Increased ketonaemia in hyperthyroidism. Evidence for a beta-adrenergic mechanism.

Abstract

The metabolic status of 16 hyperthyroid patients and 22 control subjects was studied in the post-absorptive state after 3 days on a standard diet (35 kcal/kg body weight/day). In hyperthyroidism the ranges of blood ketone body (19–1159 vs 17–233 μmol/l, p<0.001) and glycerol (59–285 vs 15–69 μmol/l, p<0.001) concentrations were increased relative to controls despite slight hyperglycaemia (4.9±0.6 vs 4.6±0.4 mmol/l, mean±SD p<0.05). Plasma non-esterified fatty acids, immunoreactive insulin and glucagon levels were not significantly different. A positive correlation was found between thyroid hormone and ketone body (p<0.02) and glycerol (p<0.05) levels and between glycerol and ketone bodies (p<0.05). There was no correlation of non-esterified fatty acids with either thyroid hormone or ketone body concentrations. In hyperthyroid patients propranolol administration for 4 days induced a decrease in triiodothyronine (349±140 to 229±107 ng/100ml, p<0.01) and a dramatic fall in ketone body (18–295 μmol/l, p<0.001) and glycerol (44–130 μmol/l, p<0.001) levels. Non esterified fatty acids were unchanged. There was no longer a correlation between thyroid hormones and ketone bodies or glycerol. Placebo administration to 6 other hyperthyroid patients had no significant effect. In euthyroid obese subjects on a 600 kcal/day diet, propranolol administration did not change ketone body or glycerol levels. These data provide evidence for an increase in both lipolysis and ketogenesis in hyperthyroidism which might, at least in part, be dependent upon a catecholamine β-receptor mediated mechanism.