Control of glucose phosphorylation and glucose usage in clonal insulinoma cells
- PMID: 2834251
- DOI: 10.2337/diab.37.5.563
Control of glucose phosphorylation and glucose usage in clonal insulinoma cells
Abstract
Glucose metabolism was investigated in two established clonal insulinoma cell lines (RINm5F and HIT) and in a newly developed line of mouse insulinoma cells (IgSV195). The hexokinase capacity in the homogenates of RINm5F cells was 22.1 +/- 3.23 U/g protein, but glucokinase was barely detectable (0.06 +/- 0.013 U/g protein). In contrast, both HIT and IgSV195 cells contained glucokinase (1.5 +/- 0.17 and 1.0 +/- 0.16 U/g protein, respectively) in addition to hexokinase activity. Glucose usage by the intact cells qualitatively reflected the glucose phosphorylation found in the cell-free extracts. RINm5F cells exhibited a high glucose usage rate with one high-affinity component, whereas both HIT and IgSV195 cells showed two components with different glucose affinities. HIT and IgSV195 cells may be useful for a model of pancreatic beta-cell glycolysis.
Similar articles
-
Control of glucose metabolism in pancreatic beta-cells by glucokinase, hexokinase, and phosphofructokinase. Model study with cell lines derived from beta-cells.Diabetes. 1988 Nov;37(11):1524-30. doi: 10.2337/diab.37.11.1524. Diabetes. 1988. PMID: 2972577
-
Porin proteins in mitochondria from rat pancreatic islet cells and white adipocytes: identification and regulation of hexokinase binding by the sulfonylurea glimepiride.Arch Biochem Biophys. 1994 Jan;308(1):8-23. doi: 10.1006/abbi.1994.1002. Arch Biochem Biophys. 1994. PMID: 8311478
-
Glucose transport by radiation-induced insulinoma and clonal pancreatic beta-cells.Diabetes. 1986 Dec;35(12):1340-4. doi: 10.2337/diab.35.12.1340. Diabetes. 1986. PMID: 3021551
-
Mitochondria and diabetes. Genetic, biochemical, and clinical implications of the cellular energy circuit.Diabetes. 1996 Feb;45(2):113-26. doi: 10.2337/diab.45.2.113. Diabetes. 1996. PMID: 8549853 Review.
-
New perspectives on pancreatic islet glucokinase.Am J Physiol. 1984 Jan;246(1 Pt 1):E1-13. doi: 10.1152/ajpendo.1984.246.1.E1. Am J Physiol. 1984. PMID: 6364828 Review.
Cited by
-
Cation-Independent Mannose 6-Phosphate Receptor Deficiency Enhances β-Cell Susceptibility to Palmitate.Mol Cell Biol. 2018 Mar 29;38(8):e00680-17. doi: 10.1128/MCB.00680-17. Print 2018 Apr 15. Mol Cell Biol. 2018. PMID: 29378831 Free PMC article.
-
[Insulin producing cells as therapy in diabetes mellitus].Naturwissenschaften. 1996 Jan;83(1):1-5. Naturwissenschaften. 1996. PMID: 8637602 Review. German.
-
Inhibition of the high-affinity glucose transporter GLUT 1 affects the sensitivity to glucose in a hamster-derived pancreatic beta cell line (HIT).Diabetologia. 1993 Nov;36(11):1204-7. doi: 10.1007/BF00401067. Diabetologia. 1993. PMID: 8270137
-
Pancreatic beta cell line MIN6 exhibits characteristics of glucose metabolism and glucose-stimulated insulin secretion similar to those of normal islets.Diabetologia. 1993 Nov;36(11):1139-45. doi: 10.1007/BF00401058. Diabetologia. 1993. PMID: 8270128
-
Differential expression and regulation of the glucokinase gene in liver and islets of Langerhans.Proc Natl Acad Sci U S A. 1989 Oct;86(20):7838-42. doi: 10.1073/pnas.86.20.7838. Proc Natl Acad Sci U S A. 1989. PMID: 2682629 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical