There exists a complex relationship between liver and thyroid hormones. Liver plays an important role in the activation, inactivation, transportation, and metabolism of thyroid hormones. At the same time, thyroid hormones also affect hepatocytes activity and liver metabolism, such as lipid and bilirubin metabolism. Importantly, thyroid hormone levels often change abnormally in patients with liver cirrhosis. Therefore, studying the change of thyroid hormone levels in patients with liver cirrhosis has a certain clinical value for assessing the severity, prognosis, diagnosis and treatment. This paper reviews the research progress on the relationship between liver cirrhosis and thyroid hormone.
Bilirubin ; Humans ; Liver/metabolism* ; Liver Cirrhosis/metabolism* ; Thyroid Hormones/metabolism*

Gastrins ; metabolism ; Gonadal Steroid Hormones ; metabolism ; Growth Hormone ; metabolism ; Hormones ; metabolism ; Humans ; Liver Diseases ; metabolism ; Thyroid Hormones ; metabolism

Thyroglobulin is the most important and abundant protein in thyroid follicles and has been widely studied as a tumor marker of thyroid cancer recurrence and persistence. Tg is considered the material basis of thyroid hormone synthesis and does not participate in the regulation of thyroid hormone synthesis and secretion. This review summarizes the recent progress in the research of thyroid hormone synthesis and secretion regulation via a negative feedback regulation mechanism by the thyroid-hypothalamus-pituitary axis. Thyroglobulin can negatively regulate the synthesis of thyroid hormone by thyroid follicular cells and antagonize the positive regulation of thyrotropin TSH. The function of thyroid follicular cells is presumably a result of Tg and TSH interaction, and a follicular cycle model is proposed to explain the causes of follicular heterogeneity in glands. We also discuss the prospects and clinical significance of studies into the negative feedback regulation mechanism of the thyroid-hypothalamus-pituitary axis and compare two theories for this mechanism.
Feedback, Physiological ; Humans ; Hypothalamo-Hypophyseal System ; physiology ; Neoplasm Recurrence, Local ; Thyroglobulin ; metabolism ; Thyroid Gland ; physiology ; Thyroid Hormones ; metabolism ; Thyrotropin ; metabolism

Thyroid hormone plays pivotal roles in growth, differentiation, development and metabolic homeostasis via thyroid hormone receptors (TRs) by controlling the expression of TR target genes. The transcriptional activity of TRs is modulated by multiple factors including various TR isoforms, diverse thyroid hormone response elements, different heterodimeric partners, coregulators, and the cellular location of TRs. In the present review, we summarize recent advance in understanding the molecular mechanisms of thyroid hormone action obtained from human subject research, thyroid hormone mimetics application, TR isoform-specific knock-in mouse models, and mitochondrion study with highlights in metabolic regulations. Finally, as future perspectives, we share our thoughts about current challenges and possible approaches to promote our knowledge of thyroid hormone action in metabolism.
Animals ; Gene Knockout Techniques ; Humans ; Mice ; Mitochondria ; metabolism ; Protein Isoforms ; genetics ; metabolism ; physiology ; Receptors, Thyroid Hormone ; metabolism ; Thyroid Diseases ; metabolism ; pathology ; Thyroid Hormones ; genetics ; metabolism ; physiology

The changes of thyroid hormones are expected in patients with chronic renal failure(CRF) because the kidney plays an important role in metabolism and excretion of thyroid hormones. In spite of many studies about this issue, there have not been full consensus about the nature and mechanism of thyroid hormone changes. We undertook the present study to reveal the dialysis effects on these hormones. We measured basal levels of serum total T3 (T3), total T4(T4), free T4(FT4), reverse T3(rT3) and TSH, and then calculated the ratio of T3/T4, rT3/T3 and rT3/T4. The following groups were identifed : Group I-10 cases of normal controls, Group II-18 cases of pre-dialysis or treated conservatively, Group III-20 cases treated by maintenance hemodialysis(HD), Group IV-18 cases treated by continuous ambulatory peritoneal dialysis(CAPD). Patients from group II, III and IV revealed significantly decreased levels of T3 and T4, and increased ratio of rT3/T4 in comparison to the control group(P<0.05). Especially, CAPD group revealed significantly increased levels of T4 and FT4 in comparison to HD group(P<0.05). In the long-term dialysis group(>36months), the mean concentrations of free T4 levels revealed signifcantly decreased in comparison to the short-term dialysis group(P<0.05). Thyroid dysfunction are observed in CRF patients with partial recovery after dialysis therapy. Especially, CAPD achieves significantly improved thyroid dysfunction compared to HD, but further study would be necessary.
Consensus ; Dialysis ; Humans ; Kidney ; Kidney Failure, Chronic* ; Metabolism ; Peritoneal Dialysis* ; Peritoneal Dialysis, Continuous Ambulatory ; Renal Dialysis* ; Thyroid Gland* ; Thyroid Hormones

