Regulation of Adiponectin Receptor 2 Expression via PPAR-.ALPHA. in NIT-1 Cells
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- JUNG Tae Woo
- Samsung Biomedical Institute
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- LEE Myung Won
- Department of Family Medicine, Brain Korea 21 Project Medical Science, College of Medicine, Korea University Department of Anatomy, College of Medicine, Korea University
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- LEE Yong Jik
- Division of Clinical Research, Seoul Medical Center Research Institute
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- KIM Seon Mee
- Department of Family Medicine, Brain Korea 21 Project Medical Science, College of Medicine, Korea University
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- LEE Kyoung Tae
- College of Pharmacy, Chung-Ang University
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- WHANG Wan Kyunn
- College of Pharmacy, Chung-Ang University
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- CHEON Hwan Ju
- Samsung Biomedical Institute
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- JEONG Yeon Taek
- Samsung Biomedical Institute
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- CHUNG Kun Wook
- Samsung Biomedical Institute
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- CHO Jae Min
- Samsung Biomedical Institute
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- KIM Do Hoon
- Samsung Biomedical Institute
説明
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 β 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 β cells. Expression was significantly increased under acute hyperlipidemic conditions but impaired under chronic conditions. The impaired AdiR2 expression may play a role in worsened β cell function. Clofibrate, an agonist of peroxisome proliferator-activated receptor-alpha (PPAR-α) delayed the palmitate-induced impairment of AdiR2 expression and PPAR-α; this delay was abolished by PPAR-α targeted small interfering RNA. The results suggest that AdiR2 expression is regulated by palmit ate via PPAR-α.
収録刊行物
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- Endocrine Journal
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Endocrine Journal 56 (3), 377-382, 2009
一般社団法人 日本内分泌学会
