title: Lack of beta-adrenergic role for catecholamines in the development of hyperglycemia and ketonaemia following acute insulin withdrawal in type I diabetic patients.
abstract: In order to evaluate the role of beta-receptor mediated effects of catecholamines in the metabolic deterioration following insulin withdrawal in insulin-dependent diabetic patients we have measured in 5 patients metabolic substrate and hormone concentrations during a 6 hours arrest of insulin infusion, without or with a simultaneous infusion of propranolol. During insulin deprivation plasma epinephrine and norepinephrine increased slightly (from 107 +/- 10 ng/L to 173 +/- 6 ng/L and from 307 +/- 37 ng/L to 518 +/- 77/ng/L respectively (p less than 0.05), cortisol decreased physiologically, but growth hormone and glucagon were not significantly modified. Free insulin decreased progressively from 12.2 +/- 2.5 mU/L to 5.4 +/- 1.1 mU/L (p less than 0.01). Blood glucose and ketone bodies rose sharply before any significant change in catecholamine levels. Plasma free fatty acids and blood glycerol increased progressively and their rise appeared somewhat temporally related to the variations of catecholamine levels. The addition of propranolol to insulin deprivation did not modify the changes in hormone concentrations in spite of a slightly greater rise of epinephrine (from 78 +/- 4 ng/L to 179 +/- 7 ng/L, p less than 0.05) and norepinephrine (from 395 +/- 80 ng/L to 679 +/- 153 ng/L, p less than 0.05). The rises of glucose and ketone bodies were unaffected whereas the increases of free fatty acids and glycerol were slightly blunted. In conclusion, we have no evidence for a beta-adrenergic mediated role for catecholamines in the development of hyperglycaemia and ketonaemia in non-stressed insulin deprived diabetic patients, and only small evidence for a permissive effect on lipolysis.
authors.forename: M
authors.initials: M
authors.lastname: Beylot
authors.forename: G
authors.initials: G
authors.lastname: Sautot
authors.forename: H
authors.initials: H
authors.lastname: Dechaud
authors.forename: R
authors.initials: R
authors.lastname: Cohen
authors.forename: J P
authors.initials: JP
authors.lastname: Riou
authors.forename: P
authors.initials: P
authors.lastname: Serusclat
authors.forename: R
authors.initials: R
authors.lastname: Mornex
mesh_terms: D000328:Adult; D002395:Catecholamines / Q000502:physiology*; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D004837:Epinephrine / Q000097:blood; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005934:Glucagon / Q000097:blood; D005990:Glycerol / Q000097:blood; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006943:Hyperglycemia / Q000209:etiology*; D007328:Insulin / Q000008:administration & dosage* / Q000097:blood; D007657:Ketone Bodies / Q000097:blood*; D008297:Male; D009638:Norepinephrine / Q000097:blood; D011433:Propranolol; D011943:Receptors, Adrenergic, beta / Q000502:physiology*
chemical_list: D002395:Catecholamines; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D007657:Ketone Bodies; D011943:Receptors, Adrenergic, beta; D013006:Growth Hormone; D005934:Glucagon; D011433:Propranolol; D005990:Glycerol; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine