Indole-3-carbinol prevents diet-induced obesity through modulation of multiple genes related to adipogenesis, thermogenesis or inflammation in the visceral adipose tissue of mice

Inflammation Male 2. Zero hunger 0301 basic medicine Adipogenesis Indoles Cell Differentiation Thermogenesis Intra-Abdominal Fat Diet, High-Fat Lipids 3. Good health Mice, Inbred C57BL Mice 03 medical and health sciences Adipose Tissue Gene Expression Regulation 3T3-L1 Cells Dietary Supplements Animals Anti-Obesity Agents Obesity
DOI: 10.1016/j.jnutbio.2011.12.005 Publication Date: 2012-05-07T15:34:50Z
ABSTRACT
Indole-3-carbinol (I3C) is a compound found in high concentrations in Brassica family vegetables, including broccoli, cauliflower and cabbage, and is regarded as a promising chemopreventive agent against various cancers. This study assesses the protective effect of I3C against diet-induced obesity in mice. Mice were randomly grouped to receive either a normal diet, high-fat (40% energy as fat) diet (HFD) or I3C-supplemented diet (1 g/kg diet) for 10 weeks. I3C supplementation significantly ameliorated HFD-induced increases in body weight gain, visceral fat pad weights and plasma lipid levels. The visceral adipose tissue mRNA levels of uncoupling proteins 1 and 3, crucial factors of thermogenesis, and their regulators such as sirtuin 1, peroxisome proliferator-activated receptor (PPAR) α and PPARγ coactivator 1α, which were down-regulated by HFD, were normalized by supplementation with I3C. In contrast, I3C supplementation significantly decreased expression levels of a key adipogenic transcription factor, PPARγ2, and its target genes, such as leptin and adipocyte protein 2, in the visceral adipose tissue of mice maintained on the HFD. Furthermore, HFD-induced up-regulation in mRNA levels of inflammatory cytokines (tumor necrosis factor α, interferon β and interleukin 6) was significantly ameliorated by I3C. These findings suggest that I3C has a potential benefit in preventing obesity and metabolic disorders, and the action for I3C in vivo may involve multiple mechanisms including decreased adipogenesis and inflammation, along with activated thermogenesis.
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