These findings provide new evidence of the central role of insulin resistance and hyperinsulinemia in the development of risk factors associated with coronary heart disease.
The clinicopathologic features of an adult with insulinoma and pancreatic islet cell hyperplasia, who presented with hyperinsulinemic hypoglycemia are reported, together with in vitro studies on the patient's pancreatic islets. Islet cell hyperplasia with ductal proliferation and budding and beta cell degranulation was demonstrated by immunochemical means. The in vitro studies of cultured hyperplastic islet cells support the clinicopathologic features. Thus, in comparison with control islets maintained in culture for up to 14 days, hyperplastic islets could be cultured for up to 60 days, during which time cell overgrowth required subculture on three occasions. Furthermore, in contrast to control islets the release of both insulin and somatostatin from cultured hyperplastic islets was refractory to glucose, glucagon, and tolbutamide; theophylline was the only secretagogue to stimulate insulin and somatostatin release from hyperplastic islets in vitro. Indirect immunofluorescence revealed the presence of islet cell surface autoantibodies in the plasma of this patient reactive with both normal human islets and a rat insulinoma line (RIN-m5F). These studies demonstrate the proliferative capacity and relatively undifferentiated functional state of hyperplastic islets in vitro. They provide further evidence that islet cell division is capable of being stimulated in adult life. The pathogenic significance of islet cell surface autoantibodies in hyperplastic islet cell disease and insulinoma warrants further investigation.
Hormonal and metabolic responses to hypothermic coronary artery bypass grafting (CABG) were studied in three groups: 8 non-diabetic patients, 8 patients with non-insulin-dependent diabetes mellitus (NIDDM) given a glucose pump priming solution and 8 NIDDM patients given a non-glucose infusion. There were no significant differences in stress hormone responses between NIDDM and non-diabetic patients, with adrenaline concentrations rising 10-fold, noradrenaline 4-fold and cortisol 2 to 3-fold. Glucagon rose significantly during bypass only in the NIDDM patients who did not receive a glucose prime. Comparable marked hyperglycaemia was seen in both glucose primed groups during bypass and exclusion of glucose from the prime in NIDDM patients prevented this major rise. Postoperatively, the rise in insulin in the glucose primed NIDDM patients contrasted with the slower rise in the non-glucose primed NIDDM patients who were also hyperglycaemic by this stage. Perioperative hyperglycaemia in NIDDM patients undergoing CABG can be prevented by using a non-glucose priming solution and by giving insulin infusion, particularly postoperatively.
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