Diets high in monounsaturated and polyunsaturated fatty acids decrease fatty acid synthase protein levels in adipose tissue but do not alter other markers of adipose function and inflammation in diet-induced obese rats
Diets high in monounsaturated and polyunsaturated fatty acids decrease fatty acid synthase protein levels in adipose tissue but do not alter other markers of adipose function and inflammation in diet-induced obese rats
Year: 2014
Authors: Enns, J.E. Hanke, D. Park, A. Zahradka, P. Taylor, C.G.
Publication Name: Prostaglandins, Leukotrienes and Ess. Fatty Acids
Publication Details: Volume 90; Pages 77-84
Abstract:
This study investigates the effects of monounsaturated and polyunsaturated fatty acids from different fat sources (High Oleic Canola, Canola, Canola Flaxseed (3 to 1 blend), Safflower, or Soybean Oil, or a Lard based diet) on adipose tissue function and markers of inflammation in Obese Prone rats fed high fat (55 per cent energy) diets for 12 weeks. Adipose tissue fatty acid composition reflected the dietary fatty acid profiles. Protein levels of fatty acid synthase, but not mRNA levels, were lower in adipose tissue of all groups compared to the Lard group. Adiponectin and fatty acid receptors GPR41 and GPR43 protein levels were also altered, but other metabolic and inflammatory mediators in adipose tissue and serum were unchanged among groups. Overall, rats fed vegetable oil or lard based high fat diets appear to be largely resistant to major phenotypic changes when the dietary fat composition is altered, providing little support for the importance of specific fatty acid profiles in the context of a high fat diet. (Authors abstract)
Once thought to serve merely as an energy storage depot, adipose tissue is now known to be a dynamic endocrine organ, secreting bioactive molecules termed “adipokines” that contribute to the regulation of metabolic homeostasis. In obesity, excessive adiposity and the dysregulated production of adipokines, such as adiponectin, leptin, and several classes of proinflammatory molecules, contribute to the chronic low grade inflammation that drives the pathogenesis of related conditions, including insulin resistance and cardiovascular disease. Although the etiology of obesity is complex, diet is one of the most important determinants. In this regard, little is known about the essential n3 fatty acid alpha linolenic acid (ALA C18 3n3), found in plant based products such as canola and flaxseed oils. The effects of ALA in obesity have not been well studied, despite reports that ALA blood levels and cardiovascular endpoints are inversely associated. Other promising findings include the inflammation reducing effects of ALA supplementation in obese subjects. Diets rich in MUFA, which have been studied mainly in relation to the oleic acid (C18 1n9) rich Mediterranean Diet, may also be beneficial in reducing the risk of co morbidities associated with obesity. Given the high prevalence of obesity and obesity related conditions as well as dietary recommendations to reduce SFA intake, it is important to determine the contributions of MUFA and PUFA to the development of these metabolic imbalances. This study compared the effects of MUFA and PUFA rich diets containing different amounts and ratios of n6 andn3 fatty acids in a diet-induced obesity rodent model, which closely mimics the phenotype and pathogenesis of human obesity. The fatty acid profiles of the vegetable oils making up the fat content of the diets allowed us to evaluate the metabolic consequences of two high n6 PUFA diets containing very low or moderate levels of ALA, and three high MUFA diets with relatively constant amounts of linoleic acid and low, moderate and high levels of ALA. The objective of the study was to investigate the effects of the different fatty acid profiles of vegetable oils on adipose tissue function and inflammation and relationships with adipose tissue fatty acid composition in diet induced obese rats. Although the groups fed the MUFA rich diets had 10 per cent lower body weight at the end of the study, there was no difference in adiposity based on relative fat pad mass. One of the main findings of the study is the decrease in fatty acid synthase protein observed in all dietary treatment groups compared to the Lard group. The adipose tissue is one of two major sites of fatty acid synthesis, second only to the liver. The mechanism for the observed decrease in fatty acid synthase protein in the dietary treatment groups consuming PUFA or MUFA rich diets remains uncertain, since there were no changes in fatty acid synthase mRNA levels in the adipose tissue. Thus, the change in fatty acid synthase protein may instead be the result of regulation at either the post transcriptional or the translational level. Changes to the fatty acid composition in the phospholipids and triglycerides of adipose tissue occurred as expected, corresponding to the content of SFA, MUFA and PUFA in the diets. Despite the large differences in linoleic acid and ALA intake, there were no changes in arachidonic acid and only small differences in EPA in phospholipids, suggesting that the pool of substrates for eicosanoid production was relatively unchanged. Furthermore, enrichment of n6 PUFA in the Safflower and Soybean Oil diets and a high level of n3 PUFA in the Canola Flaxseed Oil diet did not produce changes in protein levels of pro or anti inflammatory adipokines in the adipose tissue. Although the diets varied in the amounts and ratios of n6 andn3 fatty acids, in adipose tissue, there were no differences among groups in the n6 per n3 ratio in either phospholipid or triglyceride fatty acids. Even though the n6 to n3 ratios varied across the dietary treatments, a dietary n6 to n3 ratio of 8 to 1 or less did not produce differences in adipose tissue n6 per n3 ratios. However, DHA, the main n3PUFA in adipose tissue phospholipids was similar across all groups, indicating that the range of dietary ALA intakes was able to maintain tissue DHA by elongation and desaturation of ALA. The study indicates that very few obesity related parameters were altered by 12 weeks of feeding MUFA or PUFA rich diets containing different proportions of n3 and n6 PUFA in the context of a high-fat diet. The study found changes in fatty acid synthase, adiponectin and short chain fatty acid receptors GPR41 and GPR43 in animals fed high fat diets containing different proportions of MUFA and PUFA. These findings indicate that different types of dietary fatty acids regulate adipokine production and proteins involved in fatty acid metabolism in adipose tissue. However, although the fatty acid compositions of the diets were variable (particularly in PUFA, MUFA and ALA contents) and there were changes in the fatty acid profile of adipose tissue, the diets had little impact on adipose tissue function. Additionally, although there were some differences in body weight among groups at the end of the study, these differences did not translate into changes in adiposity (fat mass) or inflammation, suggesting that the dietary treatments had little impact on the broader physiological function of these obese animals. Overall, the findings of this study indicate that using vegetable oils to replace PUFA with MUFA and to increase intake of ALA has minimal effects on altering adipose tissue function and inflammation in the context of a long term high fat diet. (Editors comments)
