Nutrient regulation of pancreatic beta-cell function in diabetes: problems and potential solutions

Peter Flatt, B. D. Green

Research output: Contribution to journalArticle

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 beta-cell glucose responsiveness. Mechanisms underlying beta-cell dysfunction include glucose toxicity, lipotoxicity and beta-cell hyperactivity. Defects at various sites in beta-cell signal transduction pathways contribute, but no single lesion can account for the common form of Type 2 diabetes. Recent studies highlight diverse beta-cell actions of GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide). These intestinal hormones target the beta-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 beta-cells. Incretin hormones therefore represent an exciting future multi-action solution to correct beta-cell defect in Type 2 diabetes.
LanguageEnglish
Pages774-778
JournalBiochemical Society Transactions
Volume34
Issue numberPart 5
Publication statusPublished - Nov 2006

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Insulin-Secreting Cells
Food
Glucose
Insulin
Type 2 Diabetes Mellitus
Gastrointestinal Hormones
Incretins
Proinsulin
Glucagon-Like Peptide 1
Cyclic AMP-Dependent Protein Kinases
Signal Transduction
Obesity
Hormones
Apoptosis
Gene Expression
Peptides

Cite this

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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 beta-cell glucose responsiveness. Mechanisms underlying beta-cell dysfunction include glucose toxicity, lipotoxicity and beta-cell hyperactivity. Defects at various sites in beta-cell signal transduction pathways contribute, but no single lesion can account for the common form of Type 2 diabetes. Recent studies highlight diverse beta-cell actions of GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide). These intestinal hormones target the beta-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 beta-cells. Incretin hormones therefore represent an exciting future multi-action solution to correct beta-cell defect in Type 2 diabetes.",
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Nutrient regulation of pancreatic beta-cell function in diabetes: problems and potential solutions. / Flatt, Peter; Green, B. D.

In: Biochemical Society Transactions, Vol. 34, No. Part 5, 11.2006, p. 774-778.

Research output: Contribution to journalArticle

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