4.7 Article

The effects of fatty acid composition on cardiac hypertrophy and function in mouse models of diet-induced obesity

期刊

JOURNAL OF NUTRITIONAL BIOCHEMISTRY
卷 46, 期 -, 页码 137-142

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2017.05.009

关键词

Lipid overload; Lipid metabolism; Cardiomyopathy; Fatty acid profiling; Mouse strain

资金

  1. American Heart Association [14SDG18590020, 15POST21620006]
  2. National Institutes of Health [HL088634, HL110349, HL118989, HL129510]
  3. Coordenacao de Aperfeicoamento Pessoal de Nivel Superior [CAPES 7231-12-1]
  4. Sao Paulo Research Foundation

向作者/读者索取更多资源

High-fat diets (HFDs) are used frequently to study the development of cardiac dysfunction in animal models of obesity and diabetes. However, impairment in systolic function, often reported as declining ejection fraction, may not consistently occur in a given time frame which could be contributable to a variety of factors within the experimental design. One major factor may be the amounts of saturated and unsaturated fatty acids (FAs) that are present in the diet. To determine whether the FA content and composition were critical determinants in the development of cardiac dysfunction in response to high-fat feeding, we fed adult, male mice Western diet (45% fat, 60% saturated), Surwit diet (60% fat, 90% saturated), milk-fat-based diet (60% fat, 60% saturated) or high-fat Western diet (HFWD, 60% fat, 32% saturated) for 12 weeks. We report that neither the amount of total fat nor the ratio of saturated to unsaturated FM in the diets differentially affects body weight and adiposity in mice. In addition, no evidence of systolic dysfunction is present after 12 weeks. Interestingly, the HFWD, with equal parts saturated, monounsaturated and polyunsaturated FM, induces mild cardiac hypertrophy and diastolic dysfunction after 12 weeks, which coincides with elevated serum levels of arachidonic acid. Our results suggest that the dietary FA content and composition may be a primary determinant of diastolic, but not systolic, dysfunction in animal models of diet-induced obesity. (C) 2017 Elsevier Inc. All rights reserved.

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