Quantitative analysis of major lipid classes and the fatty acids carried out on lipid extracts of brain from young and adult alloxan diabetic rats revealed decreases in total lipid, cholesterol, the more polar cerebroside, and phospha-tidylethanolamine in brain from young diabetic rats. No significant changes in lipid class composition were found in brains from adult rats with alloxan diabetes. No significant changes in fatty acids were detected in the total brain lipids of young or adult rats as a result of alloxan diabetes. In contrast, similar studies on the lipids of sciatic nerve revealed an increase in cholesterol balanced by a decrease of triglycerides in young rats and a decrease of total lipid and the more polar cerebroside only in adult rats with alloxan diabetes. Compared to normal rats, total lipids from sciatic nerves of young alloxan diabetic rats showed relative decreases in palmitate (16:0), oleate (18:1), and linoleate (18:2) with increases in stearate (18:0), eicosanoate (20:0), eicosenoate (20:1), arachidonate (20:4), docosanoate (22:0), docosapentaenoate (22:5), docosahexaenoate (22:6), lignocerate (24:0). In lipid extracts from sciatic nerves of adult diabetic rats, only oleate (18:1) was increased and linoleate (18:2) decreased compared to normal.

The data suggest that two forms of NIDDM may exist, crudely distinguished by the clinical decision to use insulin to control blood glucose levels. The insulin-taking diabetic individuals may experience a greater likelihood of pancreatic failure, whereas non-insulin-taking diabetic individuals probably experience stable pancreatic function over the course of their disease. Longitudinal observation of the Wadena cohort will provide more insight into this possibility.

Glucagon response to insulin hypoglycemia was tested in diabetics with autonomic neuropathy (N=9), diabetics without neuropathy (N=8), and normals (N=9). With similar levels of hypoglycemia, growth hormone and plasma cortisol increased in all groups. The glucagon response in normals (121+/-19 vs. 308+/-30 pg./ml., mean+/-S.E.M. of baseline vs. hypoglycemia peak) was significantly less in nonneuropathic diabetics than in normals (128+/-13 vs. 209+/-30) and absent in neuropathic diabetes (128+/-23 vs. 115+/-20). Arginine stimulation produced a glucagon response in the neuropathic diabetics (106+/-16 vs. 523+/-103). The data indicate that the capacity to release glucagon during hypoglycemia is lost in diabetic neuropathy while glucagon responsiveness to arginine is retained. Neuropathy in diabetes may contribute to metabolic instability.

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