Unawareness of hypoglycemia by insulin-dependent diabetics
Autor: | Bosquet F, P. Davidoff, Landault C, C Sachon, A Grimaldi, F. Zoghbi, Digy Jp, Thervet F, J. C. Legrand |
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Rok vydání: | 1990 |
Předmět: |
Adult
Blood Glucose medicine.medical_specialty Time Factors Epinephrine Hydrocortisone Endocrinology Diabetes and Metabolism medicine.medical_treatment Clinical Biochemistry Adrenergic Hypoglycemia Biochemistry Glucagon Subcutaneous injection Norepinephrine Endocrinology Risk Factors Internal medicine Diabetes mellitus medicine Humans Insulin Aged business.industry Biochemistry (medical) General Medicine Middle Aged medicine.disease Diabetes Mellitus Type 1 Basal (medicine) Growth Hormone Perception business Hormone |
Zdroj: | Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 22(2) |
ISSN: | 0018-5043 |
Popis: | 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. |
Databáze: | OpenAIRE |
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