Lipid metabolism thyroid hormone effect

Metabolic Effects. Thyroid hormones affect energy substrate utilization in a number of ways. For instance, these hormones increase intestinal glucose absorption and increase the activity of several enzymes involved in carbohydrate metabolism. Thyroid hormones enhance lipolysis by increasing the response of fat cells to other lipolytic hormones. In general, these and other metabolic effects help to increase the availability of glucose and lipids for increased cellular activity. 

Thyroid hormone effects on metabolism arc diverse. The rates of protein and carbohydrate synthesis and catabolism are inlluenced. An example of the effect of thyroid hormones on lipid metabolism is the observation of a high serum cholesterol in some hypothyroid patients. This is a consequence of a reduction in cholesterol metabolism due to down regulation of low-density lipoprotein (LDL) receptors on liver cell membranes, with a subsequent failure of sterol excretion via the gut. 

Triiodothyronine (3, 5,3-L-triiodothyronine, T3) is a thyroid hormone. It is producedby outer ring deiodination of thyroxine (T4) in peripheral tissues. The biologic activity of T3 is 3-8 times higher than that of T4. T3 is 99.7% protein-bound and is effective in its free non-protein-bound form. The half-life of triiodothyronine is about 19 h. The daily tur nover of T3 is 75%. Triiodothyronine acts via nuclear receptor binding with subsequent induction of protein synthesis. Effects of thyroid hormones are apparent in almost all organ systems. They include effects on the basal metabolic rate and the metabolisms of proteins, lipids and carbohydrates. 

Thyroid hormone has multiple effects on the cardiovascular system with various physiological consequences. Several genes that encode important regulatory and structural proteins in the heart have been shown to be thyroid hormone responsive. Thyroid hormone increases cardiac contractility, induces vasorelaxation and angiogenesis, prevents fibrosis and has favorable effects on lipid metabolism (reviewed by Pantos73). 

Thyroid hormone decreases hepatic hpase activity [14] deficiency of thyroid hormone does not result in significant effects on HDL levels, however. Individuals wifh hypothyroidism have either unchanged or slightly elevated HDL levels [15]. It is possible fhat EL expression in the thyroid is regulated by thyroid hormone or that EL is involved in thyroid lipid metabolism. 

Thyroid hormones at the levels present in hyperthyroidism are catabolic they lead to the mobilization of tissue protein and, especially, of muscle tissue protein for gluconeogenetic processes (20). Thus, the depletion of liver glycogen, the increased breakdown of lipids, and the negative nitrogen balance observed in hyperthyroidism represent toxic effects. The metabolic processes of hypermetabolism are wasteful. In hyperthyroidism, a smaller-than-normal amount of liberated energy is available for useful work, and an excessive amount is wasted as heat. 

Thyroid hormones act on tissues all over the body and have far-reaching effects on energy metabolism, turnover of proteins, lipids and carbohydrates and consequently growth. Thyroid deficiency in early childhood, if untreated, leads to stunted growth and poor development of the nervous system. Such individuals are termed cretins. This is a word that has unfortunately passed into common usage as a term of abuse but refers to a specific clinical condition brought about by endocrine insufficiency. 

Thyroid hormones have long been known to affect lipid metabolism. Thyroxine undoubtedly controls cholesterol metabolism serum cholesterol levels are markedly increased in hypothyroidism and decreased in hyperthyroidism. There are various ways by which thyroxine could cause cholesterol to accumulate in blood direct stimulation of the pathway involved in cholesterol biosynthesis block of cholesterol use for further biosynthesis indirect stimulation of cholesterol synthesis by acceleration of pathways that provide precursors of coenzymes needed for cholesterol synthesis and indirect stimulation of cholesterol synthesis by blocking pathways that use those precursors involved in cholesterol synthesis. The exact mechanism by which thyroxine induces the accumulation of cholesterol in serum needs to be elucidated. The effect of thyroid hormones on blood cholesterol must be understood because hypothyroidism is known to enhance the development of experimental arteriosclerosis in animals. 

Thyroid hormones are active by reducing abnormal serum lipid concentrations with the greatest effect on cholesterol-rich low-density lipoproteins with much less effect on TG-rich very low-density lipoproteins. Use of thyroid hormones in patients with ischaemic heart disease should be cautious as their action stimulates tissue oxygen consumption. However, with D-thyroxine a good dissociation of the calori-genic effect from the action on cholesterol metabolism has been obtained. 

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