Jung Tae Woo, Lee Myung Won, Lee Yong Jik, Kim Seon Mee, Lee Kyoung Tae, Whang Wan Kyunn, Cheon Hwan Ju, Jeong Yeon Taek, Chung Kun Wook, Cho Jae Min, Kim Do Hoon, Jung Tae Woo
Samsung Biomedical Institute, Seoul, Korea.
Endocr J. 2009;56(3):377-82. doi: 10.1507/endocrj.k08e-354. Epub 2009 Apr 1.
Adiponectin receptors mediate the antidiabetic effects of adiponectin. Although suggested to be mainly expressed in muscle, liver, and adipocyte cells, the expression of adiponectin receptors in beta cells is unclear. Given the primary involvement of this cell type in diabetes mellitus, we presently examined the expression level of adiponectin receptor 2 (AdiR2) in beta cells. Expression was significantly increased under acute hyperlipidemic conditions but impaired under chronic conditions. The impaired AdiR2 expression may play a role in worsened beta cell function. Clofibrate, an agonist of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) delayed the palmitate-induced impairment of AdiR2 expression and PPAR-alpha; this delay was abolished by PPAR-alpha targeted small interfering RNA. The results suggest that AdiR2 expression is regulated by palmitate via PPAR-alpha.
脂联素受体介导脂联素的抗糖尿病作用。尽管有研究表明脂联素受体主要在肌肉、肝脏和脂肪细胞中表达，但β细胞中脂联素受体的表达情况尚不清楚。鉴于这种细胞类型在糖尿病中起主要作用，我们目前检测了β细胞中脂联素受体2（AdiR2）的表达水平。在急性高脂血症条件下，AdiR2的表达显著增加，但在慢性条件下则受损。AdiR2表达受损可能在β细胞功能恶化中起作用。氯贝丁酯是过氧化物酶体增殖物激活受体α（PPAR-α）的激动剂，它可延缓棕榈酸诱导的AdiR2表达和PPAR-α的损伤；PPAR-α靶向小干扰RNA可消除这种延缓作用。结果表明，棕榈酸通过PPAR-α调节AdiR2的表达。
