Faulhaber-Walter Robert
National Institute of Diabetes, Digestive & Kidney Diseases; National Institutes of Health; Bethesda, MD USA; and Dialysepraxis Emden; Emden, Germany.
Adipocyte. 2012 Apr 1;1(2):108-111. doi: 10.4161/adip.19285.
Adenosine A1 receptor-deficient mice develop a phenotype of insulin resistance and grow fat. Participating pathophysiological pathways are not understood in detail yet, as discussed in our recent manuscript. This commentary further explores possible pathophysiological mechanisms with emphasis on the roles of the adipokines resistin, retinol-binding protein 4, adiponectin and the function of the gastric hormone ghrelin in adenosine mediated central regulation of energy balance. The postulate of an important function of ghrelin/A1AR axis provides a good hypothetical basis for further investigations to clarify the mechanism of A1AR-dependent metabolic homeostasis.
腺苷 A1 受体缺陷型小鼠会出现胰岛素抵抗的表型并发胖。正如我们最近的论文中所讨论的，参与其中的病理生理途径尚未完全明确。本评论进一步探讨了可能的病理生理机制，重点关注脂肪因子抵抗素、视黄醇结合蛋白 4、脂联素的作用以及胃激素 ghrelin 在腺苷介导的能量平衡中枢调节中的功能。ghrelin/A1AR 轴具有重要功能这一假设为进一步研究阐明 A1AR 依赖性代谢稳态机制提供了良好的理论基础。
