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Insulin resistance cellular mechanisms

It has been shown that fish oil can not only suppress proinflammatory mediators but also can increase the anti-inflammatory ones such as adiponectin (Duda et al., 2009 Kalupahana et al., 2010b). Increased adipo-nectin levels can reduce inflammation and beneficially improve the metabolism. Specifically, the increased levels of adiponectin can significantly reduce the insulin resistance. Oster et al. (2010) showed that DHA increases cellular adiponectin mRNA and secreted adiponectin protein in 3T3-L1 adipocytes, possibly by a mechanism involving PPARy. A recent dietary intervention study conducted on healthy Japanese female subjects by Kondo et al. (2010) showed that a fish-based diet intervention increased the serum adiponectin concentration in young, nonobese, healthy Japanese female subjects. Also, the same study indicated that the increment in serum -3 PUFA may regulate the serum adiponectin concentration (Kondo et al., 2010). [Pg.217]

Rudich A, Ben-Romano R, Etzion S, Bashan N. Cellular mechanisms of insulin resistance, lipodystrophy and atherosclerosis induced by HIV protease inhibitors. Acta Physiol Scand. 2005 183 75-88. [Pg.544]

Shulman, G.I., 2000, Cellular mechanisms of insulin resistance. J. Clin. Invest. 106 171-176. [Pg.290]

R539 G. I. Shulman, Cellular Mechanisms of Insulin Resistance , J. Clin.-Invest., 2000,106, 171... [Pg.37]

A review of cellular mechanisms of insulin resistance has been produced with 46 references. The use of NMR to study glycogen in exercise has been reviewed with many references. The quantification of the contribution of gluconeogenesis to glucose production in fasted human subjects, using stable isotopes and NMR, has been reviewed with 72 references. A review of the use of magnetic resonance imaging and spectroscopy in biomedicine has been produced with 180 references. The beginnings and later applications of NMR for clinical studies has been reviewed with 18 references. [Pg.411]

Analogous to FFA, tumor necrosis factor-a (TNF-a) is a cytokine secreted by adipose tissue, which has also been implicated as a mediator of insulin resistance in skeletal muscle and the liver. Thiazolidinediones suppress the secretion of TNF-a as well as antagonize the effects of this cytokine at the cellular level in insulin target tissues [5]. Additional mechanisms of thiazolidinedione action have also been recently identified. For example, the levels of adiponectin, a recently described protein with insulin-sensitizing properties specifically secreted by adipose tissue that circulates in... [Pg.87]


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See also in sourсe #XX -- [ Pg.1340 ]




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