Description:
<jats:p>Bitter melon (<jats:italic>Momordica charantia</jats:italic>, MC) has been shown to improve markers of insulin resistance including adiposity, glucose and lipid profile in mice fed high fat diet. Fatty acids can activate toll‐like receptor (TLR) 4 signaling pathway resulting in the enhanced production and secretion of proinflammatory cytokines which may contribute to insulin resistance associated with diet induced obesity (DIO). The objective of this study was to examine the effect of MC on glucose and lipid homeostasis in an animal model of DIO and the role of TLR4 in mediating these effects. Eight week old male TLR4 mutant (C3H/HeJ) and control (C57BL/6) mice were randomly assigned to four dietary treatment groups for eight weeks (n=12–13/group): control (10% calories from fat), high fat (HF, 60% calories from fat), HF+1% (w/w) MC, and HF+10% (w/w) MC. Our preliminary data suggests that the C3H/HeJ strain exhibited significantly higher body weight, body fat, plasma cholesterol, and triglycerides in response to a high fat diet when compared to the C57BL/6 strain regardless of dietary treatment. However, C3H/HeJ strain had significantly lower area under the curve after a glucose tolerance test, plasma fructosamine and free fatty acid in comparison to the C57BL/6 strain. Mice fed the 10% MC, but not the 1% MC, improved glucose tolerance in the C57BL/6 but not the C3H/HeJ strain, suggesting MC may act through TLR4 signaling to modulate glucose homeostasis. The effects of MC and TLR4 mutation on mRNA expression of genes involved in glucose and lipid metabolism are currently being assessed. <jats:italic>(Supported by USDA,#2008‐35200‐18692)</jats:italic></jats:p>