Once thought to serve merely as an energy storage depot, adipose tissue is now known to be a dynamic endocrine organ, secreting bioactive molecules termed “adipokines” that contribute to the regulation of metabolic homeostasis. In obesity, excessive adiposity and the dysregulated production of adipokines, such as adiponectin, leptin, and several classes of proinflammatory molecules, contribute to the chronic low grade inflammation that drives the pathogenesis of related conditions, including insulin resistance and cardiovascular disease. Although the etiology of obesity is complex, diet is one of the most important determinants. In this regard, little is known about the essential n3 fatty acid alpha linolenic acid (ALA C18 3n3), found in plant based products such as canola and flaxseed oils. The effects of ALA in obesity have not been well studied, despite reports that ALA blood levels and cardiovascular endpoints are inversely associated. Other promising findings include the inflammation reducing effects of ALA supplementation in obese subjects. Diets rich in MUFA, which have been studied mainly in relation to the oleic acid (C18 1n9) rich Mediterranean Diet, may also be beneficial in reducing the risk of co morbidities associated with obesity. Given the high prevalence of obesity and obesity related conditions as well as dietary recommendations to reduce SFA intake, it is important to determine the contributions of MUFA and PUFA to the development of these metabolic imbalances. This study compared the effects of MUFA and PUFA rich diets containing different amounts and ratios of n6 andn3 fatty acids in a diet-induced obesity rodent model, which closely mimics the phenotype and pathogenesis of human obesity. The fatty acid profiles of the vegetable oils making up the fat content of the diets allowed us to evaluate the metabolic consequences of two high n6 PUFA diets containing very low or moderate levels of ALA, and three high MUFA diets with relatively constant amounts of linoleic acid and low, moderate and high levels of ALA. The objective of the study was to investigate the effects of the different fatty acid profiles of vegetable oils on adipose tissue function and inflammation and relationships with adipose tissue fatty acid composition in diet induced obese rats. Although the groups fed the MUFA rich diets had 10 per cent lower body weight at the end of the study, there was no difference in adiposity based on relative fat pad mass. One of the main findings of the study is the decrease in fatty acid synthase protein observed in all dietary treatment groups compared to the Lard group. The adipose tissue is one of two major sites of fatty acid synthesis, second only to the liver. The mechanism for the observed decrease in fatty acid synthase protein in the dietary treatment groups consuming PUFA or MUFA rich diets remains uncertain, since there were no changes in fatty acid synthase mRNA levels in the adipose tissue. Thus, the change in fatty acid synthase protein may instead be the result of regulation at either the post transcriptional or the translational level. Changes to the fatty acid composition in the phospholipids and triglycerides of adipose tissue occurred as expected, corresponding to the content of SFA, MUFA and PUFA in the diets. Despite the large differences in linoleic acid and ALA intake, there were no changes in arachidonic acid and only small differences in EPA in phospholipids, suggesting that the pool of substrates for eicosanoid production was relatively unchanged. Furthermore, enrichment of n6 PUFA in the Safflower and Soybean Oil diets and a high level of n3 PUFA in the Canola Flaxseed Oil diet did not produce changes in protein levels of pro or anti inflammatory adipokines in the adipose tissue. Although the diets varied in the amounts and ratios of n6 andn3 fatty acids, in adipose tissue, there were no differences among groups in the n6 per n3 ratio in either phospholipid or triglyceride fatty acids. Even though the n6 to n3 ratios varied across the dietary treatments, a dietary n6 to n3 ratio of 8 to 1 or less did not produce differences in adipose tissue n6 per n3 ratios. However, DHA, the main n3PUFA in adipose tissue phospholipids was similar across all groups, indicating that the range of dietary ALA intakes was able to maintain tissue DHA by elongation and desaturation of ALA. The study indicates that very few obesity related parameters were altered by 12 weeks of feeding MUFA or PUFA rich diets containing different proportions of n3 and n6 PUFA in the context of a high-fat diet. The study found changes in fatty acid synthase, adiponectin and short chain fatty acid receptors GPR41 and GPR43 in animals fed high fat diets containing different proportions of MUFA and PUFA. These findings indicate that different types of dietary fatty acids regulate adipokine production and proteins involved in fatty acid metabolism in adipose tissue. However, although the fatty acid compositions of the diets were variable (particularly in PUFA, MUFA and ALA contents) and there were changes in the fatty acid profile of adipose tissue, the diets had little impact on adipose tissue function. Additionally, although there were some differences in body weight among groups at the end of the study, these differences did not translate into changes in adiposity (fat mass) or inflammation, suggesting that the dietary treatments had little impact on the broader physiological function of these obese animals. Overall, the findings of this study indicate that using vegetable oils to replace PUFA with MUFA and to increase intake of ALA has minimal effects on altering adipose tissue function and inflammation in the context of a long term high fat diet. (Editors comments)
