Effect of endocrine factors on cholesterol turnover in young and old rats

Hruza, Z

doi:10.1016/0531-5565(71)90031-3

Cited by 17 publications

(3 citation statements)

References 9 publications

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“…In addition, hormone replacement therapy in hypothyroid patients quadruples the receptor-mediated FCR for LDL in vivo (8). Since the major lipid component of LDL is cholesterol, it is probable that thyroid-stimulated, receptor-mediated uptake of LDL contributes to the high turnover of cholesterol seen in T 3 -treated rats (127), consistent with the slow clearance of cholesterol from the plasma of hypothyroid rats (122). The LDL cholesterol drops to near-normal levels in hypothyroid patients (128) and PTU-treated rats (18) when T 4 is administered.…”

Section: Lipoprotein and Apolipoprotein Metabolismmentioning

confidence: 97%

Plasma Lipoproteins and Regulation of Hepatic Metabolism of Fatty Acids in Altered Thyroid States*

1985

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This article reviews our understanding of effects of thyroid hormone excess and deficiency on hepatic metabolism of FFA, and consequent effects on production, secretion, and metabolism of plasma lipoproteins. In the hyperthyroid state the following alterations are observed. Fatty acid oxidation and ketogenesis are stimulated simultaneously with a paradoxical stimulation of fatty acid synthesis, which may be linked by virtue of a blunted response of mitochondrial carnitine palmitoyltransferase I (CPT-I) to malonyl coenzyme A (CoA). Esterification of fatty acid to triglyceride (TG) is reduced, as is the secretion of the very low density lipoprotein (VLDL) (including VLDL TG, cholesterol, and apoprotein); this may be due, in part, to decreased concentrations of glycerol-3-phosphate (G3P) in the hepatic cell. In the intact animal or patient, however, serum TG concentration is variable, which may reflect increased adipose tissue lipolysis and elevated concentrations of plasma FFA, which would tend to drive VLDL secretion by the liver. Clearance of the VLDL and its metabolic product, the low density lipoprotein (LDL), is increased, resulting in decreased plasma total and LDL cholesterol. Although high density lipoprotein (HDL) cholesterol may also be reduced, the ratio of LDL/HDL cholesterol is further decreased. The regulatory role of the lipoprotein apoproteins is less clear, but hepatic apolipoprotein (apo) B secretion (required for VLDL) is diminished, while apo-AI secretion (required for HDL) is stimulated, perhaps both reflecting rates of synthesis. Plasma concentrations of apo-AI are variable, dependent on relative rates of secretion and clearance. In the hypothyroid, many of these effects are reversed, which results in hyperlipoproteinemias and greater risk for the development of atherosclerotic cardiovascular disease.

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Section: Lipoprotein and Apolipoprotein Metabolismmentioning

confidence: 97%

Plasma Lipoproteins and Regulation of Hepatic Metabolism of Fatty Acids in Altered Thyroid States*

1985

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“…It may be that a lack of GH in the hypophysectomized rats accounted for the decreased turnover in the old animals (Hruza, 1971b).…”

Section: The Precise Mechanisms By Which Dietary Manipulations and Almentioning

confidence: 99%

“…A possible factor in the age related slowing of lipid metabolism is decreased thyroid secretion rate in old animals (Grad and Hoffman, 1955). The sensitivity of cholesterol metabolism to thyroxine is also decreased in old amimais (Hruza, 1971b).…”

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confidence: 99%