TSH signaling pathways that regulate MCP-1 in human differentiated adipocytes

Gagnon, AnneMarie; Langille, Melanie L.; Chaker, Seham; Antunes, Tayze T.; Durand, Jason; Sorisky, Alexander

doi:10.1016/j.metabol.2014.02.015

Cited by 36 publications

(23 citation statements)

References 41 publications

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“…It has been suggested that TSH in the upper part of the reference range may indicate an early stage of hypothyroidism [30]. TSH may promote inflammation by stimulating proinflammatory cytokines in adipose tissue [31]. Low-normal thyroid function is associated with a myriad of cardiometabolic disorders [32] that may increase the risk of mortality.…”

Section: Discussionmentioning

confidence: 99%

Prognostic value of thyroid-stimulating hormone within reference range in patients with coronary artery disease

Ndrepepa¹,

Braun²,

Mayer³

et al. 2015

Metabolism

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Section: Discussionmentioning

confidence: 99%

Prognostic value of thyroid-stimulating hormone within reference range in patients with coronary artery disease

Ndrepepa¹,

Braun²,

Mayer³

et al. 2015

Metabolism

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“…It has been shown that TSH upregulates IL-6 and MCP-1 mRNA expression and release from adipose tissue. Serum concentrations of proinflammatory cytokines such as IL-6 and MCP-1 have been found to be elevated in chronic thyroidits with mild hypothyroidism; therefore, higher levels of TSH could be pro-inflammatory stimuli of adipocytes [40]. It has been shown that elevated TSH through TSHR is expressed in microvascular endothelial cells and attenuates NO and prostacyclin release [41].…”

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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“…Introduction ▼ Adipocytes express TSH (thyroid stimulating hormone) receptors, and are increasingly recognized as extra-thyroidal targets of TSH [1,2]. Human adipocytes stimulated by TSH in culture undergo lipolysis, and release interleukin (IL) 6 and monocyte chemoattractant protein-1 [3][4][5][6]. When TSH is acutely administered to patients on thyroid hormone treatment who have been treated for thyroid cancer (thyroidectomy and radioablation) for cancer surveillance, the rise in TSH levels induces a brief induction of metabolic and vascular stress.…”

Section: Interacting Effects Of Tsh and Insulin On Human Differentiatmentioning

confidence: 99%

Interacting Effects of TSH and Insulin on Human Differentiated Adipocytes

2014

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Subclinical hypothyroidism, characterized by an isolated rise in TSH serum levels with normal thyroid function, is a pro-inflammatory state associated with insulin resistance. Adipocytes express TSH receptors, but it is not known if TSH can directly inhibit insulin signaling. Using primary human differentiated adipocytes, we examined the effects of TSH on insulin-stimulated Akt phosphorylation, and whether conventional PKC (cPKC) were involved. The effect of insulin on TSH-stimulated lipolysis was also investigated. TSH inhibited insulin-stimulated Akt phosphorylation in adipocytes by 54%. TSH activated cPKC, and Gö6976, a PKCα and -β1 inhibitor, prevented the inhibitory effect of TSH on the insulin response. Insulin reduced the ability of TSH to activate cPKC and to stimulate lipolysis.Our data reveal novel interactions between TSH and insulin. TSH inhibits insulin-stimulated Akt signaling in a cPKC-dependent fashion, whereas insulin blocks TSH-stimulated cPKC activity and lipolysis. TSH and insulin act on differentiated human adipocytes to modulate their respective intracellular signals.

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TSH signaling pathways that regulate MCP-1 in human differentiated adipocytes

Cited by 36 publications

References 41 publications

Prognostic value of thyroid-stimulating hormone within reference range in patients with coronary artery disease

Prognostic value of thyroid-stimulating hormone within reference range in patients with coronary artery disease

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

Interacting Effects of TSH and Insulin on Human Differentiated Adipocytes

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