Poster Topical Area: Nutrient-Gene Interactions
Location: Hall D
Poster Board Number: 449
Objectives: Brown adipose tissue (BAT) plays a critical role in energy expenditure through its thermogenic function. Therefore, its activation may help prevent and/or treat obesity. We have previously reported that eicosapentaenoic acid (EPA), an omega 3 polyunsaturated fatty acid, significantly increased the thermogenic uncoupling protein 1 (UCP1) as well as gene expression of other key thermogenic markers in BAT of diet-induced obese male mice. However, whether female mice respond similarly to EPA has not been investigated. Further, it is unknown whether metabolic effects of EPA on BAT require UCP1 expression. We hypothesize that EPA reduces obesity and insulin resistance and activates BAT in female mice, and these effects are dependent on UCP1 expression.
Methods: We used wild type (WT) and UCP1 knockout (KO) female mice housed at thermoneutral temperature (30°C), a temperature shown to induce obesity in the KO animals. Mice were fed high fat diets (HF) without or with EPA for up to 14 weeks. Body weight (BW), body composition, and insulin tolerance tests were measured. Serum, BAT and other tissues were harvested for future analyses.
Results: WT female mice (both HF and EPA) consumed significantly more food compared to the KO mice (P<0.05). However, both WT groups gained significantly less weight than the two KO groups (P<0.05). Additionally, in both WT and KO mice, EPA significantly reduced the total body fat percentage (P<0.05) along with decreases in BAT and white adipose tissue (WAT) weights compared to HF-fed WT and KO mice. Furthermore, in both genotypes, insulin sensitivity was significantly higher in the EPA groups compared to the HF groups (P<0.05).
Conclusions: These findings demonstrate that inactivation of the UCP1 gene in female mice dysregulates energy metabolism. Further, EPA protects female mice from diet-induced obesity, and these effects were independent of UCP1. Additional mechanistic studies in BAT and other tissues from these mice are necessary to determine mechanisms mediating the effects of EPA.
NIH/NCCIH grant # R15AT008879-01A1
Texas Tech University