Thyroid hormone action on intermediary metabolism

Abstract

Despite their enhanced endogenous de novo cholesterol synthesis, hyperthyroid patients exhibit decreased total and low-density lipoprotein (LDL) cholesterol levels in the serum because of a concomitant increase in LDL catabolism, cholesterol excretion by bile and a reduced enterohepatic bile acid circulation. Hypothyroidism exhibits a reduction (1) in the synthesis of cholesterol and (2) in LDL catabolism, whereas cholesterol reabsorption is unchanged or even enhanced. In addition, obese hypothyroid patients showed an increased cholesterol synthesis which is independent of thyroid hormones and which contributes to the observed LDL cholesterolaemia. Thyroid hormones per se have only a minor influence on plasma triglyceride (TG) levels, but they induce an acceleration of TG turnover and chylomicron clearance rate. In addition, the hepatic lipogenic capacity is increased in hyperthyroidism and reduced in hypothyroidism. However, hepatic total and very low-density lipoprotein (VLDL) triglyceride output is decreased by thyroid hormones due to a reduced re-esterification and a simultaneously increased oxidation of newly synthesized fatty acids. Hypothyroid livers, by contrast, reveal an increased VLDL secretion. Despite their reduced lipogenesis, obese hypothyroidism is often accompanied by a hypertriglyceridaemia type III. The simultaneous stimulation of the synthesis of fatty acids, which are still in part converted to TG, and the degradation of TG contributes to the enhanced thermogenesis in hyperthyroid patients. The concentration and turnover of free fatty acids (FFA) are increased in hyperthyroidism, resulting from a thyroid hormone-induced increase in: (1) lipolysis, explained by an increased adipose tissue sensitivity for lipolytic hormones; and (2) oxidation of fatty acids to CO2 as well as to ketone bodies (KB).(ABSTRACT TRUNCATED AT 250 WORDS)

Glucoregulatory function of glucagon in hypo-, eu- and hyperthyroid miniature pigs

“…It is obvious that hepatic glycogen content is conserved in hyperthyroid pigs (Table 3). These data are contrary to previous data obtained in hyperthyroid starved rats and dogs [2]. Since glucagon fails to increase Ra despite sufficient amounts of hepatic glycogen, it is tempting to speculate that experimental hyperthyroidism impairs glucagon-induced glycogen mobilisation.…”

“…In euthyroid pigs hepatic glycogen decreased from 220 to 25 within 24 h after food withdrawal and to 11 ymol glycosyl units/g liver wet weight (ww) within 72 h after food withdrawal. The data for fed/fasted euthyroid pigs resemble those for euthyroid rat, dog and man [2]. By contrast, in hyperthyroid pigs glycogen decreased from 211 only to 131 ymol glycosyl units/g liver ww within 24 h after food withdrawal.…”

“…We conclude that moderate experimental hyperthyroidism reduces glucagon action due to reduced glycogen mobilisation. This may in part result from increased insulin sensitivity.Key words: Insulin, glucagon, thyroid hormones, glucose turnover, glucose production, glucose utilisation, glucoregulation.Glucose intolerance is frequently seen in hyperthyroidism and may be explained by thyroid hormone-induced 1) increase in intestinal glucose absorption, 2) rise in hepatic glucose production, 3) enhanced sensitivity and/or altered response to glucagon even after glucose ingestion [1,2]. With respect to insulin we could show recently that moderate hyperthyroidism may increase hepatic as well as peripheral insulin sensitivity [3,4].…”

Soy sterols in the regulation of thyroid functions, glucose homeostasis and hepatic lipid peroxidation in mice

“…Despite these beneficial effects of soy bean, little is known on the biological effects of its sterol components (AbuMweis & Jones, 2008;Hallikainen et al, 2008). Therefore, in the present investigation an attempt was made to isolate soy sterols (a well characterized mixture of beta-sitosterol, campesterol and stigma sterol) and to reveal its therapeutic potential in the alteration of serum glucose, thyroid hormones and insulin and in the activity of hepatic glucose-6-phospatase (G-6-Pase), an important thyroid hormone dependent parameter (Andersen, Friis, & Ottesen, 1977;Larsen & Ingbar, 1992;Muller & Seitz, 1984;Sandler, Robinson, & Rabin, 1983). Simultaneously, changes in lipid peroxidation (LPO); in the activity of superoxide dismutase (SOD) and catalase (CAT), and in reduced glutathione (GSH) content were also evaluated in liver, the major target organ of a drug to ascertain the antioxidative efficacy, if any.…”

Effect of Iron, Zinc, Vitamin E and Vitamin C Supplementation on Thyroid Hormones in Rats with Hypothyroidism

“…It was clear that, PTU produced hypercholesterolemia that remarkable significant (P<0.05) increase in TC, TG, VLDL-C and LDL-C levels, compared to the normal group, however, no significant changes was observed in the mean value of HDL-C for the group treated with PTU, compared with control negative group. The most common abnormalities of lipoprotein metabolism associated with hypothyroidism are elevated levels of TC and LDL-C, which are attributable to the effect of thyroid hormone on lipoprotein lipase activity [69].…”