Overexpression of hexokinase I but not GLUT1 glucose transporter alters concentration dependence of glucose-stimulated insulin secretion in pancreatic β-cell line MIN6

Hisamitsu Ishihara, Tomoichiro Asano, Katsunori Tsukuda, Hideki Katagiri, Kouichi Inukai, Motonobu Anai, Masatoshi Kikuchi, Yoshio Yazaki, Jun Ichi Miyazaki, Yoshitomo Oka

Research output: Contribution to journalArticlepeer-review

55 Citations (Scopus)

Abstract

The recently established pancreatic β-cell line MIN6 retains the ability to secrete insulin in response to physiological glucose concentrations. To investigate the role of glucose transport and phosphorylation in glucose- stimulated insulin secretion by β-cells, MIN6 cells were stably transfected with a rabbit GLUT1 glucose transporter cDNA or a rat hexokinase I cDNA cloned in an expression vector. Overexpression of GLUT1 increased 3-O- methylglucose uptake, but did not alter either glucose utilization or glucose-stimulated insulin secretion. In contrast, clones overexpressing hexokinase I exhibited enhanced glucose-stimulated insulin secretion at glucose concentrations below 10 mM with a concomitant increase in glucose utilization. Maximal insulin secretion as well as the maximal rate of glucose utilization were not altered in these clones. Insulin secretion stimulated by 2-ketoisocaproate, a non-glucose secretagogue, was not affected by hexokinase I expression. These results strongly suggest that the glucose phosphorylating step, but not glucose transport step, regulates glucose-stimulated insulin secretion by modulating the glycolytic rate in the β-cell.

Original languageEnglish
Pages (from-to)3081-3087
Number of pages7
JournalJournal of Biological Chemistry
Volume269
Issue number4
Publication statusPublished - 1994 Jan 28
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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