GLUCOSE AND FREE FATTY ACID TURNOVER IN THYROTOXICOSIS AND HYPOTHYROIDISM, BEFORE AND AFTER TREATMENT
J. Saunders, S. E. H. HALL, Peter H. Sönksen
Abstract
J. Saunders, S. E. H. HALL, Peter H. Sönksen
Abstract
Glucose and free fatty acid (FFA) turnover (RT) were measured by isotopic methods in groups of patients with thyrotoxicosis and hypothyroidism and compared with normal subjects. Patients with thyrotoxicosis were then studied after treatment with oral propranolol and again after treatment with carbimazole. Patients with hypothyroidism were studied again after treatment with thyroxine. Glucose RT was increased by about a third in thyrotoxicosis (12.7 mumol. min.-1 kg-1 +/- 1.0 SEM compared to 9.5 +/- 0.5 in normal subjects) while FFA RT was doubled (12.5 mumol. min.-1 kg-1 +/- 1.2 compared to 6.3 +/- 0.9 in normals). Propranolol was without effect, but carbimazole normalized these variables. In hypothyroidism both glucose and FFA RT were normal (9.1 +/- 0.7 and 6.7 +/- 0.9 respectively). Mean glucose and FFA RT both rose following thyroxine treatment, but not significantly; the post-treatment values remaining within the normal range (10.3 +/- 0.7 and 7.0 +/- 1.3 respectively). Oxidation of FFA, as estimated by 14CO2 excretion, was increased in thyrotoxicosis (42.8% +/- 2.9 SEM compared to 34.8 +/- 2.3 in normal subjects) and fell with carbimazole treatment (34.7 +/- 4.1). In hypothyroid subjects FFA oxidation increased following thyroxine treatment (from 34.4 +/- 4.1). In hypothyroid subjects FFA oxidation increased following thyroxine treatment (from 34.4 +/- 3.3 to 46.2 +/- 3.6).
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Glucose and free fatty acid (FFA) turnover (RT) were measured by isotopic methods in groups of patients with thyrotoxicosis and hypothyroidism and compared with normal subjects. Patients with thyrotoxicosis were then studied after treatment with oral propranolol and again after treatment with carbimazole. Patients with hypothyroidism were studied again after treatment with thyroxine. Glucose RT was increased by about a third in thyrotoxicosis (12.7 mumol. min.-1 kg-1 +/- 1.0 SEM compared to 9.5 +/- 0.5 in normal subjects) while FFA RT was doubled (12.5 mumol. min.-1 kg-1 +/- 1.2 compared to 6.3 +/- 0.9 in normals). Propranolol was without effect, but carbimazole normalized these variables. In hypothyroidism both glucose and FFA RT were normal (9.1 +/- 0.7 and 6.7 +/- 0.9 respectively). Mean glucose and FFA RT both rose following thyroxine treatment, but not significantly; the post-treatment values remaining within the normal range (10.3 +/- 0.7 and 7.0 +/- 1.3 respectively). Oxidation of FFA, as estimated by 14CO2 excretion, was increased in thyrotoxicosis (42.8% +/- 2.9 SEM compared to 34.8 +/- 2.3 in normal subjects) and fell with carbimazole treatment (34.7 +/- 4.1). In hypothyroid subjects FFA oxidation increased following thyroxine treatment (from 34.4 +/- 4.1). In hypothyroid subjects FFA oxidation increased following thyroxine treatment (from 34.4 +/- 3.3 to 46.2 +/- 3.6).
Key concepts: Carbimazole, Internal medicine, Endocrinology, Medicine, Propranolol, Excretion, Fatty acid, Antithyroid agent