BACKGROUND: The purpose of this prospective study is to define the effect of cardiopulmonary bypass (CPB) on the concentration of thyroid hormones and metabolites. METHODS: Blood samples were obtained from 15 patients undergoing open heart surgery at 1) pre-induction, 2) after heparinization, 3) during CPB, 4) 2 hours after CPB, 5) 24 hours after CPB and 6) 48 hours after CPB. Thyroid stimulating hormone, albumin, thyroxine (T4), free thyroxine (FT4), triiodothyronine (T3), free triiodothyronine (FT3) and reverse T3 (T3) were measured. RESULTS: Concentration of T3 significantly decreased after infusion of heparin and maintained at the decreased level until postbypass 24 hours. Concentration of FT3 significantly increased after heparin administration but maintained at a control level during CPB and decreased after postbypass 24 , 48 hours (p<0.05). Reverse T3 increased at 24 and 48 hours after CPB (p<0.05). Thyroxine decreased during CPB and return to control level after CPB. Free thyroxine did not change significantly. Thyroid stimulating hormone was significantly depressed at 24 hours after CPB (p<0.05). CONCLUSIONS: This result suggest that the thyroid function is depressed until 48 hours after CPB and it seems to be associated with abnormal metabolism of thyroid hormones.
Cardiopulmonary Bypass ; Heart* ; Heparin ; Humans ; Metabolism ; Prospective Studies ; Thoracic Surgery* ; Thyroid Gland* ; Thyroid Hormones ; Thyrotropin ; Thyroxine ; Triiodothyronine

Bone is a dynamic tissue undergoing life-long remodeling, a process of bone resorption by osteoclast and bone formation by osteoblast, regulated by diverse hormones including estrogen. Recently, several pituitary hormones have been identified as a modulator of this process. Here, we reviewed the role of thyroid stimulating hormone signaling per se in bone metabolism.
Bone Remodeling ; Bone Resorption ; Estrogens ; Metabolism* ; Osteoblasts ; Osteoclasts ; Osteogenesis ; Pituitary Hormones ; Thyroid Gland* ; Thyrotropin*

Bone is a dynamic tissue undergoing life-long remodeling, a process of bone resorption by osteoclast and bone formation by osteoblast, regulated by diverse hormones including estrogen. Recently, several pituitary hormones have been identified as a modulator of this process. Here, we reviewed the role of thyroid stimulating hormone signaling per se in bone metabolism.
Bone Remodeling ; Bone Resorption ; Estrogens ; Metabolism* ; Osteoblasts ; Osteoclasts ; Osteogenesis ; Pituitary Hormones ; Thyroid Gland* ; Thyrotropin*

BACKGROUND: Thyroid dysfunction (TD) and metabolic syndrome (MetS) are known risk factors for atherosclerotic cardiovascular disease (ASCVD). TD is risk factor for ASCVD mediated by the effects of thyroid hormones on lipid metabolism and blood pressure hence the components of MetS. It is possible that coexistence of these two disease entities and unrecognized TD in patients with MetS might substantially increase ASCVD risk. Moreover, little is known about the relationship between TD and the components of MetS. Thus, the purpose of this study was to evaluate the pattern of TD in patients with MetS and its relationship with components of the MetS. METHODS: A total of 358 previously diagnosed patients with MetS were recruited in the study. The thyroid function test parameters were measured to classify TD at Dhulikhel Hospital-Kathmandu University Hospital, Dhulikhel, Nepal. Statistical analyses were performed using SPSS version 16.0 to evaluate pattern and relationship. RESULTS: The overall prevalence of TD in patients with MetS was 31.84% with high prevalence of subclinical hypothyroidism (29.32%). We found no evidence of a relationship between TD and components of MetS, although there was significant difference in waist circumference between four groups of TD. CONCLUSION: Patients with MetS had subclinical hypothyroidism greatly. Although there was no evidence of any relationship between thyroid status and all components of MetS, TD should be taken into account when evaluating and treating patients with MetS to reduce the impending risk.
Blood Pressure ; Cardiovascular Diseases ; Humans ; Hypothyroidism ; Lipid Metabolism ; Nepal ; Prevalence ; Risk Factors ; Thyroid Function Tests ; Thyroid Gland* ; Thyroid Hormones ; Waist Circumference

OBJECTIVETo study the interaction between insulin-like growth factor binding protein-3 (IGFBP-3) and thyroid hormone receptor α1 (TRα1) and the modulatory effect of IGFBP-3 on transcription of the thyroid hormone responsive gene.

METHODSThe interaction between IGFBP-3 and TRα1 was detected with glutathione-S-transferase pull-down method, co-immunoprecipitation, fluorescence resonance energy transfer test. The cellular distribution of these two proteins was observed by confocal laser scanning microscopy. The effect of IGFBP-3 on the growth hormone promoter activity stimulated by triiodothyronine (T3) was determined by dual-luciferase reporter assay.

RESULTSIGFBP-3 interacted with TRα1 both in vivo and in vitro. IGFBP-3 and TRα1 were shown to co-localize in the nucleus of HEK-293 cells. The overexpressed IGFBP-3 inhibited the growth hormone promoter activity stimulated by T3 (P<0.01).

CONCLUSIONSIGFBP-3 interacts with TRα1 and inhibits T3 responsive gene transcription. This finding further confirms the insulin-like growth factor-independent role of IGFBP-3 in the nucleus.

HEK293 Cells ; Humans ; Insulin-Like Growth Factor Binding Protein 3 ; metabolism ; Promoter Regions, Genetic ; Thyroid Hormone Receptors alpha ; metabolism ; Thyroid Hormones ; genetics ; metabolism ; Transcription, Genetic ; Triiodothyronine ; pharmacology