Cellular and molecular effects of n−3 polyunsaturated fatty acids on adipose tissue biology and metabolism

2008 ◽  
Vol 116 (1) ◽  
pp. 1-16 ◽  
Author(s):  
Pavel Flachs ◽  
Martin Rossmeisl ◽  
Morten Bryhn ◽  
Jan Kopecky

Adipose tissue and its secreted products, adipokines, have a major role in the development of obesity-associated metabolic derangements including Type 2 diabetes. Conversely, obesity and its metabolic sequelae may be counteracted by modulating metabolism and secretory functions of adipose tissue. LC-PUFAs (long-chain polyunsaturated fatty acids) of the n−3 series, namely DHA (docosahexaenoic acid; C22:6n−3) and EPA (eicosapentaenoic acid; C20:5n−3), exert numerous beneficial effects, such as improvements in lipid metabolism and prevention of obesity and diabetes, which partially result from the metabolic action of n−3 LC-PUFAs in adipose tissue. Recent studies highlight the importance of mitochondria in adipose tissue for the maintenance of systemic insulin sensitivity. For instance, both n−3 LC-PUFAs and the antidiabetic drugs TZDs (thiazolidinediones) induce mitochondrial biogenesis and β-oxidation. The activation of this ‘metabolic switch’ in adipocytes leads to a decrease in adiposity. Both n−3 LC-PUFAs and TZDs ameliorate a low-grade inflammation of adipose tissue associated with obesity and induce changes in the pattern of secreted adipokines, resulting in improved systemic insulin sensitivity. In contrast with TZDs, which act as agonists of PPARγ (peroxisome-proliferator-activated receptor-γ) and promote differentiation of adipocytes and adipose tissue growth, n−3 LC-PUFAs affect fat cells by different mechanisms, including the transcription factors PPARα and PPARδ. Some of the effects of n−3 LC-PUFAs on adipose tissue depend on their active metabolites, especially eicosanoids. Thus treatments affecting adipose tissue by multiple mechanisms, such as combining n−3 LC-PUFAs with either caloric restriction or antidiabetic/anti-obesity drugs, should be explored.

RSC Advances ◽  
2019 ◽  
Vol 9 (71) ◽  
pp. 41903-41912
Author(s):  
Yu Peng ◽  
Huixia Ren ◽  
Hongxun Tao ◽  
Chengwei He ◽  
Peng Li ◽  
...  

Low-grade inflammation is usually defined as the chronic production and a low-grade state of inflammatory factors, it often does not have symptoms, and has been associated with neurodegenerative disease, obesity, and diabetes.


2013 ◽  
Vol 38 (3) ◽  
pp. 361-361 ◽  
Author(s):  
Justine M. Tishinsky

Adipose tissue represents an important endocrine organ that secretes a multitude of adipokines known to mediate inflammation, lipid metabolism, and insulin sensitivity in peripheral tissues, such as skeletal muscle. Specifically, adiponectin stimulates skeletal muscle fatty acid oxidation and is associated with improvements in insulin response. Long-chain n-3 polyunsaturated fatty acids (PUFA) are well known for their anti-inflammatory and insulin-sensitizing properties, and their dietary consumption is associated with a more favourable circulating adipokine profile, including increased adiponectin. However, whether n-3 PUFA can directly stimulate adiponectin secretion from human adipocytes, as well as the underlying mechanisms involved, is unknown. In contrast to n-3 PUFA, diets high in saturated fatty acids (SFA) are thought to decrease adiponectin and increase pro-inflammatory adipokines, as well as blunt skeletal muscle response to both adiponectin and insulin, possibly via activation of inflammatory pathways. The role of n-3 PUFA in mediating the communication between adipose tissue and skeletal muscle, as well as preventing SFA-induced impairments in skeletal muscle function, has yet to be examined. In this thesis, it was found that long-chain n-3 PUFA increase adiponectin secretion from human adipocytes via a peroxisome proliferator-activated receptor γ-dependent mechanism. The effects of n-3 PUFA on adiponectin secretion were additive when combined with the thiazolidinedione, rosiglitazone. Second, incorporation of n-3 PUFA into a high SFA diet prevented impairments in adiponectin response and both prevented and restored impairments in insulin response in rodent skeletal muscle. Interestingly, these findings were paralleled by prevention of SFA-induced increases in toll-like receptor 4 expression by n-3 PUFA, suggesting inflammatory changes may be involved. Finally, dietary n-3 PUFA and SFA modulated the secretion of adipose tissue-derived factors from visceral rodent adipose tissue and subsequent exposure of isolated skeletal muscle to such factors induced acute changes in inflammatory gene expression without affecting insulin sensitivity. Together, the findings in this thesis suggest that n-3 PUFA modulate adipokine secretion from adipose tissue and that adipose-derived factors mediate skeletal muscle inflammation and response to adiponectin and insulin. Ultimately, this work highlights the importance of considering n-3 PUFA as a therapeutic strategy in the prevention and treatment of obesity and related pathologies.


2021 ◽  
Vol 12 ◽  
Author(s):  
Minjeong Kim ◽  
Brynn H. Voy

Modern broiler chickens are incredibly efficient, but they accumulate more adipose tissue than is physiologically necessary due to inadvertent consequences of selection for rapid growth. Accumulation of excess adipose tissue wastes feed in birds raised for market, and it compromises well-being in broiler-breeders. Studies driven by the obesity epidemic in humans demonstrate that the fatty acid profile of the diet influences adipose tissue growth and metabolism in ways that can be manipulated to reduce fat accretion. Omega-3 polyunsaturated fatty acids (n-3 PUFA) can inhibit adipocyte differentiation, induce fatty acid oxidation, and enhance energy expenditure, all of which can counteract the accretion of excess adipose tissue. This mini-review summarizes efforts to counteract the tendency for fat accretion in broilers by enriching the diet in n-3 PUFA.


