Ingested Capsaicinoids Can Prevent Low‐Fat/High‐Carbohydrate diet and High‐Fat Diet‐Induced Obesity by Regulating the Expression of Genes for Metabolism

Abstract

BACKGROUNDWe previously found that ingested capsaicinoids (CAPs) inhibit pancreatic lipase and the mRNA levels of adipogenic genes such as peroxisome proliferator‐activated receptor‐gamma (PPAR‐gamma) and CCAAT enhancer‐binding protein‐alpha (C/EBP‐alpha) decreased in in vitro models. The aim of this study was to investigate the capsaicinoids (CAPs) effects on regulating the gene protein levels in low fat/high carbohydrate diet (LF/HCD) and high fat diet (HFD) induced obesity in rats.METHODSEight week male Wistar rats were fed on a LF/HCD and HFD with and without capsaicinoids compared with control group (CTL, +/− CAPs) for 8 weeks to induce obesity. Subsequently they were divided into different groups and were maintained on a CTL (+/− 0.2mg CAPs, 10 mg/kg bw CapsimaxTM, LF/HCD (+/− 0.2mg CAPs, 10 mg/kg bw CapsimaxTM) and HFD (+/−0.2 mg CAPs, 10 mg/kg bw CapsimaxTM) for 8 weeks. Changes in the gene protein levels of gp91phox (NOX2), Sirtuin 1 (SIRT1), nuclear factor NF‐κB, endothelial NO synthase (eNOS), NFkB, p22phox Protein (CYBA) and nuclear factor erythroid 2–related factor 2 (Nrf2) were analyzed. Serum and liver TBARS and total antioxidant capacity (TAC) were analyzed in all treatments.RESULTSExperimental diets supplemented with CAPs lowered the levels of mRNA levels of gp91phox (NOX2), NFkB, p22phox Protein (CYBA) and However, the mRNA levels of SIRT an important regulator of energy metabolism, Nrf2 an emerging regulator of cellular resistance to oxidant, eNOS a vasoprotective molecule nitric oxide (NO·) were significantly increased. CAPs treated groups had significant decrease in TBARS in serum and liver tissue and an increase in serum TAC were observed.CONCLUSIONThese results suggest that CAPs effectively reduces TBARS and increased TAC. These effects might be at least partially mediated via regulation of the gene proteins involved in energy metabolism, oxidative stress and vasoprotection.Support or Funding InformationOmniActive Health Technologies Inc.