Hypertension induced by omega-3 polyunsaturated fatty acid deficiency is alleviated by alpha-linolenic acid regardless of dietary source
Hypertension induced by omega-3 polyunsaturated fatty acid deficiency is alleviated by alpha-linolenic acid regardless of dietary source
Year: 2010
Authors: Begg, D.P. Sinclair, A.J. Stahl, L.A. Premaratna, S.D. Hafandi, A. Jois, M. Weisinger . R.S.
Publication Name: Hypertension Research
Publication Details: Volume 33: Pages 808 – 813.
Abstract:
n-3 polyunsaturated fatty acid deficiency, particularly during the prenatal period, can cause hypertension in later life. This study examined the effect of different sources of alpha-linolenic acid (canola oil or flaxseed oil) in the prevention of hypertension and other metabolic symptoms induced by an ω -3 fatty acid-deficient diet. Dams were provided one of three experimental diets from 1 week before mating. Diets were either deficient (10% safflower oil-DEF) or sufficient (7% safflower oil+3% flaxseed oil-SUF-F; or 10% canola oil-SUF-C) in ω -3 fatty acids. The male offspring were continued on the maternal diet from weaning for the duration of the study. Body weight, ingestive behaviors, blood pressure, body composition, metabolic rate, plasma leptin and brain fatty acids were all assessed. The DEF animals were hypertensive at 24 weeks of age compared with SUF-F or SUF-C animals; this was not evident at 12 weeks. These results suggest that different sources of ALA are effective in preventing hypertension related to ω -3 fatty acid deficiency. However, there were other marked differences between the DEF and, in particular, the SUF-C phenotype including lowered body weight, adiposity, leptin and food intake in SUF-C animals. SUF-F animals also had lower, but less marked reductions in adiposity and leptin compared with DEF animals. The differences observed between DEF, SUF-F and SUF-C phenotypes indicate that body fat and leptin may be involved in ω -3 fatty acid deficiency hypertension. (Author�s abstract)
When deficiency of dietary ω-3 fatty acid is reversed in later life brain ω-3 fatty acid levels are essentially restored, although not in all brain membrane lipid fractions, but deficiency induced hypertension remains. Research to date indicates that prenatal ω-3 fatty acid supply has an important role in the development of the cardiovascular system and the regulation of blood pressure. The use of canola oil as the source of ω-3 fatty acids could act as a major confounding variable in studies of hypertension. Therefore, this study aimed to establish the effect of ALA source (canola oil or flaxseed oil) on prevention of ω-3 fatty acid deficiency-induced hypertension, and to determine if there are other effects on metabolic function in these animals. This study shows that the hypertension induced by ω-3 fatty acid deficiency from a safflower oil-based diet can be prevented by diets containing vegetable oils rich in ALA; either a canola oil diet or a combination of flax seed oil with safflower oil. It was not expected that the two ALA-containing diets would have significantly altered the phenotype of the animals in a number of ways including body weight and body composition. Given that both SUF-F and SUF-C groups had less body fat, the hypertension in DEF animals may be due to an increase in adipose tissue and body fat percentage, as obesity has a well-documented effect on hypertension. ω-3 fatty acids affect hypertension through an interaction with angiotensin (ANG) II a hormone that can be produced in adipocytes. Higher levels of vasodilative eicosanoid metabolites from the ω-3 fatty acid eicosapentaenoic acid in SUF animals may be causing a reduction in the vasoconstrictive effects of ANG II. The elevated leptin levels in DEF animals may be a mechanism for hypertension in DEF animals. Increases in leptin may be an underlying mechanism that contributes to hypertension in ω-3 fatty acid-deficient animals. The concentrations of docosahexaenoic acid in the prefrontal cortex were related to the ω-3 fatty acid deficiency/sufficiency of the diet the animals were fed. Despite the difference in ALA content of the SUF-F (B1.8%) and SUF-C (B0.8%) diets, there was no difference in the proportion of docosahexaenoic acid in the frontal cortex of animals fed the SUF-F and SUF-C diets. Future research should extend this work by determining the role of leptin in hypertension followingo-3 fatty acid deficiency. Overall, the results of the current study indicate that hypertension caused by ω-3 fatty acid deficiency can be prevented by either of the two different vegetable oil sources of ALA. These data suggest a contributing cause of the hypertension induced by the ω-3 fatty acid deficiency might be related to the higher body weight, body fat and plasma leptin levels. This should be explored further in future studies. (Editor�s comments)
When deficiency of dietary ω-3 fatty acid is reversed in later life brain ω-3 fatty acid levels are essentially restored, although not in all brain membrane lipid fractions, but deficiency induced hypertension remains. Research to date indicates that prenatal ω-3 fatty acid supply has an important role in the development of the cardiovascular system and the regulation of blood pressure. The use of canola oil as the source of ω-3 fatty acids could act as a major confounding variable in studies of hypertension. Therefore, this study aimed to establish the effect of ALA source (canola oil or flaxseed oil) on prevention of ω-3 fatty acid deficiency-induced hypertension, and to determine if there are other effects on metabolic function in these animals. This study shows that the hypertension induced by ω-3 fatty acid deficiency from a safflower oil-based diet can be prevented by diets containing vegetable oils rich in ALA; either a canola oil diet or a combination of flax seed oil with safflower oil. It was not expected that the two ALA-containing diets would have significantly altered the phenotype of the animals in a number of ways including body weight and body composition. Given that both SUF-F and SUF-C groups had less body fat, the hypertension in DEF animals may be due to an increase in adipose tissue and body fat percentage, as obesity has a well-documented effect on hypertension. ω-3 fatty acids affect hypertension through an interaction with angiotensin (ANG) II a hormone that can be produced in adipocytes. Higher levels of vasodilative eicosanoid metabolites from the ω-3 fatty acid eicosapentaenoic acid in SUF animals may be causing a reduction in the vasoconstrictive effects of ANG II. The elevated leptin levels in DEF animals may be a mechanism for hypertension in DEF animals. Increases in leptin may be an underlying mechanism that contributes to hypertension in ω-3 fatty acid-deficient animals. The concentrations of docosahexaenoic acid in the prefrontal cortex were related to the ω-3 fatty acid deficiency/sufficiency of the diet the animals were fed. Despite the difference in ALA content of the SUF-F (B1.8%) and SUF-C (B0.8%) diets, there was no difference in the proportion of docosahexaenoic acid in the frontal cortex of animals fed the SUF-F and SUF-C diets. Future research should extend this work by determining the role of leptin in hypertension followingo-3 fatty acid deficiency. Overall, the results of the current study indicate that hypertension caused by ω-3 fatty acid deficiency can be prevented by either of the two different vegetable oil sources of ALA. These data suggest a contributing cause of the hypertension induced by the ω-3 fatty acid deficiency might be related to the higher body weight, body fat and plasma leptin levels. This should be explored further in future studies. (Editor�s comments)
