Abstract
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 palmitate via PPAR-α.
Original language | English |
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Pages (from-to) | 377-382 |
Number of pages | 6 |
Journal | Endocrine Journal |
Volume | 56 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2009 |
Externally published | Yes |
Keywords
- Adiponectin receptor 2
- Clofibrate
- Palmitate
- Peroxisome proliferator-activated receptor-alpha
- β cells
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrinology