Reduction of increased levels of blood glycerol and ketone bodies by propranolol in human hyperthyroidism: Role of the fall of the triiodothyronine level

Beylot, M.; Riou, Jean‐Paul; Borson, F.; Cohen, Richard A.; Sautot, G; Mornex, R

doi:10.1016/0026-0495(84)90091-x

Cited by 7 publications

(3 citation statements)

References 17 publications

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“…Increased levels of blood glycerol and ketone bodies and increased urinary hydroxyproline excretion in hyperthyroid patients are reduced by pro¬ pranolol but not by timolol (which has no effect on plasma T3). (43,44) Propranolol decreased oxygen consumption in rela¬ tion to the decrease of plasma T3 in one study'45' but not in another.146' The fall in oxygen consumption, if any, appears to be unrelated to a diminished plasma T3, since atenolol also decreased oxygen consumption in the absence of T3 changes/25' Neither propranolol nor metoprolol modified the increased protein synthesis and degradation in hyperthyroidism. '47·48' Taken together, these studies indicate no metabolic improve¬ ment or only modest benefit due to ß-blockade in thyrotoxicosis.…”

Section: Clinical Response In Hyperthyroidismmentioning

confidence: 99%

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Propranolol and Thyroid Hormone Metabolism

Wiersinga

1991

Thyroid

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Propranolol decreases plasma T3 and increases plasma rT3 in a dose-dependent manner due to a decreased production rate of T3 and a decreased metabolic clearance rate of rT3, respectively, caused by inhibition of the conversion of T4 into T3 and of rT3 into 3,3'-T2. This inhibition of 5'-deiodination is not secondary to inhibition of thyroid hormone transport across the plasma membrane. Propranolol and its major metabolite, 4-hydroxypropranolol, are not directly responsible for these effects, but an unidentified metabolite of propranolol might be involved. beta-blockers ameliorate clinical symptoms and signs of thyrotoxicosis independent of the decrease of plasma 13, that is confined to beta-blockers with membrane-stabilizing activity, such as propranolol and alprenolol. The decrease of plasma T3, however, appears responsible for some of the metabolic responses to beta-blockers.

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Section: Clinical Response In Hyperthyroidismmentioning

confidence: 99%

“…'50' 44 27,36,42b aISA, intrinsic sympathicomimetic activity; MSA, membrane-stabilizing activity. bA decrease of plasma T3 was observed in studies 37 and 42.…”

Section: Clinical Response In Hyperthyroidismmentioning

confidence: 99%

Propranolol and Thyroid Hormone Metabolism

Wiersinga

1991

Thyroid

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“…I roidism, and diabetes mellitus (1)(2)(3)(4)(5)(6)(7)(8). Plasma ketone levels are regulated both by hepatic ketogenesis and by peripheral clearance of ketone bodies.…”

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confidence: 99%

Uptake of Ketone Bodies in Perfused Hindquarter and Kidney of Starved, Thyrotoxic, and Diabetic Rats

Ikeda

Ishimura

Terasawa

et al. 1993

Experimental Biology and Medicine

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To elucidate the peripheral disposal of ketone bodies in hyperketonemia accompanied with starvation, hyperthyroidism, or diabetes mellitus, the uptake of acetoacetic acid (AcAc) and beta-hydroxybutyrate (BOHB) was investigated in the perfused hindquarter and kidney of starved, thyrotoxic, and diabetic rats. Thyrotoxicity was induced by daily subcutaneous injection of thyroxine (100 micrograms/kg/day) for 7 days, and diabetes mellitus was induced by intraperitoneal streptozotocin (50 mg/kg) injection. Plasma concentration of AcAc and BOHB was significantly higher in starved, thyrotoxic, and diabetic rats than in controls. The hindquarter or kidney of rats was perfused with synthetic medium containing 0.2 or 1.5 mM AcAc or BOHB for 30 min at a flow rate of 0.5 ml/g muscle wt/min or 3.2-3.5 ml/kidney/min, respectively. In perfused hindquarter, the uptake of AcAc and BOHB was significantly reduced in starved and diabetic rats, but not in thyrotoxic rats. In perfused kidney, the uptake of AcAc and BOHB was not significantly different between the experimental and control rats. These results suggest that in starvation or diabetes mellitus, disposal of AcAc and BOHB was impaired in the hindquarter but not in the kidney, and that disposal of AcAc and BOHB by hindquarter and kidney was not impaired in thyrotoxic rats.

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