Body adiposity dictates different mechanisms of increased coronary reactivity related to improved in vivo cardiac function.

Evangelia Mourmoura,Guillaume Vial,Jean-Paul Rigaudiere,Kasra Azarnoush,Luc Demaison,Béatrice Morio,Karine Couturier,Valérie Chaté,Brigitte Laillet,Corinne Malpuech-Brugère

doi:10.1186/1475-2840-13-54

Abstract

BackgroundSaturated fatty acid-rich high fat (HF) diets trigger abdominal adiposity, insulin resistance, type 2 diabetes and cardiac dysfunction. This study was aimed at evaluating the effects of nascent obesity on the cardiac function of animals fed a high-fat diet and at analyzing the mechanisms by which these alterations occurred at the level of coronary reserve.Materials and methodsRats were fed a control (C) or a HF diet containing high proportions of saturated fatty acids for 3 months. Thereafter, their cardiac function was evaluated in vivo using a pressure probe inserted into the cavity of the left ventricle. Their heart was isolated, perfused iso-volumetrically according to the Langendorff mode and the coronary reserve was evaluated by determining the endothelial-dependent (EDV) and endothelial-independent (EIV) vasodilatations in the absence and presence of endothelial nitric oxide synthase and cyclooxygenase inhibitors (L-NAME and indomethacin). The fatty acid composition of cardiac phospholipids was then evaluated.ResultsAlthough all the HF-fed rats increased their abdominal adiposity, some of them did not gain body weight (HF- group) compared to the C group whereas other ones had a higher body weight (HF+). All HF rats displayed a higher in vivo cardiac activity associated with an increased EDV. In the HF- group, the improved EDV was due to an increase in the endothelial cell vasodilatation activity whereas in the HF+ group, the enhanced EDV resulted from an improved sensitivity of coronary smooth muscle cells to nitric oxide. Furthermore, in the HF- group the main pathway implicated in the EDV was the NOS pathway while in the HF+ group the COX pathway.ConclusionsNascent obesity-induced improvement of cardiac function may be supported by an enhanced coronary reserve occurring via different mechanisms. These mechanisms implicate either the endothelial cells activity or the smooth muscle cells sensitivity depending on the body adiposity of the animals.

Highlights

Saturated fatty acid-rich high fat (HF) diets trigger abdominal adiposity, insulin resistance, type 2 diabetes and cardiac dysfunction
In the HF- group, the improved endothelial-dependent vasodilatation (EDV) was due to an increase in the endothelial cell vasodilatation activity whereas in the HF+ group, the enhanced EDV resulted from an improved sensitivity of coronary smooth muscle cells to nitric oxide
Since the HF diet-fed rats did not display necessarily an increased body weight but had systematically a higher abdominal adiposity, the improved EDV was rather related to the increased abdominal fat mass

Summary

Introduction

Saturated fatty acid-rich high fat (HF) diets trigger abdominal adiposity, insulin resistance, type 2 diabetes and cardiac dysfunction. This study was aimed at evaluating the effects of nascent obesity on the cardiac function of animals fed a high-fat diet and at analyzing the mechanisms by which these alterations occurred at the level of coronary reserve. High-fat (HF) diets are common in the Western societies and may induce insulin resistance (IR) when the absorbed lipids are rich in saturated fatty acids (SFAs) and poor in n-3 polyunsaturated fatty acids (PUFAs) [1]. As exemplified by postnatal over nutrition-induced obesity, the in vivo ejection fraction increases firstly until the third month of age and decreases only after a longer period of obesity [8]. That improvement is only transitory and could be responsible for the later cardiomyopathy

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