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Differential impacts of high fat and high Se diets on tissue lipid profiles of young adult and old wild‐type and GPX1‐/‐ mice (374.5)
Author(s) -
Zhao Zeping,
Kim Jonggun,
Lei Xin Gen
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.374.5
Subject(s) - endocrinology , medicine , nefa , adipose tissue , hyperinsulinemia , chemistry , white adipose tissue , lipogenesis , biology , obesity , insulin resistance , insulin
Our previous research has demonstrated hyperinsulinemia and elevated lipogenesis by feeding pigs and rats with Se at 3.0 mg/kg of diet. This study was to determine the impacts of a moderately high Se (1.0 vs. 0.3 mg/kg as selenite) and(or) high fat (60 vs. 16% energy from fat) on lipid profiles in plasma, adipose and liver tissues of young adult (2‐4 mo of age) and old (6‐10 mo of age) wild‐type (WT) and GPX1‐/‐ (KO) male mice. A total of 80 mice were divided into 4 parallel (genotype by age) experiments (n = 5/group) and fed one of 4 diets for 6 wk. Body weight was elevated (P < 0.05) by the high fat diet in old WT and young KO mice, but decreased by high Se diet (P < 0.05) in young WT mice. Both high fat and Se intakes enhanced (P < 0.05) plasma glucose concentrations in old WT mice. High Se intake decreased plasma non‐esterified fatty acids (NEFA) concentrations in young WT mice. There was little effect of high fat or Se intake on plasma lipid profiles of KO mice. Adipose tissue concentrations of triglycerides, cholesterol, and NEFA were consistently elevated by high fat and Se in both young WT and KO mice. In comparison, such effects of the dietary treatments on adipose tissue of old WT and KO mice or on liver of all 4 groups of mice were less obvious or consistent. In conclusion, our results revealed a uniquely high response of adipose tissue lipid profile to dietary intakes of high fat and Se and a strong interaction of age by GPX1 knockout on the response (NIH DK 53018). Grant Funding Source : (NIH DK 53018).