Role of Ca2+ in the stimulation of glucose transport by insulin in adipocytes.
- Author:
Sung Hoe CHANG
1
;
Yeon Jin JANG
;
Koo Kun PARK
;
Ghi Su KIM
;
Hee Jeong RYU
;
Chun Sik PARK
Author Information
1. Department of Physiology, University of Ulsan College of Medicine, 388-1 Poongnap-dong Songpa-ku, Seoul, 138-736 South Korea.
- Publication Type:Original Article
- MeSH:
Adipocytes*;
Animals;
Cyclosporine;
Glucose*;
Insulin*;
Okadaic Acid;
Rats;
Staphylococcal Protein A
- From:The Korean Journal of Physiology and Pharmacology
1999;3(3):357-364
- CountryRepublic of Korea
- Language:English
-
Abstract:
We investigated the role of Ca2+ and protein kinases/phosphatases in the stimulatory effect of insulin on glucose transport. In isolated rat adipocytes, the simple omission of CaCl2 from the incubation medium significantly reduced, but did not abolish, insulin-stimulated 2-deoxy glucose (2-DG) uptake. Pre-loading adipocytes with intracellular Ca2+ chelator, 5,5'-dimethyl bis (o-aminophenoxy)ethane-N,N,N'N' tetraacetic acetoxymethyl ester (5,5'-dimethyl BAPTA/AM) completely blocked the stimulation. Insulin raised intracellular Ca2+ concentration ((Ca2+)i) about 1.7 times the basal level of 72+/-5 nM, and 5,5'-dimethyl BAPTA/AM kept it constant at the basal level. This correlation between insulin-induced increases in 2-DG uptake and (Ca2+)i indicates that the elevation of (Ca2+)i may be prerequisite for the stimulation of glucose transport. Studies with inhibitors (ML-9, KN-62, cyclosporin A) of Ca2+-calmodulin dependent protein kinases/phosphatases also indicate an involvement of intracellular Ca2+. Additional studies with okadaic acid and calyculin A, protein phosphatase-1 (PP-1) and 2A (PP-2A) inhibitors, indicate an involvement of PP-1 in insulin action on 2-DG uptake. These results indicate an involvement of Ca2+-dependent signaling pathway in insulin action on glucose transport.
