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Metabolism ; 30(1): 6-17, 1981. tab, gra
Artigo em Inglês | MedCarib | ID: med-3530


The possible role of epinephrine deficiency in abnormal utilization of energy sources during fasting was investigated in three pairs of discordant identical twins with recurrent fasting hypoglycemia. The hypoglycemic twins, ages 2, 8 and 9 years, each had beens smaller at birth. Defective epinephrine responsiveness to hypoglycemia was established by administration of 2-deoxyglucose, 50 mg/kg, i.v. In the control twins, this resulted in a rapid increase of plasma glucose (+39 mg/100 ml), free fatty acids (+0.3 mM), and urinary epinephrine (+224 ng/mg creatine). These changes did not occur in the affected twins. Fasting metabolism in the epinephrine-deficient twins was compared to the unaffected twins as controls. Oxidation of carbohydrate and fat were estimated from hourly measurements of oxygen consumption and carbon dioxide production, and utilization of protein was determined from nitrogen excretion. PLasma glucose decreased more rapidly in the affected twins during the 8 hours prior to appearance of symptoms. During this period, carbohydrate was oxidized more rapidly than in the controls (average: 3.1 versus 1.7 mg/kg/min). Plasma á-hydroxybutyrate and free fatty acids was frequently less in relation to glucose. Symptoms occurred when the sum of both glucose and á-hydroxybutyrate was lower than in the controls. Urinary epinephrine excretion increased from an average baseline of 18 to a maximum of 134 ng/mg creatinine in the control twins. The average maximum urinary epinephrine reached in the deficient twins was only 51 ng/mg creatinine, in spite of lower glucose. Plasma insulin decreased in relation to glucose below 40 mg/100 ml in the control twins (r = 0.65), but this did not occur in the deficient twins (r = -0.38). Cortisol and growth hormone responses were similar in the two groups. THerefore, the consequences of inability to increase epinephrine when availability of glucose became acutely limiting were inappropriate persistent oxidation of carbohydrate, decreased circulating alternate substrates from fat, and lack of suppression of insulin. (AU)

Pré-Escolar , Feminino , Humanos , Masculino , Doenças em Gêmeos , Metabolismo Energético , Epinefrina/deficiência , Jejum , Gêmeos , Gêmeos Monozigóticos , Hipoglicemia/metabolismo , Peso ao Nascer , Glicemia/metabolismo , Carboidratos/metabolismo , Desoxiglucose/diagnóstico , Epinefrina/urina , Ácidos Graxos não Esterificados/sangue , Hidroxibutiratos/sangue , Oxirredução