Dietary Fatty Acids Alter Lipid Profiles and Induce Myocardial Dysfunction without Causing Metabolic Disorders in Mice.

Bainian Chen,Mark Bernards,Rui Ni,Dong Zheng,Yifan Huang

doi:10.3390/nu10010106

Abstract

Oversupply of bulk saturated fatty acids (SFA) induces metabolic disorders and myocardial dysfunction. We investigated whether, without causing metabolic disorders, the uptake of individual dietary SFA species alters lipid profiles and induces myocardial dysfunction. C57BL/6 mice were fed various customized long-chain SFA diets (40% caloric intake from SFA), including a beef tallow (HBD), cocoa butter (HCD), milk fat (HMD) and palm oil diet (HPD), for 6 months. An isocaloric fat diet, containing medium-chain triglycerides, served as a control (CHD). Long-term intake of dietary long-chain SFA differentially affected the fatty acid composition in cardiac phospholipids. All long-chain SFA diets increased the levels of arachidonic acid and total SFA in cardiac phospholipids. The preferential incorporation of individual SFA into the cardiac phospholipid fraction was dependent on the dietary SFA species. Cardiac ceramide content was elevated in all mice fed long-chain SFA diets, while cardiac hypertrophy was only presented in mice fed HMD or HPD. We have demonstrated that the intake of long-chain SFA species differentially alters cardiac lipid profiles and induces cardiac dysfunction, without causing remarkable metabolic disorders.

Highlights

Obesity and type-2 diabetes are prevalent in Western countries and countries elsewhere that have adopted a Western lifestyle
There were no significant differences in heart weight and heart/body weight ratio among the different high saturated fatty acid (SFA) diets groups, including CHD (Table S2 of Supplementary File 2)
HMD induced a slight increase in the area under curve (AUC) for intraperitoneal glucose tolerance (IPGTT), compared with that of CHD

Summary

Introduction

Obesity and type-2 diabetes are prevalent in Western countries and countries elsewhere that have adopted a Western lifestyle In both conditions, lipotoxic cardiomyopathy commonly ensues, due to excessive fatty acid uptake by cardiomyocytes. Cardiomyocytes, isolated from high-fat fed mice, displayed contractile defects, compared with those from control animals [6] In these animal models of obesity, myocardial dysfunction may be directly associated with saturated fatty acid (SFA) oversupply. Previous investigations have shown that oversupply of SFA directly impairs contractile performance and induces apoptosis of cardiac myocytes, in vitro [7,8,9] Whether these effects are mediated by bulk SFA or by individual lipid species in vivo remains largely elusive

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Conclusion