Role of extrathyroidal TSHR expression in adipocyte differentiation and its association with obesity

Lu, Sumei; Guan, Qingbo; Liu, Yuantao; Wang, Haibo; Xu, Wei; Li, Xia; Fu, Yue; Gao, Ling; Zhao, Jiajun; Wang, Xiangdong

doi:10.1186/1476-511x-11-17

Cited by 96 publications

(96 citation statements)

References 24 publications

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“…Previous studies have confirmed that there might be a direct effect of TSH in the adipose tissue via adipocyte TSH receptors (TSHr) [34, 35] independently of its effect on thyroid function. Previously, TSH acting on TSHr has been shown to be involved in regulating lipolysis in neonates [36], inducing adipogenesis in mouse embryonic stem cells [37], directly stimulating leptin secretion in human adipose tissue [38], and inducing differentiation of preadipocytes [39], supporting the hypothesis that there is a relationship between adipose tissue and TSH. In theory, the regulation of thyroid function could be impaired due to a reduction of TSHr in the adipose tissue of obese individuals.…”

Section: Discussionmentioning

confidence: 81%

Thyroid-Stimulating Hormone, Degree of Obesity, and Metabolic Risk Markers in a Cohort of Swedish Children with Obesity

et al. 2017

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Background/Aims: Thyroid-stimulating hormone (TSH) is affected in obesity and might influence metabolic risk. It is unclear what mechanisms cause elevated TSH in obesity. We aimed to investigate TSH status within the normal range and the association of TSH with degree of obesity and metabolic parameters in children with obesity. Methods: A total of 3,459 children, aged 3.0–17.9 years, were identified in the Swedish Childhood Obesity Treatment Registry, BORIS. Age, gender, TSH, free triiodothyronine (fT3), free thyroxine (fT4), body mass index standard deviation scores (BMI SDS), as well as variables of lipid and glucose metabolism were examined. Results: Children with high-normal TSH (>3.0 mU/L) (28.8%) had higher BMI SDS compared to children with low-normal TSH (<3.0 mU/L) (p < 0.001). Multivariable regression analysis adjusted for age and gender showed that TSH levels were associated with BMI SDS (β: 0.21, 95% CI: 0.14–0.28, p < 0.001). Associations of thyroid hormones with markers of lipid and glucose metabolism were observed, where TSH was associated with fasting insulin, HOMA (homeostatic model assessment of insulin resistance), total cholesterol, and triglycerides. Conclusions: A positive association between TSH levels and BMI SDS was seen in children with obesity. Associations of TSH and free thyroid hormones with glucose metabolism indicated that TSH might be one of several factors acting to determine body weight and obesity co-morbidities, although the underlying mechanism remains unclear.

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Section: Discussionmentioning

confidence: 81%

Thyroid-Stimulating Hormone, Degree of Obesity, and Metabolic Risk Markers in a Cohort of Swedish Children with Obesity

et al. 2017

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“…WAT cells were isolated from the inguinal pads of adult mice by collagenase treatment and stained with BODIPY neutral lipid probe and Alexa fluor 647-labeled antibody to Tshr; Tshr was used as a cell surface marker of adipogenesis, since its expression increases during adipogenesis (18,31).…”

Section: Resultsmentioning

confidence: 99%

Heritability of fat accumulation in white adipocytes

Katz

Geras‐Raaka

Gershengorn

2014

American Journal of Physiology-Endocrinology and Metabolism

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Since individual cells from freshly isolated white adipose tissue (WAT) exhibit variable levels of fat accumulation, we attempted to determine which factor(s) cause this variation. We used primary WAT cells from adult mice and the mouse 3T3-L1 cell-line of preadipocytes for these studies. Cells were labeled with BODIPY (boron-dipyrromethene) lipid probe, a marker for fat accumulation in live cells, and sorted on a fluorescence-activated cell sorter into two populations exhibiting low or high BODIPY fluorescence intensity. After more than 12 doublings as dedifferentiated cells in growth medium, the sorted populations were exposed to adipogenic medium for 7 days and analyzed for BODIPY accumulation and mRNA expression of adipogenic markers. WAT-derived cells initially sorted to have low or high BODIPY fluorescence intensity maintained a similar low or high lipid phenotype after redifferentiation. Cell surface TSH receptor expression, which is known to increase when preadipocytes are differentiated, correlated with BODIPY staining in all states. mRNA levels of Pparγ, Srebp1c, aP2, and Pref1, key regulators of adipogenesis, and leptin, Glut4, Fasn, and Tshr, markers of adipocyte differentiation, correlated with the levels of fat accumulation. Overexpression of Pparγ in 3T3-L1 cells, as expected, caused cells from low- and high-BODIPY populations to accumulate more fat. More importantly, prior to differentiation, the endogenous Pparγ promoter exhibited higher levels of acetylated histone H3, an activatory modification, in high-BODIPY- compared with low-BODIPY-derived populations. We conclude that fat accumulation is a heritable trait in WAT and that epigenetic modification on the Pparγ promoter contributes to this heritability.

