Beta cells in type 2 diabetes - a crucial contribution to pathogenesis.
The healthy beta-cell has an enormous capacity to adapt to conditions of higher insulin demand (e.g. in obesity, pregnancy, cortisol excess) to maintain normoglycaemia with an increase in its functional beta-cell mass. This compensates in 80-90% of individuals for insulin resistance. However, in 10-20% of individuals, the beta-cells are unable to match the demands of insulin resistance and insulin levels are relatively insufficient to maintain normal glycaemic control. This eventually leads to glucose intolerance and type 2 diabetes (T2DM). Accordingly, preservation of functional beta-cell mass has become central in the treatment of type 1 diabetes as well as T2DM. The purpose of this review is to summarize the recently described mechanisms of beta-cell death in T2DM and to postulate possible new targets for treatment.
Maedler
Kathrin
K
Department of Medicine, Larry L. Hillblom Islet Research Center, University of California at Los Angeles, Los Angeles, CA 90095-7345, USA. kmaedler@mednet.ucla.edu
D000818:Animals; D017209:Apoptosis; D001786:Blood Glucose / Q000502:physiology; D049109:Cell Proliferation; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology* / Q000503:physiopathology; D018149:Glucose Intolerance; D006801:Humans; D007249:Inflammation / Q000473:pathology; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000473:pathology* / Q000502:physiology; D016328:NF-kappa B / Q000502:physiology; D019014:fas Receptor / Q000502:physiology
D001786:Blood Glucose; D016328:NF-kappa B; D019014:fas Receptor