Stimulation by Eicosapentaenoic Acids of Leptin mRNA Expression and Its Secretion in Mouse 3T3-L1 Adipocytes in Vitro

Morimoto, Masahiro; Kaji, Hidesuke; Takahashi, Yutaka; Iida, Keiji; Mizuno, Ishikazu; Okimura, Yasuhiko; Abe, Hiromi; Chihara, Kazuo

doi:10.1006/bbrc.2000.2424

Cited by 47 publications

(33 citation statements)

References 48 publications

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“…We speculate that EPA can improve insulin sensitivity and dyslipidemia possibly through its stimulation of the insulininduced tyrosine-phosphorylated IRS-1 as well as PPAR activation in accordance with dietary EPA intake. The second possibility is the involvement of hexosamine biosynthetic pathway, which mediates EPA-induced leptin expression as shown in our previous report (8). In this study, however, DON failed to affect EPA-induced tyrosine phosphorylation of IRS-1, suggesting that the involvement of hexosamine biosynthetic pathway in this mechanism is unlikely.…”

Section: Resultssupporting

confidence: 40%

“…We also reported that EPA up-regulates leptin mRNA expression and its secretion through hexosamine biosynthetic pathway in 3T3-L1 adipocytes (8). Increased inflow of free fatty acid to HepG2 cells produces increased amounts of fatty acyl-CoA, causing the inhibition of glycolysis, and subsequently increases fluctose 6-phosphate, which increases the substrate for glutamine:fructose-6-phosphate amidotransferase, which plays a critical role as the rate-limiting enzyme in glucosamine biosynthesis.…”

Section: Resultsmentioning

confidence: 77%

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Dual Action of Eicosapentaenoic Acid in Hepatoma Cells

Morimoto¹,

Kaji²,

Iida³

et al. 2001

Journal of Biological Chemistry

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Exogenous administration of eicosapentaenoic acid (EPA) improves insulin sensitivity, but its precise mechanism remains unknown. Here we show that EPA stimulates the intracellular insulin signaling pathway in hepatoma cells. Exposure of these cells to EPA caused up-regulation of several insulin-induced activities including tyrosine phosphorylation of insulin receptor substrate-1, insulin receptor substrate-1-associated phosphatidylinositol 3-kinase, and its downstream target Akt kinase activity as well as down-regulation of gluconeogenesis. In contrast, EPA decreased mitogenactivated protein kinase activity and inhibited cell proliferation. These findings raise the possibility that EPA up-regulates metabolic action of insulin and inhibits cell growth in humans.

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Section: Resultssupporting

confidence: 40%

Section: Resultsmentioning

confidence: 77%

Dual Action of Eicosapentaenoic Acid in Hepatoma Cells

Morimoto¹,

Kaji²,

Iida³

et al. 2001

Journal of Biological Chemistry

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“…Leptin, the product of the ob gene, is a hormone that is primarily secreted from adipose tissue, and regulates energy expenditure and food intake (Weigle et al, 1995). Expression of leptin is regulated by several substances like insulin, glucocorticoids and TNF-a (Murata et al, 2000). Here, we found that aP2 and leptin mRNA expression was inhibited by RE ( Fig.…”

Section: Discussionmentioning

confidence: 56%

Red yeast rice extracts suppress adipogenesis by down-regulating adipogenic transcription factors and gene expression in 3T3-L1 cells

et al. 2004

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“…Thus, in vitro studies with EPA (0 . 1-200 ml) showed the ability of this fatty acid to stimulate in a dose-dependent manner leptin mRNA expression and leptin secretion in 3T3-L1 cells (55) and in primary rat adipocytes (34) . Little is still known about the mechanisms underlying this stimulatory action of EPA on leptin.…”

Section: Leptinmentioning

confidence: 99%

Regulation of adipokine secretion byn-3 fatty acids

2010

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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...

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Stimulation by Eicosapentaenoic Acids of Leptin mRNA Expression and Its Secretion in Mouse 3T3-L1 Adipocytes in Vitro

Cited by 47 publications

References 48 publications

Dual Action of Eicosapentaenoic Acid in Hepatoma Cells

Dual Action of Eicosapentaenoic Acid in Hepatoma Cells

Red yeast rice extracts suppress adipogenesis by down-regulating adipogenic transcription factors and gene expression in 3T3-L1 cells

Regulation of adipokine secretion byn-3 fatty acids

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