Key result
Insulin-dependent diabetics with poor perception of hypoglycemia had a delayed adrenergic secretion with a lower blood glucose threshold compared to those with good perception.
Why the study?
Does hormonal counterregulation differ during induced hypoglycemia in insulin-dependent diabetics with versus without hypoglycemia unawareness?
Case-Control (n=14)
Does hormonal counterregulation differ during induced hypoglycemia in insulin-dependent diabetics with versus without hypoglycemia unawareness?
Hypoglycemia unawareness in insulin-dependent diabetics is associated with a delayed adrenergic response to falling blood glucose levels, rather than an absolute defect in catecholamine secretion.
Answers are grounded in this paper and cite their sources.
May support awareness screening in insulin-dependent diabetes; leaves open whether threshold restoration improves outcomes.
After several years of insulin therapy, about 20% of insulin-dependent diabetics have little or no perception of hypoglycaemia because of a loss of the adrenergic warning symptoms. This defect, poorly correlated with the presence of autonomic neuropathy, has been classically explained by a defect in the catecholamine secretion. We compared the hormonal counterregulation during hypoglycaemia induced by subcutaneous injection of insulin in 7 insulin-dependent diabetics with poor perception of hypoglycaemia and experiencing repeated episodes of severe hypoglycaemia (group A) and 7 insulin-treated diabetics with very good perception of hypoglycaemia and not experiencing severe hypoglycaemia (group B). Groups A and B were similar in terms of age, duration of diabetes, HbA1c level and degenerative complications. The glucagon levels were identical and non-reactive in the two groups. The basal levels and secretion peaks of adrenaline, noradrenaline, growth hormone and cortisol were similar between the two groups, but there was a significant delay in secretion in group A with a blood glucose threshold of adrenergic secretion of between 3.1 +/- 0.5 and 1.6 +/- 0.2 mmoles/l in group A and between 4.6 +/- 0.3 and 3.2 +/- 0.2 mmoles/l in group B (P less than 0.05). This delayed secretion could be explained by desensitisation of the hypothalamic glucostat and could be due to the frequency and/or severity of hypoglycaemic episodes.
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Grimaldi et al. (1990) conducted a case-control in Insulin-dependent diabetes (n=14). Poor perception of hypoglycemia vs. Good perception of hypoglycemia was evaluated on Blood glucose threshold of adrenergic secretion (p=<0.05). Insulin-dependent diabetics with poor perception of hypoglycemia had a delayed adrenergic secretion with a lower blood glucose threshold compared to those with good perception.
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