PPAR Research ◽  
2009 ◽  
Vol 2009 ◽  
pp. 1-15 ◽  
Author(s):  
Weimin He

The nuclear hormone receptor peroxisome proliferator activated receptor gamma (PPAR) is an important transcription factor regulating adipocyte differentiation, lipid and glucose homeostasis, and insulin sensitivity. Numerous genetic mutations of PPAR have been identified and these mutations positively or negatively regulate insulin sensitivity. Among these, a relatively common polymorphism of PPAR, Pro12Ala of PPAR2, the isoform expressed only in adipose tissue has been shown to be associated with lower body mass index, enhanced insulin sensitivity, and resistance to the risk of type 2 diabetes in human subjects carrying this mutation. Subsequent studies in different ethnic populations, however, have revealed conflicting results, suggesting a complex interaction between the PPAR2 Pro12Ala polymorphism and environmental factors such as the ratio of dietary unsaturated fatty acids to saturated fatty acids and/or between the PPAR2 Pro12Ala polymorphism and genetic factors such as polymorphic mutations in other genes. In addition, this polymorphic mutation in PPAR2 is associated with other aspects of human diseases, including cancers, polycystic ovary syndrome, Alzheimer disease and aging. This review will highlight findings from recent studies.


2018 ◽  
Vol 28 (12) ◽  
pp. 1237-1244 ◽  
Author(s):  
K.S. Flannagan ◽  
M. Ramírez-Zea ◽  
A.V. Roman ◽  
A.K. Das ◽  
E. Villamor

2015 ◽  
Vol 31 (4) ◽  
pp. 543-550 ◽  
Author(s):  
T. Popova ◽  
J. Nakev ◽  
Y. Marchev

The aim of this study was to provide information on the fatty acid profile of different adipose depots - subcutaneous (upper and inner backfat layers) and intramuscular (m. Longissimus dorsi) in East Balkan pigs. The animals were reared in free-range conditions and slaughtered at an average live weight of 107?1.65kg. The results of the study showed that the various adipose tissues in pigs have different lipid metabolism and hence differ in their fatty acid composition. Intramuscular fat had significantly higher content of the saturated C16:0 and C18:0 (P<0.001), as well as the C16:1 (P<0.001) than the subcutaneous fat. In regards to the content of the polyunsaturated fatty acids, the latter displayed considerably higher content of both C18:2 and C18:3 (P<0.001) in comparison to the intramuscular fat in m. Longissimus dorsi. The differences between the subcutaneous and intramuscular adipose tissue in the individual fatty acids determined the similar trend of change in the total content of saturated and polyunsaturated fatty acids. Significant differences between the backfat layers were detected for C16:1, C18:0 and C18:3 (P<0.001). Stearic acid (C18:0) displayed higher content of the inner, while both C16:1 and C18:3 had higher proportion in the outer backfat layer in the East Balkan pigs. Except for C20:2, the long chain polyunsaturated n-6 and n-3 fatty acids had significantly higher proportions in the intramuscular fat, however no differences were determined between the two backfat layers.


Diabetologia ◽  
2010 ◽  
Vol 53 (5) ◽  
pp. 850-857 ◽  
Author(s):  
D. Iggman ◽  
J. Ärnlöv ◽  
B. Vessby ◽  
T. Cederholm ◽  
P. Sjögren ◽  
...  

2013 ◽  
Vol 98 (2) ◽  
pp. 549S-555S ◽  
Author(s):  
Hans Hauner ◽  
Stefanie Brunner ◽  
Ulrike Amann-Gassner

2006 ◽  
Vol 92 (2) ◽  
pp. 386-395 ◽  
Author(s):  
Arya M. Sharma ◽  
Bart Staels

Abstract Context: Adipose tissue is a metabolically dynamic organ, serving as a buffer to control fatty acid flux and a regulator of endocrine function. In obese subjects, and those with type 2 diabetes or the metabolic syndrome, adipose tissue function is altered (i.e. adipocytes display morphological differences alongside aberrant endocrine and metabolic function and low-grade inflammation). Evidence Acquisition: Articles on the role of peroxisome proliferator-activated receptor γ (PPARγ) in adipose tissue of healthy individuals and those with obesity, metabolic syndrome, or type 2 diabetes were sourced using MEDLINE (1990–2006). Evidence Synthesis: Articles were assessed to provide a comprehensive overview of how PPARγ-activating ligands improve adipose tissue function, and how this links to improvements in insulin resistance and the progression to type 2 diabetes and atherosclerosis. Conclusions: PPARγ is highly expressed in adipose tissue, where its activation with thiazolidinediones alters fat topography and adipocyte phenotype and up-regulates genes involved in fatty acid metabolism and triglyceride storage. Furthermore, PPARγ activation is associated with potentially beneficial effects on the expression and secretion of a range of factors, including adiponectin, resistin, IL-6, TNFα, plasminogen activator inhibitor-1, monocyte chemoattractant protein-1, and angiotensinogen, as well as a reduction in plasma nonesterified fatty acid supply. The effects of PPARγ also extend to macrophages, where they suppress production of inflammatory mediators. As such, PPARγ activation appears to have a beneficial effect on the relationship between the macrophage and adipocyte that is distorted in obesity. Thus, PPARγ-activating ligands improve adipose tissue function and may have a role in preventing progression of insulin resistance to diabetes and endothelial dysfunction to atherosclerosis.


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