Anatomical versus functional beta-cell mass in experimental diabetes.
The ability of pancreatic beta-cell mass to vary according to insulin requirements is an important component of optimal long-term control of glucose homeostasis. It is generally assumed that alteration of this property largely contributes to the impairment of insulin secretion in type 2 diabetes. However, data in humans are scarce and it is impossible to correlate beta-cell mass and function with the various stages of the disease. Thus, the importance of animal models is obvious. In rodents, increased beta-cell mass associated with an increase in the function of individual beta-cells contributes to the adaptation of the insulin response to insulin resistance in late pregnancy and in obesity. A reduction in beta-cell mass always corresponds to an alteration in insulin secretory capacity of islet tissue (Zucker diabetic fatty and Goto-Kakisaki rats, db/db mice). During regenerative processes following experimental reduction of beta-cell mass [partial pancreatectomy, streptozocin (STZ) injection], beta-cell mass increase is not associated with a corresponding improvement of beta-cell function, thus indicating that regenerative beta-cells did not achieve functional maturity. The main lesson from experimental diabetes is therefore that beta-cell mass cannot always predict functional capacity of the beta-cell tissue and that the functional beta-cell mass rather than the anatomical beta-cell mass must be taken into account at all times.
Kargar
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C
Diabetes and Metabolic Diseases Research Department, Institut de Recherches Servier, Suresnes, France. catherine.kargar@fr.netgrs.com
Ktorza
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A
D000818:Animals; D001786:Blood Glucose / Q000032:analysis / Q000502:physiology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000473:pathology*; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007333:Insulin Resistance / Q000502:physiology; D050417:Insulin-Secreting Cells / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D051379:Mice; D009765:Obesity / Q000378:metabolism*; D010179:Pancreas / Q000473:pathology*; D010180:Pancreatectomy; D011247:Pregnancy; D051381:Rats; D013311:Streptozocin / Q000008:administration & dosage
D001786:Blood Glucose; D013311:Streptozocin