Regulation of adipokine secretion byn-3 fatty acids

Abstract

Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. The n-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact, n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability of n-3 PUFA to regulate adipokine gene expression and secretion has been observed both in vitro and in vivo in rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immunemodulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions of n-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability of n-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.Leptin: Adiponectin: Visfatin: n-3 fatty acids: Obesity: Inflammation Adipokines, obesity and inflammationObesity represents an increasing problem of health care. It leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome (1) . Obesity also predisposes individuals to an increased risk of developing non-alcoholic fatty liver disease and certain cancers (2) . Furthermore, obesity and impaired immune function have been described in both human subjects and genetically obese rodents, supporting a link between adipose tissues and immunocompetent cells (3) .Adipose tissues play crucial roles in the development of obesity, with white adipose tissue (WAT) functioning as an energy storage organ and brown adipose tissue as an energy consumption organ. Several studies have suggested the importance of WAT metabolism and WAT-derived factors (fatty acids and adipokines) in the development of obesity and systemic insulin resistance, the key event in the pathophysiology of the metabolic syndrome (1) .WAT is an important secretory organ which produces a number of molecules that putatively play critical roles in fuel homeostasis and contribute to maintain metabolic control. These bioactive molecules, generally termed 'adip...

Effects of n‐3 PUFA on insulin resistance after an oral fat load

“…Also in this case our results are in contrast with Simão et al that reported an increase of insulin resistance with n-3 PUFA, but in line with Thorseng et al [44] and Huang et al [45] that suggested that some types of n-3 PUFA may have a protective effect against insulin resistance. Also a review conducted by Moreno-Aliaga et al [46] reached the same results, concluding that the ability of n-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of white adipose tissue metabolism and the secretion of bioactive adipokines including leptin, ADN, and visfatin. Analyzing the situation after the OFL, in the group treated with n-3 PUFA there was a better improvement of all parameters peaks, include the insulin resistance biomarkers, after the 6 months treatment, while there was a neutral effect with placebo.…”

Omega-3 fatty acids and adipose tissue function in obesity and metabolic syndrome

“…These hypertrophied adipocytes present an altered secretory pattern resulting in increased secretion of proinflammatoryadipokines, cytokines and chemokines such asmonocyte chemoattractant protein-1 (MCP-1), leptin, interleukin (IL)-6 or tumor necrosis factor (TNF)-α, and reduced production of anti-inflammatory adipokines, including adiponectin [14,15].…”

“…A significant number of studies consider that n-3PUFAs are able to improve impaired metabolism in obesity by modulating main metabolic pathways in key metabolic organs such as adipose tissue, liver and skeletal muscle [71,38,72,73,46,15,31].Here, we will focus in reviewing theactions and mechanisms of marine origin n-3 PUFAs in adipose tissue metabolism and functions.…”

Perinodal Adipose Tissue and Mesenteric Lymph Node Activation During Reactivated TNBS-Colitis in Rats

“…Additionally, PUFAs can regulate adipokine expression and secretion by adipose tissue, i.e. EPA has been shown to both up-and down-regulate leptin expression but clearly up-regulates adiponectin expression in adipocytes in culture [9]. In turn, adipokines with proinflammatory (TNF-a, leptin) or anti-inflammatory (IL-10, adiponectin) activities can modify lymph node cell activation or survival [10].…”