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Effects of a low-carbohydrate high-fat meal (LCM) versus a high-carbohydrate low-fat meal (HCM) on insulin, glucagon, and somatostatin release in nonobese healthy volunteers and in subjects with mild non-insulin-dependent diabetes mellitus (NIDDM) were compared. The meals were isocaloric. In the LCM, 26% of energy was supplied by carbohydrate, 51% by fat, and 23% by protein, whereas corresponding figures for HCM were 62, 22, and 16%. Hormonal responses were expressed as incremental areas over baseline. In healthy volunteers the HCM had a significantly greater effect on the insulin response than did the LCM. In contrast, in the diabetic group the insulin response to HCM was markedly impaired and was of the same magnitude as that to LCM. Glucagon release was significantly augmented after LCM in the nondiabetic as well as in the diabetic group, despite a pronounced and concomitant hyperglycemia in the latter. Moreover, HCM tended to stimulate glucagon release but only in the diabetic subjects. LCM and HCM induced a significant and sustained elevation of somatostatin levels in both groups; these responses were not significantly influenced by glucose tolerance or composition of meal. In conclusion, the present study suggests that at least two islet dysfunctions--decreased insulin response and enhanced glucagon release--characterize mild NIDDM. With a high-carbohydrate meal, a severe impairment of insulin secretion and a slight paradoxical glucagon release are observed. With a low-carbohydrate fat-rich meal, beta-cell responsiveness seems to be intact, but alpha-cell secretion is enhanced.
Gutniak et al. (Thu,) studied this question.