Bastie Claire C, Zong Haihong, Xu Jun, Busa Bhavin, Judex Stefan, Kurland Irwin J, Pessin Jeffrey E
Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794, USA.
Cell Metab. 2007 May;5(5):371-81. doi: 10.1016/j.cmet.2007.04.005.
Mice null for Fyn (a member of the Src family of nonreceptor tyrosine kinases) display a reduced percentage of adipose mass associated with decreased adipocyte cell size. In parallel, there is a substantial reduction in fasting plasma glucose, insulin, triglycerides, and free fatty acids concomitant with decreased intrahepatocellular and intramyocellular lipid accumulation. Importantly, the Fyn null mice exhibit improved glucose tolerance resulting from increased peripheral tissue (adipose and skeletal muscle) insulin sensitivity with a very small effect in the liver. Moreover, whole-body, adipose, and skeletal muscle fatty acid uptake and oxidation are increased along with AMP kinase activation and acetyl-CoA carboxylase inhibition. Together, these data demonstrate crosstalk between Src-family kinase activity and fatty acid oxidation and show that the loss of Fyn markedly improves peripheral tissue insulin sensitivity by relieving a selective negative modulation of AMP kinase activity in adipose tissue and skeletal muscle.
Fyn基因缺失的小鼠(Fyn是一种非受体酪氨酸激酶Src家族的成员)脂肪量的百分比降低,同时脂肪细胞大小减小。与此同时,空腹血浆葡萄糖、胰岛素、甘油三酯和游离脂肪酸大幅减少,同时肝细胞内和肌细胞内脂质积累也减少。重要的是,Fyn基因缺失的小鼠葡萄糖耐量得到改善,这是由于外周组织(脂肪和骨骼肌)胰岛素敏感性增加,而对肝脏的影响很小。此外,全身、脂肪和骨骼肌的脂肪酸摄取和氧化增加,同时AMP激酶激活和乙酰辅酶A羧化酶受到抑制。总之,这些数据证明了Src家族激酶活性与脂肪酸氧化之间的相互作用,并表明Fyn的缺失通过减轻脂肪组织和骨骼肌中AMP激酶活性的选择性负调节,显著改善了外周组织的胰岛素敏感性。