Responses to oleic, linoleic and alpha linolenic acids in high carbohydrate, high fat diet induced metabolic syndrome in rats.

We investigated the changes in adiposity, cardiovascular and liver structure and function, and tissue fatty acid compositions in response to oleic acid rich macadamia oil, linoleic acid rich safflower oil and alpha linolenic acid rich flaxseed oil (C18 unsaturated fatty acids) in rats fed either a diet high in simple sugars and mainly saturated fats or a diet high in polysaccharides (cornstarch) and low in fat. The fatty acids induced lipid redistribution away from the abdomen, more pronounced with increasing unsaturation; only oleic acid increased whole-body adiposity. Oleic acid decreased plasma total cholesterol without changing triglycerides and nonesterified fatty acids, whereas linoleic and ALAs decreased plasma triglycerides and nonesterified fatty acids but not cholesterol. ALA improved left ventricular structure and function, diastolic stiffness and systolic blood pressure. Neither oleic nor linoleic acid changed the left ventricular remodeling induced by high carbohydrate, high fat diet, but both induced dilation of the left ventricle and functional deterioration in low fat diet fed rats. ALA improved glucose tolerance, while oleic and linoleic acids increased basal plasma glucose concentrations. Oleic and ALA, but not linoleic acid, normalized systolic blood pressure. Only oleic acid reduced plasma markers of liver damage. The C18 unsaturated fatty acids reduced trans fatty acids in the heart, liver and skeletal muscle with lowered stearoyl CoA desaturase 1 activity index; linoleic and ALA increased accumulation of their C22 elongated products. These results demonstrate different physiological and biochemical responses to primary C18 unsaturated fatty acids in a rat model of human metabolic syndrome. (Authors abstract)

It is generally accepted that dietary saturated fatty acids (SFAs) and trans fatty acids are detrimental and unsaturated fatty acids are beneficial to cardiovascular health. There is considerable controversy as to the biological responses to dietary fatty acids in disease states such as metabolic syndrome. Despite being structurally similar, different dietary fatty acids, even within the same class, elicit different physiological responses. The differences in physiological responses to dietary oleic, linoleic and ALAs have not been evaluated in the same disease model. The main aim of this study was to characterize systematically the effects of dietary supplementation of oleic, linoleic and ALAs in rats fed either a low fat, high starch diet as control or a high fructose, high tallow diet as a model of metabolic syndrome. Dietary supplementation of C18 unsaturated fatty acids elicits different responses in adiposity, cardiovascular remodeling, plasma lipids, hepatic structure and function, and tissue fatty acid compositions. Here, oleic acid, linoleic acid and ALA induced lipid redistribution away from the abdomen and that this effect is more pronounced with increasing degree of unsaturation. the authors have previously shown that ALA rich chia seed and oil but not eicosapentaenoic or docosahexaenoic acid rich fish oil induce lipid redistribution in diet-induced obese rats. These results suggest that the C18 unsaturated fatty acids favor lipid partitioning away from the abdomen. However, only linoleic and ALAs induced lipid partitioning without affecting wholebody adiposity, as oleic acid supplementation increased whole body adiposity.

Additionally, oleic acid decreased total plasma cholesterol but did not change plasma triglycerides and nonesterified fatty acids, whereas the PUFAs (linoleic and ALA) decreased plasma triglycerides and nonesterified fatty acids but not cholesterol. ALA supplementation improved left ventricular structure and function, diastolic stiffness and systolic blood pressure. Oleic or linoleic acid supplementation did not change the left ventricular remodeling induced by high diet feeding, but both fatty acids induced dilation of the left ventricle and subsequent deterioration in function in the rats fed the low fat (C) diet.  These effects were associated with unique tissue fatty acid profiles induced by oleic, linoleic and ALA. While all three fatty acids inhibited the desaturation of C16:0 in all tissues, linoleic acid induced preferential oxidation of trans fat and therefore loss of vaccenic acid from all tissues; ALA induced the selective storage of trans fat in the adipose tissue and oleic acid in the organs. In conclusion, ALA but not oleic acid and linoleic acid attenuated the risk factors of metabolic syndrome. Although oleic acid and linoleic acid were both associated with cardiovascular remodeling, oleic acid decreased blood pressure and improved liver structure and function, and linoleic acid only decreased plasma triglyceride concentrations without affecting other risk factors of metabolic syndrome. However, the three fatty acids were all associated with trafficking of fat away from the abdomen, proportional to the number of double bonds. (Editors comments)