Intracellular signal transduction pathways that control pancreatic beta-cell proliferation.
This review focuses on the factors that regulate the proliferation of pancreatic islet beta-cells in vitro, and in particular on the intracellular pathways that convey the mitogenic signal into a proliferative response. Substances as diverse as nutrients, polypeptides, cytokines, adrenergic agents, lithium, phorbol esters and cyclic AMP analogs are all able to stimulate or inhibit beta-cell proliferation in a time- and concentration-dependent manner. The evidence for involvement of cyclic AMP, cyclic GMP, protein kinase C, inositol polyphosphates, GTP-binding proteins, polyamines and oncogenes is reviewed.
Sjöholm
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Department of Endocrinology, Rolf Luft Center for Diabetes Research, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.
D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D000242:Cyclic AMP / Q000502:physiology; D019204:GTP-Binding Proteins / Q000502:physiology; D005947:Glucose / Q000494:pharmacology; D007295:Inositol Phosphates / Q000378:metabolism; D007515:Islets of Langerhans / Q000166:cytology* / Q000378:metabolism; D010455:Peptides / Q000494:pharmacology; D011073:Polyamines / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism; D015398:Signal Transduction
D000596:Amino Acids; D007295:Inositol Phosphates; D010455:Peptides; D011073:Polyamines; D000242:Cyclic AMP; D011493:Protein Kinase C; D019204:GTP-Binding Proteins; D005947:Glucose