almendro Vanessa,
Fuster Gemma,
Busquets Sílvia,
Ametller Elisabet,
Figueras Maite,
Argilés Josep M.,
LópezSoriano Francisco J.
Publication year - 2008
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2007.47
Subject(s) - brown adipose tissue , adipose tissue , uncoupling protein , thermogenin , endocrinology , medicine , chemistry
Objectives: Interleukin‐15 (IL‐15) plays an important role in lipid metabolism as its administration to rats causes a marked depletion of white adipose tissue (WAT). This reduction in fat mass seems to be caused by and related to hipotriglyceridemia as a result of a lower hepatic lipogenesis and an increased fatty acid oxidation. We have previously observed that IL‐15 treatment induces the expression of uncoupling proteins (UCPs) in muscle. The aim of this study was to investigate the effects of IL‐15 on brown adipose tissue (BAT), and in particular on genes related to lipid metabolism in this tissue. Methods and Procedures: Male Wistar rats were treated daily with IL‐15 for 7 days. Adipose tissues were collected and the mRNA content of UCPs, peroxisome proliferator–activated receptors (PPARs) and several genes implicated in fatty acid transport and oxidation were evaluated on BAT. Results: IL‐15 treatment in rats causes a decrease in the mass of both WAT and BAT (35 and 24%, respectively). In BAT, an important upregulation of the mRNA content of thermogenic proteins (UCP1 and UCP3), lipid‐related transcription factors (PPARδ and PPARα) and other proteins implicated in membrane transport (fatty acid translocase (FAT) and fatty acid transport protein (FATP)), mitochondrial transport (carnitine palmitoyl transferase‐I (CPT‐I) and CPT‐II) and consumption (acyl‐CoA synthetase 4 (ACS4)) of fatty acids was observed as a consequence of the treatment. Discussion: The changes observed in BAT suggest that IL‐15 could be implicated in lipid consumption in this tissue by regulating lipid oxidation and probably thermogenesis, processes mediated by UCPs and PPARs.