Liver X receptor β: new player in the regulatory network of thyroid hormone and ‘browning’ of white fat

Miao, Yifei; Warner, Margaret; Gustafsson, Jan Åke

doi:10.1080/21623945.2016.1142634

Cited by 9 publications

(10 citation statements)

References 26 publications

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“…Depletion of LXR in mice activated thyroid stimulating hormone (TSH)-releasing hormone (TRH)-positive neurons in the hypothalamus and stimulated TSH from the pituitary gland leading to increased secretion of thyroid hormone. Also, decreased expressions of perinatal deiodinase 2 in hepatocytes greatly reduce the susceptibility to diet induced steatosis and obesity [ 16 ].…”

Section: Biology Of the Metabolic Syndromementioning

confidence: 99%

The Global Epidemic of the Metabolic Syndrome

2018

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Metabolic syndrome, variously known also as syndrome X, insulin resistance, etc., is defined by WHO as a pathologic condition characterized by abdominal obesity, insulin resistance, hypertension, and hyperlipidemia. Though there is some variation in the definition by other health care organization, the differences are minor. With the successful conquest of communicable infectious diseases in most of the world, this new non-communicable disease (NCD) has become the major health hazard of modern world. Though it started in the Western world, with the spread of the Western lifestyle across the globe, it has become now a truly global problem. The prevalence of the metabolic syndrome is often more in the urban population of some developing countries than in its Western counterparts. The two basic forces spreading this malady are the increase in consumption of high calorie-low fiber fast food and the decrease in physical activity due to mechanized transportations and sedentary form of leisure time activities. The syndrome feeds into the spread of the diseases like type 2 diabetes, coronary diseases, stroke, and other disabilities. The total cost of the malady including the cost of health care and loss of potential economic activity is in trillions. The present trend is not sustainable unless a magic cure is found (unlikely) or concerted global/governmental/societal efforts are made to change the lifestyle that is promoting it. There are certainly some elements in the causation of the metabolic syndrome that cannot be changed but many are amenable for corrections and curtailments. For example, better urban planning to encourage active lifestyle, subsidizing consumption of whole grains and possible taxing high calorie snacks, restricting media advertisement of unhealthy food, etc. Revitalizing old fashion healthier lifestyle, promoting old-fashioned foods using healthy herbs rather than oil and sugar, and educating people about choosing healthy/wholesome food over junks are among the steps that can be considered.

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Section: Biology Of the Metabolic Syndromementioning

confidence: 99%

The Global Epidemic of the Metabolic Syndrome

2018

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“…Nevertheless, LXR KO mice showed enhanced secretion of TSH, thereby stimulating THs levels. Collectively, these results provide evidence that depletion of LXRs would abrogate the TH negative feedback loop in the hypothalamus and cause a loss of TRs in the PVN area [ 136 , 137 ].…”

Section: Tr Crosstalk With Ppar and Lxr To Regulate Metabolismmentioning

confidence: 98%

“…Thus, activated LXR represses TRH levels and induces the orexigenic peptides, which may promote weight gain and obesity. In contrast, specific inactivation of LXRs enhances Trh expression in the hypothalamus [ 135 ] and induces the browning of WAT, thereby ameliorating obesity outcomes [ 136 , 137 ].…”

Section: Nuclear Receptors Integrators Of Metabolic Regulationmentioning

confidence: 99%

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Integrating Thyroid Hormone Signaling in Hypothalamic Control of Metabolism: Crosstalk Between Nuclear Receptors

Kouidhi

Clerget-Froidevaux

2018

IJMS

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The obesity epidemic is well recognized as a significant global health issue. A better understanding of the energy homeostasis mechanisms could help to identify promising anti-obesity therapeutic strategies. It is well established that the hypothalamus plays a pivotal role governing energy balance. The hypothalamus consists of tightly interconnected and specialized neurons that permit the sensing and integration of several peripheral inputs, including metabolic and hormonal signals for an appropriate physiological response. Current evidence shows that thyroid hormones (THs) constitute one of the key endocrine factors governing the regulation and the integration of metabolic homeostasis at the hypothalamic level. THs modulate numerous genes involved in the central control of metabolism, as TRH (Thyrotropin-Releasing Hormone) and MC4R (Melanocortin 4 Receptor). THs act through their interaction with thyroid hormone receptors (TRs). Interestingly, TH signaling, especially regarding metabolic regulations, involves TRs crosstalk with other metabolically linked nuclear receptors (NRs) including PPAR (Peroxisome proliferator-activated receptor) and LXR (Liver X receptor). In this review, we will summarize current knowledge on the important role of THs integration of metabolic pathways in the central regulation of metabolism. Particularly, we will shed light on the crosstalk between TRs and other NRs in controlling energy homeostasis. This could be an important track for the development of attractive therapeutic compounds.

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“…In particular, LXR β suppressed the induction of the BAT phenotype in subcutaneous WAT in male rodents fed a normal diet. Depletion of LXRs activates release of thyroid-stimulating hormone (TSH) from the pituitary which, after a number of signal transduction events, is thought to lead to the browning of WAT [60]. The secretory product C-terminal fragment of Slit2, a member of the Slit extracellular protein family, acts via Prdm16 in order to regulate beige adipocyte induction.…”

Section: Transgenic Models Of Browningmentioning

confidence: 99%

Novel Browning Agents, Mechanisms, and Therapeutic Potentials of Brown Adipose Tissue

Wankhade

Shen

Yadav

et al. 2016

BioMed Research International

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Nonshivering thermogenesis is the process of biological heat production in mammals and is primarily mediated by brown adipose tissue (BAT). Through ubiquitous expression of uncoupling protein 1 (Ucp1) on the mitochondrial inner membrane, BAT displays uncoupling of fuel combustion and ATP production in order to dissipate energy as heat. Because of its crucial role in regulating energy homeostasis, ongoing exploration of BAT has emphasized its therapeutic potential in addressing the global epidemics of obesity and diabetes. The recent appreciation that adult humans possess functional BAT strengthens this prospect. Furthermore, it has been identified that there are both classical brown adipocytes residing in dedicated BAT depots and “beige” adipocytes residing in white adipose tissue depots that can acquire BAT-like characteristics in response to environmental cues. This review aims to provide a brief overview of BAT research and summarize recent findings concerning the physiological, cellular, and developmental characteristics of brown adipocytes. In addition, some key genetic, molecular, and pharmacologic targets of BAT/Beige cells that have been reported to have therapeutic potential to combat obesity will be discussed.

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Liver X receptor β: new player in the regulatory network of thyroid hormone and ‘browning’ of white fat

Cited by 9 publications

References 26 publications

The Global Epidemic of the Metabolic Syndrome

The Global Epidemic of the Metabolic Syndrome

Integrating Thyroid Hormone Signaling in Hypothalamic Control of Metabolism: Crosstalk Between Nuclear Receptors

Novel Browning Agents, Mechanisms, and Therapeutic Potentials of Brown Adipose Tissue

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