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The insulinogenic index was investigated as a possible means for distinguishing between prirnary and secondary diabetes. This index is defined as the ratio.1 IRI/.1 glucose, where IRI is the plasma immunoreactive insulin level determined after the administration of a prescribed oral glucose load. The insulinogenic index values as measured 30 minutes after a 50 grn glucose load were as follows in normal subjects and those with primary diabetes: normal, 1.43 ± 0.17 (Mean ± SEM); mild diabetes, 0.39 ± 0.08; and moderate diabetes, 0.08 ± 0.02. In certain diseases associated with abnormal glucose tolerance, the values were as folIows; pheochromocytoma, 0.18 ± 0.12, acromegaly associated with severe glucose intolerance, 0.16 ± 0.08; acromegaly associated with mild glucose intolerance, 0.54 ± 0.20; and liver cirrhosis, 0.59 ± 0.10. These va lues were not significantly different from those in primary diabetes. On the other hand, in other diseases associated with abnormal glucose tolerance a marked difference was noted as folIows: hyperthyroidism, 1.01 ± 0.20; Cushing's syndrome, 1.37 ± 0.42; steroid diabetes, 1.22 ± 0.32; acute hepatitis, 1.16 ± 0.31; and chronic hepatitis, 1.48 ± 0.34. It was concluded, therefore, that in the latter cases, the insulinogenie index is a supplementary tool for distinguishing between primary and secondary diabetes.

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Effects of voglibose (an alpha-glucosidase inhibitor) and pioglitazone (an insulin sensitizer) on glycemic control and on the function of pancreatic islets were evaluated using Goto-Kakizaki (GK) rats with non-insulin-dependent diabetes mellitus (NIDDM). Five week administration (8-13 weeks of age in GK rats) of voglibose alone (added to the chow at a concentration of 10 ppm), pioglitazone alone (10 mg/kg daily p.o.), or both of the agents together significantly improved fasting plasma glucose levels and those at 120 min in oral glucose tolerance tests. Insulin secretory capacity in response to glucose of the isolated islets, assessed by batch incubation, was significantly improved in the voglibose and in the voglibose plus pioglitazone groups. Eight-week administration (5-13 weeks of age) of voglibose and voglibose plus pioglitazone successfully lowered the fasting levels of plasma glucose and triglyceride. The glucose-responsiveness in insulin release from the islets was also significantly recovered by the therapy. The treatment increased the insulin content of the islets to almost twice that in untreated controls. Thus, treatment by these drugs can not only effectively ameliorate the metabolic derangement of NIDDM in GK rats, but it can also restore the deteriorated islet function, possibly through protection from glucose toxicity.