Portal de Periódicos da CAPES

Heterogeneity in glucose sensitivity among pancreatic beta-cells is correlated to differences in glucose phosphorylation rather than glucose transport.

1993; Springer Nature; Volume: 12; Issue: 7 Linguagem: Inglês

10.1002/j.1460-2075.1993.tb05949.x

1460-2075

Harry Heimberg, A. De Vos, A. Vandercammen, Emile Van Schaftingen, Daniël Pipeleers, F. Schuit,

Metabolism, Diabetes, and Cancer

Research Article1 July 1993free access Heterogeneity in glucose sensitivity among pancreatic beta-cells is correlated to differences in glucose phosphorylation rather than glucose transport. H. Heimberg H. Heimberg Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author A. De Vos A. De Vos Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author A. Vandercammen A. Vandercammen Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author E. Van Schaftingen E. Van Schaftingen Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author D. Pipeleers D. Pipeleers Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author F. Schuit F. Schuit Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author H. Heimberg H. Heimberg Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author A. De Vos A. De Vos Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author A. Vandercammen A. Vandercammen Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author E. Van Schaftingen E. Van Schaftingen Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author D. Pipeleers D. Pipeleers Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author F. Schuit F. Schuit Department of Biochemistry, Vrije Universiteit Brussel, Belgium. Search for more papers by this author Author Information H. Heimberg1, A. De Vos1, A. Vandercammen1, E. Van Schaftingen1, D. Pipeleers1 and F. Schuit1 1Department of Biochemistry, Vrije Universiteit Brussel, Belgium. The EMBO Journal (1993)12:2873-2879https://doi.org/10.1002/j.1460-2075.1993.tb05949.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info Rat beta-cells differ in their individual rates of glucose-induced insulin biosynthesis and release. This functional heterogeneity has been correlated with intercellular differences in metabolic redox responsiveness to glucose. The present study compares glucose metabolism in two beta-cell subpopulations that have been separated on the basis of the presence (high responsive) or absence (low responsive) of a metabolic redox shift at 7.5 mM glucose. Mean rates of glucose utilization and glucose oxidation in high responsive beta-cells were 2- to 4-fold higher than in low responsive beta-cells, whereas their leucine and glutamine oxidation was only 10–50% higher. This heterogeneity in glucose metabolism cannot be attributed to differences in GLUT2 mRNA levels or in glucose transport. In both cell subpopulations, the rates of glucose transport (13–19 pmol/min/10(3) beta-cells) were at least 50-fold higher than corresponding rates of glucose utilization. On the other hand, rates of glucose phosphorylation (0.3–0.7 pmol/min/10(3) beta-cells) ranged within those of total glucose utilization (0.2–0.4 pmol/min/10(3) beta-cells). High responsive beta-cells exhibited a 60% higher glucokinase activity than low responsive beta-cells and their glucokinase mRNA level was 100% higher. Furthermore, glucose phosphorylation via low Km hexokinase was detected only in the high responsive beta-cell subpopulation. Heterogeneity in glucose sensitivity among pancreatic beta-cells can therefore be explained by intercellular differences in glucose phosphorylation rather than in glucose transport. Previous ArticleNext Article Volume 12Issue 71 July 1993In this issue RelatedDetailsLoading ...