1. Academic Validation
  2. Dihydrocapsiate supplementation prevented high-fat diet-induced adiposity, hepatic steatosis, glucose intolerance, and gut morphological alterations in mice

Dihydrocapsiate supplementation prevented high-fat diet-induced adiposity, hepatic steatosis, glucose intolerance, and gut morphological alterations in mice

  • Nutr Res. 2018 Mar;51:40-56. doi: 10.1016/j.nutres.2017.11.006.
Ritesh K Baboota 1 Pragyanshu Khare 2 Priyanka Mangal 3 Dhirendra Pratap Singh 2 Kamlesh K Bhutani 3 Kanthi K Kondepudi 2 Jaspreet Kaur 4 Mahendra Bishnoi 5
Affiliations

Affiliations

  • 1 National Agri-Food Biotechnology Institute (NABI), SAS Nagar, Punjab, India 160071; Biotechnology division, University Institute of Engineering and Technology (UIET), Panjab University, Chandigarh, India 160036.
  • 2 National Agri-Food Biotechnology Institute (NABI), SAS Nagar, Punjab, India 160071.
  • 3 Department of Natural Products, National Institute of Pharmaceutical Education and Research (NIPER), SAS Nagar, Punjab, India 160062.
  • 4 Biotechnology division, University Institute of Engineering and Technology (UIET), Panjab University, Chandigarh, India 160036. Electronic address: jaspreet_virdi@yahoo.com.
  • 5 National Agri-Food Biotechnology Institute (NABI), SAS Nagar, Punjab, India 160071. Electronic address: mbishnoi@gmail.com.
Abstract

Despite the lipolytic and thermogenic properties of capsaicin, its putative use as a weight-lowering dietary supplement has been limited because of the burning sensation caused by capsaicin when it comes in contact with mucous membranes. A potential alternative to capsaicin are the capsinoids, nonpungent capsaicin analogs that exhibit effects similar to capsaicin. Whereas the antiobesity properties of capsinoids have been reported, the effectiveness of FDA-approved synthetic dihydrocapsiate has not yet been investigated. In the present study, we hypothesized that dihydrocapsiate might ameliorate high-fat diet (HFD)-induced metabolic disorders in a manner similar to capsaicin and therefore can be its nonpungent alternative. To test this hypothesis, HFD-fed mice were orally administered dihydrocapsiate (2 and 10mg/kg body weight) for 12weeks. Dihydrocapsiate modestly reduced the HFD-induced weight gain and significantly prevented the associated hyperglyceridemia and hyperinsulinemia while improving glucose tolerance. Histological and gene expression analysis showed that dihydrocapsiate significantly prevented the lipid accumulation in white adipose tissue and brown adipose tissue via targeting genes involved in energy expenditure and mitochondrial biogenesis, respectively. Dihydrocapsiate corrected hepatic triglyceride concentrations and normalized expression of genes regulating hepatic lipid and glucose metabolism. Moreover, dihydrocapsiate administration significantly improved gut morphology and altered gut microbial composition, resulting in reduced host energy availability. Collectively, these results indicate that dihydrocapsiate administration improved glucose tolerance, prevented adiposity and hepatic steatosis, as well as improved HFD-induced gut alterations, positing dihydrocapsiate as a potential food ingredient for the dietary management of HFD-induced metabolic alterations.

Keywords

Dihydrocapsiate; Glucose intolerance; HFD; Hepatic steatosis; Obesity.

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