There is ample evidence that thyroid hormone (T3) regulates the body’s energy metabolism. Studies from rodents show that intraperitoneal or intravenous injection of T3 causes a metabolic response in all metabolically active organs such as liver, skeletal muscle, and white- and brown adipose tissue. It has recently become clear that intra-hypothalamic injection of T3 causes similar effects in peripheral organs. This central effect is achieved through stimulation of the sympathetic nervous system. In addition, stimuli such as exercise can induce the local conversion of the precursor T4 into T3 by stimulating deodinase activity. Thus, the registered metabolic effects under different physiological or pharmacologically induced conditions depend on either the amount of circulating (free) T3 to be transported into the tissues, T3 accumulating in the hypothalamus, or local T3 production. Taking this into consideration, various questions arise. It is at present unclear to what extent the effects of intraperitoneal or intravenous injection of T3 result from central stimulation through accumulation of T3 in the hypothalamus. A second question that needs to be answered is to what extent the effect of T3 can be attributed to local conversion into metabolites such as 3,5-T2 and T1AM, which have distinct actions. Techniques involving gas chromatography coupled to mass spectrometry analysis have been developed to measure serum levels of T3 and its metabolites, but little is known about the amount of these products at the tissue level. Interestingly, it has been shown that the same hormone or metabolite can exert distinct effects at the central vs peripheral level. This Research Topic aims to bring the reader up to date on the latest developments in this field.
This Research Topic aims to provide the reader with an overview of the current state-of-the-art of central versus peripheral thyroid hormone action. All interested researchers are welcome to submit original papers or review articles regarding this topic.
There is ample evidence that thyroid hormone (T3) regulates the body’s energy metabolism. Studies from rodents show that intraperitoneal or intravenous injection of T3 causes a metabolic response in all metabolically active organs such as liver, skeletal muscle, and white- and brown adipose tissue. It has recently become clear that intra-hypothalamic injection of T3 causes similar effects in peripheral organs. This central effect is achieved through stimulation of the sympathetic nervous system. In addition, stimuli such as exercise can induce the local conversion of the precursor T4 into T3 by stimulating deodinase activity. Thus, the registered metabolic effects under different physiological or pharmacologically induced conditions depend on either the amount of circulating (free) T3 to be transported into the tissues, T3 accumulating in the hypothalamus, or local T3 production. Taking this into consideration, various questions arise. It is at present unclear to what extent the effects of intraperitoneal or intravenous injection of T3 result from central stimulation through accumulation of T3 in the hypothalamus. A second question that needs to be answered is to what extent the effect of T3 can be attributed to local conversion into metabolites such as 3,5-T2 and T1AM, which have distinct actions. Techniques involving gas chromatography coupled to mass spectrometry analysis have been developed to measure serum levels of T3 and its metabolites, but little is known about the amount of these products at the tissue level. Interestingly, it has been shown that the same hormone or metabolite can exert distinct effects at the central vs peripheral level. This Research Topic aims to bring the reader up to date on the latest developments in this field.
This Research Topic aims to provide the reader with an overview of the current state-of-the-art of central versus peripheral thyroid hormone action. All interested researchers are welcome to submit original papers or review articles regarding this topic.