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Hvorfor er betacellenes insulinfrigjöring mangelfull ved type 2-diabetes?
Engelsk titel: Why is insulin release from beta cells insufficient in type 2 diabetes? Läs online Författare: Grill V Språk: Nor Antal referenser: 26 Dokumenttyp: Översikt UI-nummer: 00101880

Tidskrift

Tidsskrift for Den Norske Laegeforening 2000;120(23)2796-8 ISSN 0029-2001 E-ISSN 0807-7096 KIBs bestånd av denna tidskrift Denna tidskrift är expertgranskad (Peer-Reviewed)

Sammanfattning

X : Insulin secretion is finely tuned to tissue requirements by tight links to prevailing blood glucose levels. The normal regulation of insulin secretion is linked to glucose metabolism in the pancreatic beta-cell, a major but not exclusive signal for secretion being closure of K+ ATP-dependent channels in the cell membrane through an increase in the cytosolic ATP/ADP. Insulin secretion in type 2 diabetes is abnormal in several respects, due to genetic causes, but also due to the metabolic environment of the pancreatic beta-cells. This environment may be particularly important for the deterioration of insulin secretion, which occurs with increasing duration of diabetes. Factors of the environment with potential importance include over-stimulation, a negative effect of hyperglycaemia per se ("glucotoxicity"), and adverse effects of elevated fatty acids ("lipotoxicity"). A better understanding of the mechanisms behind these factors and of their clinical importance will pave the way for treatment which could preserve beta-cell function in type 2 diabetic patients.