Medium-chain Triglyceride Ameliorates Insulin Resistance and Inflammation in High Fat Diet-Induced Obese Mice

Eur J Nutr. 2016 Apr;55(3):931-40. doi: 10.1007/s00394-015-0907-0. Epub 2015 Apr 25.

Abstract

Purpose: The aim of the present study was to investigate the in vivo effects of dietary medium-chain triglyceride (MCT) on inflammation and insulin resistance as well as the underlying potential molecular mechanisms in high fat diet-induced obese mice.

Methods: Male C57BL/6J mice (n = 24) were fed one of the following three diets for a period of 12 weeks: (1) a modified AIN-76 diet with 5 % corn oil (normal diet); (2) a high-fat control diet (17 % w/w lard and 3 % w/w corn oil, HFC); (3) an isocaloric high-fat diet supplemented with MCT (17 % w/w MCT and 3 % w/w corn oil, HF-MCT). Glucose metabolism was evaluated by fasting blood glucose levels and intraperitoneal glucose tolerance test. Insulin sensitivity was evaluated by fasting serum insulin levels and the index of homeostasis model assessment-insulin resistance. The levels of serum interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor-α were measured by ELISA, and hepatic activation of nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways was determined using western blot analysis.

Results: Compared to HFC diet, consumption of HF-MCT did not induce body weight gain and white adipose tissue accumulation in mice. HFC-induced increases in serum fasting glucose and insulin levels as well as glucose intolerance were prevented by HF-MCT diet. Meanwhile, HF-MCT resulted in significantly lower serum IL-6 level and higher IL-10 level, and lower expression levels of inducible nitric oxide synthase and cyclooxygenase-2 protein in liver tissues when compared to HFC. In addition, HF-MCT attenuated HFC-triggered hepatic activation of NF-κB and p38 MAPK.

Conclusions: Our study demonstrated that MCT was efficacious in suppressing body fat accumulation, insulin resistance, inflammatory response, and NF-κB and p38 MAPK activation in high fat diet-fed mice. These data suggest that MCT may exert beneficial effects against high fat diet-induced insulin resistance and inflammation.

Keywords: Inflammation; Insulin resistance; Medium-chain triglyceride; NF-κB; p38 MAPK.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / metabolism
  • Animals
  • Blood Glucose / metabolism
  • Body Weight
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Diet, High-Fat / adverse effects*
  • Dietary Supplements
  • Fasting
  • Glucose Tolerance Test
  • Inflammation / blood*
  • Insulin / blood
  • Insulin Resistance*
  • Interleukin-10 / blood
  • Interleukin-6 / blood
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Obese
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • Obesity / blood*
  • Triglycerides / administration & dosage*
  • Triglycerides / blood
  • Tumor Necrosis Factor-alpha / blood
  • p38 Mitogen-Activated Protein Kinases / genetics
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Blood Glucose
  • Insulin
  • Interleukin-6
  • NF-kappa B
  • Triglycerides
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2
  • p38 Mitogen-Activated Protein Kinases