1965EndocrinologyRequires access

Effect of Triamcinolone Administration on Corticosteroid Metabolism in the Liver

Alexander Blair, T Uete

Open publisher page 9 citations

Abstract

Despite evidence that thyroidal activity, gonadal hormones and food intake can modify steroidal metabolism in the liver, the regulatory mechanisms involved are not clear. These studies suggest that a modification of energy metabolism can influence the corticosteroid metabolism. Corticosteroids, through their stimulation of hepatic carbohydrate synthesis, can modify energy metabolism. Therefore, the influence of corticosteroids upon the Δ4-3-ketosteroid reductase activity in the liver has been investigated in male rats and hamsters. Cortisol 1,2-3H was incubated with liver slices from animals treated with triamcinolone and from untreated controls. In the intact and adrenalectomized animals, treatment caused an elevation in both the steroid reducing capacity and the glycogen content. Similarly, feeding increased the reduction of cortisol in both intact and adrenalectomized animals. Thus, this increased rate of reduction of corticosteroids in the liver caused by the administration of triamcinolone could be secondarily due to changes in energy metabolism, which are induced by adrenal cortical hormones, rather than primarily due to stimulation of Δ4-3- ketosteroid reductase activity. Conceivably, increased levels of corticosteroids in the blood could cause an increased rate of their own inactivation by the liver, suggesting a hepatic autoregulatory mechanism for adrenocortical hormones. (Endocrinology76: 52, 1965)

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What this paper is about

Despite evidence that thyroidal activity, gonadal hormones and food intake can modify steroidal metabolism in the liver, the regulatory mechanisms involved are not clear. These studies suggest that a modification of energy metabolism can influence the corticosteroid metabolism. Corticosteroids, through their stimulation of hepatic carbohydrate synthesis, can modify energy metabolism. Therefore, the influence of corticosteroids upon the Δ4-3-ketosteroid reductase activity in the liver has been investigated in male rats and hamsters. Cortisol 1,2-3H was incubated with liver slices from animals treated with triamcinolone and from untreated controls. In the intact and adrenalectomized animals, treatment caused an elevation in both the steroid reducing capacity and the glycogen content. Similarly, feeding increased the reduction of cortisol in both intact and adrenalectomized animals. Thus, this increased rate of reduction of corticosteroids in the liver caused by the administration of triamcinolone could be secondarily due to changes in energy metabolism, which are induced by adrenal cortical hormones, rather than primarily due to stimulation of Δ4-3- ketosteroid reductase activity. Conceivably, increased levels of corticosteroids in the blood could cause an increased rate of their own inactivation by the liver, suggesting a hepatic autoregulatory mechanism for adrenocortical hormones. (Endocrinology76: 52, 1965)

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Available abstract

Despite evidence that thyroidal activity, gonadal hormones and food intake can modify steroidal metabolism in the liver, the regulatory mechanisms involved are not clear. These studies suggest that a modification of energy metabolism can influence the corticosteroid metabolism. Corticosteroids, through their stimulation of hepatic carbohydrate synthesis, can modify energy metabolism. Therefore, the influence of corticosteroids upon the Δ4-3-ketosteroid reductase activity in the liver has been investigated in male rats and hamsters. Cortisol 1,2-3H was incubated with liver slices from animals treated with triamcinolone and from untreated controls. In the intact and adrenalectomized animals, treatment caused an elevation in both the steroid reducing capacity and the glycogen content. Similarly, feeding increased the reduction of cortisol in both intact and adrenalectomized animals. Thus, this increased rate of reduction of corticosteroids in the liver caused by the administration of triamcinolone could be secondarily due to changes in energy metabolism, which are induced by adrenal cortical hormones, rather than primarily due to stimulation of Δ4-3- ketosteroid reductase activity. Conceivably, increased levels of corticosteroids in the blood could cause an increased rate of their own inactivation by the liver, suggesting a hepatic autoregulatory mechanism for adrenocortical hormones. (Endocrinology76: 52, 1965)

Key concepts: Endocrinology, Internal medicine, Triamcinolone acetonide, Hormone, Metabolism, Corticosteroid, Stimulation, Glycogenolysis

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