Insulin Secretion in Maturity-Onset-Diabetes Function of Isolated Islets

Abstract

An impaired insulin response to glucose is a characteristic finding in maturity onset diabetes (MOD). To clarify whether the decreased insulin response in vivo is related to a primary defect of the beta-cells, isolated islets of MOD - obtained by intraoperative biopsy - were examined for their insulin content, biosynthesis and release. The in vitro experiments showed that despite a missing or significantly reduced insulin response in vivo the isolated beta-cells of the same patients had a normal insulin content, a normal or even high biosynthesis, and insulin release could be induced by glucose. These results suggest that the primary defect in MoD cannot be related to an intrinsic failure of the beta-cells to response to glucose; extrapancreatic factors seem to influence their reaction to glucose. These factors may be of a higher level in those patients or the reaction of the beta-cells is more inhibited by the same concentrations in diabetic patients.

Functional and morphological alterations of mitochondria in pancreatic beta cells from type 2 diabetic patients

“…However, little information is available on the insulin release properties of islets isolated from type 2 diabetic subjects. Pancreatic islets were studied from seven type 2 diabetic patients (obtained by intraoperative biopsy) [11]. The authors reported that despite a marked reduction of glucose-stimulated insulin secretion in vivo, a normal insulin release was induced by glucose from the isolated islets, suggesting that extrapancreatic factors influence beta cell reaction to glucose in type 2 diabetes.…”

Effect of human lymphoblastoid interferon on insulin synthesis and secretion in isolated human pancreatic islets

“…That high glucose concentration induces an increase in insulin secretion and proinsulin biosynthesis in isolated human islets has been reported elsewhere [14][15][16]. Total protein biosynthesis (to a lesser extent) is also significantly raised by high glucose concentrations, and this may be a reflection of increased glucose utilisation [14], as well as increased proinsulin biosynthesis.…”

Cyproheptadine Inhibits (Pro)Insulin Biosynthesis and Secretion of Isolated Human Pancreatic Islets

“…-The gestational ages of the fetuses were 18, 19 and 24 weeks, respectively. -^The biopsies were carried out chiefly for other investigations (see Lohmann et al 1980). -Two pancreata were removed because of tumors, one pancreas was from a brain-dead human cadaver.…”

“…Pancreatic islets were prepared either from fetuses of insulin dependent women (Jahr, Reiher, Ziegler, Schmidt and Hahn, unpublished data) or from pancreas specimen of non-diabetic adults or from cadaver pancreas. Preparation and incubation of the islets was carried out as described (Lohmann, Jahr, Verlohren, Schmidt, Heilmann, Ziihlke, Hartig, Mdttig 1980). Insulin release and 3 H-leucine incorporation into (pro)insulin was determined after an incubation period of 180 min (Lohmann et al 1980).…”

“…Preparation and incubation of the islets was carried out as described (Lohmann, Jahr, Verlohren, Schmidt, Heilmann, Ziihlke, Hartig, Mdttig 1980). Insulin release and 3 H-leucine incorporation into (pro)insulin was determined after an incubation period of 180 min (Lohmann et al 1980). Table 1 shows the inhibition by CPH of (pro)insulin biosynthesis and secretion in isolated human pancreatic islets.…”