Why the study?
Does hyperglycemia attenuate the rise in circulating FFA caused by acute insulin withdrawal in normal men?
Does hyperglycemia attenuate the rise in circulating FFA caused by acute insulin withdrawal in normal men?
Hyperglycemia per se significantly attenuates the rise in circulating free fatty acids caused by acute insulin withdrawal in humans.
Answers are grounded in this paper and cite their sources.
Hyperglycemia may blunt FFA rise during insulin withdrawal; leaves open relevance to metabolic control in diabetes.
The present study was undertaken to examine the influence of hyperglycemia in retarding the rise in circulating FFA noted after acute insulin withdrawal in man. The arterial FFA response to somatostatin administration was measured in the presence of (a) euglycemia and (b) hyperglycemia. In seven normal men who received somatostatin (0.9 mg/h) with euglycemia maintained by exogenous glucose infusion plasma insulin levels fell to levels 4 uU/ml and plasma FFA concentrations rose from 659 +/- 123 to 2057 +/- 268 uEq/l. When somatostatin was infused with hyperglycemia maintained at approximately 230 mg/dl, plasma insulin levels were again maintained at levels 4 uU/ml. Despite similar insulinopenia plasma FFA concentrations rose from 510 +/- 56 to only 1125 +/- 180 uEq/l, significantly less than in the previous protocol (p less than 0.01). These data indicate that hyperglycemia per se significantly attenuates the rise in circulating FFA caused by acute insulin withdrawal in man.
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Liljenquist et al. (1981) studied this question.
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