Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 307, Issue 1-2, Pages 77-82Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2009.03.024
Keywords
Insulin receptor; Insulin receptor substrate-1; Glucose; Parathyroid hormone
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Funding
- NIH [DK069965]
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Previous reports suggest that parathyroid hormone (PTH) is associated with insulin resistance. This research investigated the effects of PTH on insulin signaling in differentiated 3T3-L1 adipocytes. PTH (10 nM, 24 h) treatment induced a reduction in insulin-stimulated glucose uptake, AKT activity (phosphorylated AKT/total AKT protein expression) and a decrease in GLUT4 and IRS-1 protein expression compared to vehicle treated controls in differentiated adipocytes. PTH treatment also induced increased phosphorylation of IRS-1 on serine 307, which suppresses insulin signaling. In addition, treatment of cells with adenyl cyclase inhibitor SQ52236 ameliorated the effects of PTH on insulin-stimulated glucose uptake, whereas inhibition of phospholipase C alpha (U73122) did not significantly alter the effects of PTH. Thus, PTH treatment of differentiated 3T3-L1 adipocytes suppresses insulin-stimulated glucose uptake and insulin signaling via cAMP pathway, potentially through the phosphorylation of IRS-1 at serine 307. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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