The endocrine pancreas. Functional morphology and histopathology.

An impairment in the secretory response to glucose appears a characteristic feature of maturity-onset diabetes, which indicates that a possible defect in the glucose recognition and/or the secretory process of the B-cell might represent the pathogenic factor in this disease. It is most likely that various circumstances are capable of initiating a glucose intolerance associated with a deficient B-cell population. Such diverse pathogenic agents might affect the B-cell at different levels, which can explain the varying morphologic appearance of the endocrine pancreas in diabetic states. Both atrophic and hypertrophic islets, composed of few or several granulated or degranulated B-cells, have been described in human diabetes. No pathognomonic features can so far be identified with diabetic islets, although it is generally accepted that islet hyalinosis is frequently observed in elder diabetics; this characteristic does not seem to cause the secretory defect but appears to correspond to an accumulation of secretory products. In juvenile diabetes, an inflammatory infiltration of the islet tissue constitutes a common finding and might be related to the etiology of the disease. Genetic factors may play a part either by predisposing to some types of viral infection, or by inducing autoimmune reactions. Only in young diabetics, the reduction in the number of B-cells is sufficient to account for the secretory defect. No clear-cut quantitative or qualitative changes have so far been described in the A, D and D1 cells of diabetic islets, but the recent findings on the regulatory role of glucagon and somatostatin in normal and diabetic states certainly stress the possibility that diabetes might be a disease of the islet, and not merely one of the B-cell.SCOPUS: re.jSCOPUS: NotDefined.j