Adiponectin sphings into action
(Impact Factor: 27.36).
01/2011; 17(1):37-8. DOI: 10.1038/nm0111-37
Available from: Avner Thaler
- "Adiponectin inhibits macrophage activation through the NF-í µí¼
B pathway  resulting in markedly decreased uptake of oxidized low-density lipoproteins and foam cell formation BioMed Research International , reduces the production and activity of tumor necrosis factor í µí»¼ (TNF-í µí»¼), and inhibits (IL-6) production . It is known to exert antiapoptotic effects and to prevent myocardial apoptosis in response to myocardial ischemia reperfusion injury . Plasma adiponectin levels are decreased in critically ill patients during the acute phase of their illness . "
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ABSTRACT: Background. Adipose tissue is an important endocrine organ that secretes cytokines, including adiponectin, levels of which are negatively correlated with the severity of the inflammatory process. Aim. To assess the time course of adiponectin levels following open heart surgery with cardiopulmonary bypass and its correlation with early postoperative outcomes. Materials and Methods. Blood samples were obtained from 24 children undergoing cardiac surgery and analyzed for adiponectin, C-reactive protein, and other inflammatory markers.
Results. Baseline adiponectin levels were negatively correlated with patients' preoperative weight and age. Postoperative adiponectin levels decreased compared to baseline (P = 0.01) and correlated negatively with duration of cardiopulmonary bypass (r = −0.438, P = 0.037), length of stay in the pediatric intensive care unit (r = −0.457, P = 0.025), and the inotropic score (r = −0.471, P = 0.02). Adiponectin levels were positively correlated with sVCAM 1 levels; however, there was no correlation between adiponectin levels and sP selectin, tPA, MCP1, and sCD40. Conclusions. The inflammatory response after open heart surgery with cardiopulmonary bypass is associated with a reduction in adiponectin levels. Prolonged or more complicated surgery induced a more substantial inflammatory process characterized by a significant reduction in adiponectin levels over time and a delayed return to baseline levels.
Available from: Kazuaki Yoshioka
- "For example, S1P has been shown to counteract ceramide-induced activation of JNK (18). Thus, it has been proposed that the ceramide-to-S1P ratio may function as an intracellular rheostat (19,20). "
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ABSTRACT: The sphingolipids sphingosine-1-phosphate (S1P) and ceramide are important bioactive lipids with many cellular effects. Intracellular ceramide accumulation causes insulin resistance, but sphingosine kinase 1 (SphK1) prevents ceramide accumulation, in part, by promoting its metabolism into S1P. Despite this, the role of SphK1 in regulating insulin action has been largely overlooked. Transgenic (Tg) mice that overexpress SphK1were fed a standard chow or high-fat diet (HFD) for 6 weeks before undergoing several metabolic analyses. SphK1 Tg mice fed an HFD displayed increased SphK activity in skeletal muscle, which was associated with an attenuated intramuscular ceramide accumulation compared with wild-type (WT) littermates. This was associated with a concomitant reduction in the phosphorylation of c-jun amino-terminal kinase, a serine threonine kinase associated with insulin resistance. Accordingly, skeletal muscle and whole body insulin sensitivity were improved in SphK1 Tg, compared with WT mice, when fed an HFD. We have identified that the enzyme SphK1 is an important regulator of lipid partitioning and insulin action in skeletal muscle under conditions of increased lipid supply.
Available from: Ruth S Weinstock
- "Adipose tissue is increasingly understood to be an important endocrine organ, secreting adipokines that are important to energy homeostasis. Adiponectin is the most abundant adipokine and has important influences on insulin sensitivity, via the 5′-AMP–activated protein kinase pathway, resulting in improved glucose utilization and fatty acid oxidation and inhibition of serine kinases that antagonize insulin signaling (19,20). Recent evidence also suggests that adiponectin may also mediate insulin sensitivity through a sphingolipid pathway (21). "
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ABSTRACT: To assess the association between serum adiponectin level and all-cause mortality in people with type 2 diabetes. Because of the insulin-sensitizing, anti-inflammatory, and antiatherogenic effects of adiponectin, we hypothesized that higher adiponectin level would be associated with lower all-cause mortality.
A total of 609 men and women aged 72 ± 6.3 years with type 2 diabetes and information on total and high molecular weight adiponectin were followed for a median of 5 years. The longitudinal association between adiponectin and all-cause mortality was analyzed with Cox proportional hazards models with time from adiponectin measurement to death as the time-to-event variable. Analyses were adjusted for demographic variables and significant diabetes parameters, significant cardiovascular parameters, and significant diabetes medications.
Total and high molecular weight adiponectin were highly correlated. The highest adiponectin quartile was strongly associated with higher all-cause mortality compared with the lowest quartile (hazard ratio = 4.0 [95% CI: 1.7-9.2]) in the fully adjusted model. These results did not change in analyses stratified by sex and thiazolidinedione use, after exclusion of people who died within one year of adiponectin measurement, or when change in weight before adiponectin measurement was considered.
Contrary to our hypothesis, higher adiponectin level was related to higher all-cause mortality. This association was not explained by confounding by other characteristics, including medications or preceding weight loss.
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