Nutrient regulation of pancreatic β-cell function in diabetes: Problems and potential solutions

P. R. Flatt*, B. D. Green

*Corresponding author for this work

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Increasing prevalence of obesity combined with longevity will produce an epidemic of Type 2 (non-insulin-dependent) diabetes in the next 20 years. This disease is associated with defects in insulin secretion, specifically abnormalities of insulin secretory kinetics and pancreatic β-cell glucose responsiveness. Mechanisms underlying β-cell dysfunction include glucose toxicity, lipotoxicity and β-cell hyperactivity. Defects at various sites in β-cell signal transduction pathways contribute, but no single lesion can account for the common form of Type 2 diabetes. Recent studies highlight diverse β-cell actions of GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide). These intestinal hormones target the β-cell to stimulate glucose-dependent insulin secretion through activation of protein kinase A and associated pathways. Both increase gene expression and proinsulin biosynthesis, protect against apoptosis and stimulate replication/neogenesis of β-cells. Incretin hormones therefore represent an exciting future multi-action solution to correct β-cell defect in Type 2 diabetes.

Original languageEnglish
Pages (from-to)774-778
Number of pages5
JournalBiochemical society transactions
Volume34
Issue number5
DOIs
Publication statusPublished - 01 Nov 2006

Keywords

  • Diabetes
  • Glucagon-like peptide-1 (GLP-1)
  • Glucose-dependent insulinotropic polypeptide (GIP)
  • Incretin hormone
  • Insulin
  • Pancreatic β-cell

ASJC Scopus subject areas

  • Biochemistry

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