The role of adipokines as regulators of skeletal muscle fatty acid metabolism and insulin sensitivity

摘要: Several adipose-derived cytokines (adipokines) have been suggested to act as a link between accumulated fat mass and altered insulin sensitivity. Resistin tumour necrosis factor-alpha (TNF-alpha) implicated in impairing sensitivity rodents; conversely, two other adipokines, leptin adiponectin, increase lean obese rodents. Currently, there is considerable focus on the concept that lipid accumulation skeletal muscle leads development of resistance. Adiponectin each demonstrated rates fatty acid (FA) oxidation decrease content, which may part be underlying mechanism their sensitizing effect. These effects FA metabolism appear mediated through activation AMP-activated protein kinase. Evidence derived from animal human studies suggests ability adiponectin stimulate impaired condition. Thus, resistance an initiating factor intramuscular lipids, such diacylglycerol ceramide, ensuing Lifestyle factors diet exercise are able restore leptin. The actual physiological roles resistin TNF-alpha altering more controversial, but has shown directly impair signalling consequently, stimulated glucose uptake muscle. However, possibility reduces by this tissue leading accumulation, virtually unexamined. contribution various adipokines complex not fully understood. Finally, these generally studied isolation, making it difficult predict interactive net impact