Anatomical versus functional β-cell mass in experimental diabetes

• Published in: Diabetes, obesity & metabolism Vol. 10; no. s4; pp. 43 - 53
• Main Authors: Kargar, C, Ktorza, A
• Format: Journal Article
• Language: English
• Published: Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01-11-2008; Blackwell Publishing Ltd
• Subjects: Animals; Blood Glucose - analysis; Blood Glucose - physiology; Diabetes Mellitus, Experimental - metabolism; Diabetes Mellitus, Experimental - pathology; Diabetes Mellitus, Type 1 - physiopathology; Diabetes Mellitus, Type 2 - physiopathology; Female; Humans; Immunohistochemistry; insulin resistance; Insulin Resistance - physiology; insulin secretion; Insulin-Secreting Cells - metabolism; Insulin-Secreting Cells - pathology; Male; Mice; noninsulin-dependent diabetes mellitus; obesity; Obesity - metabolism; Pancreas - pathology; Pancreatectomy; plasticity; Pregnancy; Rats; Streptozocin - administration & dosage; type 2 diabetes; β-cell function; β-cell mass
• ISSN: 1462-8902; 1463-1326
• DOI: 10.1111/j.1463-1326.2008.00940.x

The ability of pancreatic β-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 β-cell mass and function with the various stages of the disease. Thus, the importance of animal models is obvious. In rodents, increased β-cell mass associated with an increase in the function of individual β-cells contributes to the adaptation of the insulin response to insulin resistance in late pregnancy and in obesity. A reduction in β-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 β-cell mass [partial pancreatectomy, streptozocin (STZ) injection], β-cell mass increase is not associated with a corresponding improvement of β-cell function, thus indicating that regenerative β-cells did not achieve functional maturity. The main lesson from experimental diabetes is therefore that β-cell mass cannot always predict functional capacity of the β-cell tissue and that the functional β-cell mass rather than the anatomical β-cell mass must be taken into account at all times.