Lu Jin-Ying, Huang Kuo-Chin, Chang Lin-Chau, Huang Ying-Shing, Chi Yu-Chiao, Su Ta-Chan, Chen Chi-Ling, Yang Wei-Shiung
Department of Laboratory Medicine, National Taiwan University Hospital, Taipei 100, Taiwan, ROC.
J Biomed Sci. 2008 Sep;15(5):565-76. doi: 10.1007/s11373-008-9261-z. Epub 2008 Jun 6.
Adiponectin is one of the most thoroughly studied adipocytokines. Low plasma levels of adiponectin are found to associate with obesity, metabolic syndrome, diabetes and many other human diseases. From animal experiments and human studies, adiponectin has been shown to be a key regulator of insulin sensitivity. In this article, we review the evidence and propose that hypo-adiponectinemia is not a major cause of obesity. Instead, it is the result of obesity-induced insulin resistance in the adipose tissue. Hypo-adiponectinemia then mediates the metabolic effects of obesity on the other peripheral tissues, such as liver and skeletal muscle and may also exert some direct effects on end-organ damage. We propose that deciphering the molecular details governing the adiponectin gene expression and protein secretion will lead us to more comprehensive understanding of the mechanisms of insulin resistance in the adipose tissue and provide us new avenues for the therapeutic intervention of obesity and insulin resistance-related human disorders.
脂联素是研究最为深入的脂肪细胞因子之一。血浆脂联素水平低与肥胖、代谢综合征、糖尿病及许多其他人类疾病相关。从动物实验和人体研究来看，脂联素已被证明是胰岛素敏感性的关键调节因子。在本文中，我们回顾相关证据并提出，低脂联素血症并非肥胖的主要原因。相反，它是肥胖诱导的脂肪组织胰岛素抵抗的结果。低脂联素血症进而介导肥胖对其他外周组织（如肝脏和骨骼肌）的代谢影响，还可能对终末器官损伤产生一些直接作用。我们提出，破解调控脂联素基因表达和蛋白质分泌的分子细节，将使我们更全面地了解脂肪组织中胰岛素抵抗的机制，并为肥胖及胰岛素抵抗相关人类疾病的治疗干预提供新途径。