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“…In subjects with higher TSH, different processes in adipose tissue such as adipogenesis, lipogenesis, and lipolysis could be perturbed. Thyrotropin stimulates adipogenesis by activation of preadipocyte differentiation, and increases adipocyte hypertrophy by triglycerides synthesis in mature adipocytes via TSHR expressed in adipose tissue [25]. This might explain the pathogenesis of accumulation of visceral adipose tissue mass in subclinical hypothyroid women.…”

Section: Prace Oryginalnementioning

confidence: 99%

Powiązania między zespołem metabolicznym, subkliniczną niedoczynnością i autoimmunologicznym zapaleniem tarczycy u kobiet po menopauzie oraz rola interleukiny-6

Siemińśka

Wojciechowska

Walczak

et al. 2015

Endokrynologia Polska

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Introduction: The prevalence of metabolic syndrome increases after menopause; however, the role of concomitant subclinical hypothyroidism has not been completely elucidated. The aim of the study was to identify associations between thyrotropin, immune status, inflammation, and metabolic syndrome in postmenopausal women. The specific goals were: to assess thyrotropin (TSH) and interleukin-6 (IL-6) concentrations in the serum of subclinical hypothyroid postmenopausal women with and without metabolic syndrome and compare them with euthyroid controls; to test whether immune status is related to metabolic syndrome in postmenopausal women and determine the role of IL-6; to examine the relationships between TSH and different features of metabolic syndrome: insulin resistance, waist circumferences, waist-to-hip ratio (WHR), BMI, metabolic parameters (triglycerides, total cholesterol and high-density lipoprotein cholesterol), and inflammatory cytokines (IL-6). Material and methods: Three hundred and seventy-two postmenopausal women were included in the study: 114 women had subclinical hypothyroidism (10.0 uIU/mL > TSH ≥ 4.5 uIU/mL, normal fT4), and 258 women were in euthyreosis (TSH 0.35-4.5 uIU/mL, normal fT4); both groups were matched by age. Anthropometric measurements were conducted (BMI, waist circumference, WHR) and blood pressure was measured. In all subjects the following were assessed in serum: lipid profile, glucose, insulin, TSH, fT4, thyroid antibodies (T-Abs) -TPO-Abs, TG-Abs, and IL-6 concentrations. Results: The prevalence of metabolic syndrome was 49.12% in subclinical hypothyroid women and 46.89% in euthyroid women. However, the proportion of subjects with one or two abnormalities was significantly higher in the subclinical hypothyroid group (45.61%) than in the euthyroid group (32.17%). When we compared subclinical hypothyroid women with and without metabolic syndrome, subjects with metabolic syndrome had higher BMI, abdominal circumferences, WHR, and HOMA-I. They presented higher systolic and diastolic blood pressure. Serum concentrations of cholesterol, triglycerides, fasting glucose, IL-6, TSH, T-Abs were also higher and serum cHDL was lower. There were no significant differences in fT4 concentrations. A similar comparison was made for euthyroid women with and without metabolic syndrome. Higher BMI, waist circumference, WHR, HOMA-I, and systolic blood pressure were observed in subjects with metabolic syndrome. Serum concentrations of TSH, triglycerides, glucose, and IL-6 were also higher, but the concentration of cHDL was significantly lower. There were no significant differences in fT4, T-Abs, cholesterol levels, and diastolic pressure. When we compared euthyroid women T-Abs (+) and T-Abs (-), the prevalence of metabolic syndrome was similar (48.68% vs. 46.15%). There were no differences in BMI, waist circumference, WHR, lipid profile, glucose, and HOMA-I, fT4. However, thyroid autoimmunity was associated with elevated TSH and IL-6 levels. When we analysed subclinical hypothyroid women with ...

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Role of extrathyroidal TSHR expression in adipocyte differentiation and its association with obesity

Cited by 96 publications

References 24 publications

Thyroid-Stimulating Hormone, Degree of Obesity, and Metabolic Risk Markers in a Cohort of Swedish Children with Obesity

Thyroid-Stimulating Hormone, Degree of Obesity, and Metabolic Risk Markers in a Cohort of Swedish Children with Obesity

Heritability of fat accumulation in white adipocytes

Powiązania między zespołem metabolicznym, subkliniczną niedoczynnością i autoimmunologicznym zapaleniem tarczycy u kobiet po menopauzie oraz rola interleukiny-6

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