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  • ISSN: 2333-6692
    Special Issue on Role of Thyroid Hormone in Metabolic Homeostasis
    Yan-Yun Liu
    Molecular Endocrinology Laboratory
    Department of Medicine
    David Geffen School of Medicine
    University of California
    Review Article
    Stephen Ayers* and Paul Web
    Abstract: Thyroid hormones are central regulators of lipid metabolism and energy homeostasis, which primarily act through Thyroid Hormone Receptors (TRs). Selective Thyroid Hormone Receptor Modulators (STRMs) are chemical analogues of thyroid hormone, designed to preferentially induce beneficial actions of thyroid hormone through specificity for TRβ (isoform specificity) and specific accumulation in liver (tissue selectivity). Although initial results from studies of TH analogs that combine TRβ and tissue selectivity were promising, producing impressive reductions of serum LDLC and triglycerides in animal models and human patients, none of these compounds has progressed beyond the early clinical stage so far. While recent human trials of STRMs have consistently produced impressive improvements in serum lipid parameters, they have also revealed unexpected side effects. Although STRMs have the potential to serve as treatments for hyperlipidemia, these developments make their widespread use in the future highly uncertain.
    Ting Jin and Xiaochun Teng*
    Abstract: Thyroid hormone plays an important role in the regulation of lipid metabolism. It acts predominantly through its nuclear receptors (thyroid hormone receptor á and â) to regulate the gene expression related to lipid metabolism. Both overt hypothyroidism and hyperthyroidism results in abnormalities of lipid profile. However, changes in serum lipid profiles in patients with subclinical hypothyroidism have been inconsistent. In recent years, thyroid receptor â1-selective analogue represents a new class of hypolipidemic compound have been developed. Some of these T3 analogues are very potent in lowering serum cholesterol and triglyceride in animal models and human clinical studies. This mini review will focuses on the mechanisms that affect lipid profile under pathological thyroid conditions, and give brief touch on thyroid analogues.
    Michael L Goodson1* and Brenda J Mengeling2
    Abstract: Thyroid hormone, acting through thyroid hormone receptors is a key regulator of metabolic homeostasis. Repression of transcription is critical component of thyroid hormone signaling and is mediated through the association of corepressor proteins with thyroid hormone receptors. In this review we will discuss recent results elucidating multiple roles for corepressors in mediating thyroid hormones regulation of metabolism.
    Jang-Won Lee1, Nam-Ho Kim1 and Anna Milanesi2*
    Abstract: Skeletal muscle is a plastic organ made by highly specialize fibers with specific and different structure, function and metabolism. Skeletal muscle fibers can adapt, change, recover/regenerate after injury in response to various stimulators including hormones. Thyroid hormones are important players in the homeostasis of several tissue including skeletal muscle and their genomic action mostly depend on the tissue T3 bioavailability and on the distribution of the thyroid receptor isoforms which act as transcription factors and are modulated by T3. Changing in contractile and metabolic proprieties of the muscle fibers has been described in experimental models of hyper and hypothyroidism. Animal models with disruption of thyroid hormone signaling showed different and specific skeletal muscle phenotypes. By focusing on thyroid hormone signaling in skeletal muscle homeostasis, we review T3 specific action on skeletal muscle development, postnatal growth, function and metabolism.
    Ines Donangelo1,2*
    Abstract: Thyroid Hormone (TH) regulates energy balance, lipid metabolism and cardiovascular function. These effects are largely due direct action of TH on peripheral target tissues. However, there is increasing evidence for a direct central action of TH modulating metabolic processes, including regulation of thermogenesis, food intake, hepatic glucose metabolism and cardiovascular tone through direct action in the brain. Here, we review the current understanding of mechanisms including key hypothalamic signaling involved in central TH regulation of energy balance and metabolism.
    Miriam Oliveira Ribeiro*
    Abstract: The amount of energy in the body is highly regulated. The hypothalamus is a key neural structure involved in this process, keeping the intake of food in step with the energy expenditure. The main hypothalamic nuclei involved in energetic metabolism regulation are the arcuate, periventricular, dorsomedial and ventromedial that integrates several peripheral signals, such as leptin and adiponectin. Although is well known that T3 regulates basal metabolism, it also has an important role in feeding behavior regulation since it stimulates neurons that express orexigenic neuropeptides, such as AgRP and NPY found in the arcuate hypothalamic nuclei. The amount of T3 available in the brain depends on the activity of the type 2 deiodinase (D2) that transforms T4 in T3. D2 is expressed in glial cells that are in close contact with the AgRP/NPY expressing neurons in the arcuate hypothalamic nuclei, suggesting that D2 has an important role in the regulation of the feeding behavior and in the body weight.
    Kristin Lichti-Kaiser, Gary ZeRuth, and Anton M Jetten*
    Abstract: Congenital Hypothyroidism (CH) is the most frequent endocrine disorder in neonates. While several genetic mutations have been identified that result in developmental defects of the thyroid gland or thyroid hormone synthesis, genetic factors have yet to be identified in many CH patients along with the mechanisms underlying their pathophysiology. Mutations in the gene encoding the Krüppel-like transcription factor, GLI-similar 3 (GLIS3) have been associated with the development of a syndrome characterized by congenital hypothyroidism and neonatal diabetes and similar phenotypes were observed in mouse knockout models of Glis3. Patients with GLIS3-mediated CH exhibit diminished serum levels of thyroxine (T4) and triiodothyronine (T3) and elevated Thyroid Stimulating Hormone (TSH) and thyroglobulin (TG). However, the inconsistent presentation of clinical features associated with this CH has made it difficult to ascertain a causative mechanism. Future elucidation of the biological functions of GLIS3 in the thyroid will be crucial to the discovery of new therapeutic opportunities for the treatment of CH.
    Xuan Yao1,2, Hongfeng Xia1,2, Yu-cheng Wang2,3 and Hao Ying1,2*
    Abstract: It has been known for a long time that thyroid hormone regulates metabolism. Thyroid hormone action is primarily mediated by Thyroid Hormone Receptors (TRs). The transcriptional regulation by TRs is modulated by coregulators including coactivators and corepressors. Emerging evidence suggested that coregulators are critical for metabolic regulation mediated by TR. This review describes recent in vivo findings that improve our understanding of the roles of coregulators and provides an alternative way to enhance our knowledge on TR-mediated metabolic regulation. In order to delineate the complex mechanisms involved, we compare the results obtained from the researches employing different lines of mouse genetically modified. It is found that both corepressors and coactivators are indispensible for the full function of TR. We also discuss the challenge and future direction in the research field of thyroid hormone action in metabolism.
    Mini Review
    Teresa L Mastracci* and Carmella Evans-Molina
    Abstract: A gradually expanding body of literature suggests that Thyroid Hormone (TH) and Thyroid Hormone Receptors (TRs) play a contributing role in pancreatic and islet cell development, maturation, and function. Studies using a variety of model systems capable of exploiting species-specific developmental paradigms have revealed the contribution of TH to cellular differentiation, lineage decisions, and endocrine cell specification. Moreover, in vitro and in vivo evidence suggests that TH is involved in islet β cell proliferation and maturation; however, the signaling pathway(s) connected with this function of TH/TR are not well understood. The purpose of this review is to discuss the current literature that has defined the effects of TH and TRs on pancreatic and islet cell development and function, describe the impact of hyper- and hypothyroidism on whole body metabolism, and highlight future and potential applications of TH in novel therapeutic strategies for diabetes.
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