Abstract

Animal and human studies have indicated that fatty acids such as the conjugated linoleic acids (CLA) found in milk could potentially alter the risk of developing metabolic disorders including diabetes and cardiovascular disease (CVD). Using susceptible rodent models (apoE−/− and LDLr−/− mice) we investigated the interrelationship between mouse strain, dietary conjugated linoleic acids and metabolic markers of CVD. Despite an adverse metabolic risk profile, atherosclerosis (measured directly by lesion area), was significantly reduced with t-10, c-12 CLA and mixed isomer CLA (Mix) supplementation in both apoE−/− (p<0.05, n = 11) and LDLr−/− mice (p<0.01, n = 10). Principal component analysis was utilized to delineate the influence of multiple plasma and tissue metabolites on the development of atherosclerosis. Group clustering by dietary supplementation was evident, with the t-10, c-12 CLA supplemented animals having distinct patterns, suggestive of hepatic insulin resistance, regardless of mouse strain. The effect of CLA supplementation on hepatic lipid and fatty acid composition was explored in the LDLr−/− strain. Dietary supplementation with t-10, c-12 CLA significantly increased liver weight (p<0.05, n = 10), triglyceride (p<0.01, n = 10) and cholesterol ester content (p<0.01, n = 10). Furthermore, t-10, c-12 CLA also increased the ratio of 18∶1 to 18∶0 fatty acid in the liver suggesting an increase in the activity of stearoyl-CoA desaturase. Changes in plasma adiponectin and liver weight with t-10, c-12 CLA supplementation were evident within 3 weeks of initiation of the diet. These observations provide evidence that the individual CLA isomers have divergent mechanisms of action and that t-10, c-12 CLA rapidly changes plasma and liver markers of metabolic syndrome, despite evidence of reduction in atherosclerosis.

Highlights

  • The relationship between diet and disease is of increasing importance as nutrient availability is increased and lifestyle changes put increased pressure on physiological mechanisms to maintain metabolic homeostasis [1,2]

  • In the current study we compared two common mouse models of atherosclerosis to assess the influence of two distinct conjugated linoleic acid (CLA) isomers on measurable atherosclerosis and on multiple plasma and tissue markers of atherosclerosis and metabolic dysfunction

  • An important goal of the current study was to evaluate the ability of potential biomarkers of atherosclerosis and metabolic dysfunction to identify animals at risk of developing adverse metabolic phenotypes based on dietary manipulation

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Summary

Introduction

The relationship between diet and disease is of increasing importance as nutrient availability is increased and lifestyle changes put increased pressure on physiological mechanisms to maintain metabolic homeostasis [1,2]. Animal and human studies have indicated that the two major isomeric forms of conjugated linoleic acid (CLA) are biologically active, can have highly divergent physiological properties when administered individually, and do not necessarily have synergistic effects when consumed together [3,4,5]. Some reports support a role for CLA in decreasing body fat [6,7,8] and improving insulin action, predominantly in rodents (reviewed in [9,10]). There is some evidence to support a role for CLA in the modulation of plasma lipid metabolism [15] and the development of atherosclerotic plaques (reviewed in [16,17] )

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