Absence of thyrotropin-induced increase in leptin levels in patients with history of differentiated thyroid carcinoma undergoing recombinant human thyrotropin testing

Cecoli, Francesca; Andraghetti, Gabriella; Ghiara, Carla; Briatore, L.; Cavallero, D.; Mussap, Michele; Minuto, Francesco; Giusti, Massimo

doi:10.1007/bf03346437

Cited by 4 publications

(2 citation statements)

References 25 publications

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“…We can speculate a direct effect of TSH on lipids, and not mediated by cytokine. Indeed, a previous report found that adipocytokine could interact with thyroid hormone [30,31], but acute effect of rhTSH is ineffective in changing leptin levels [32].…”

Section: Discussionmentioning

confidence: 99%

Effect of rhTSH on Lipids

Delitala

Scuteri

Maioli

et al. 2020

JCM

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Background: Subclinical hypothyroidism is associated with increased blood lipid levels. However, the exact role of thyrotropin (TSH) alone is not clear. In order to clarify this point, we analysed the acute effect of recombinant human TSH (rhTSH) administration on lipid levels. Methods: Sera of 27 premenopausal women with well-differentiated thyroid cancer were analysed. Patients that underwent a total thyroidectomy, ablation with 131I (Iodine 131) and rhTSH administration as a part of routine follow-up American Thyroid Association guidelines were included. The protocol consists of 2 intramuscular injections of 0.9 mg of rhTSH, performed on day 1 day and day 2, with blood collection on day 1 (before rhTSH administration), and day 5. TSH, free thyroxine, total cholesterol, low-density lipoprotein cholesterol (LDLc), high density lipoprotein cholesterol (HDLc), and triglycerides were assessed in all the samples, before and four days after the first administration of rhTSH. Results: Total cholesterol and triglycerides significantly increased after stimulation of rhTSH (respectively, 192 ± 33 vs. 207 ± 26, p = 0.036 and 72 ± 23 vs. 85 ± 23, p = 0.016). LDLc and HDLc showed comparable concentrations before and after the test (respectively, 115 ± 27 vs. 126 ± 22, p = 0.066, and 62 ± 15 vs. 64 ± 15, p = 0.339), while non-HDLc increased after stimulation (130 ± 30 vs. 143 ± 25, p = 0.045). Conclusion: TSH has a direct effect on total cholesterol, triglycerides, and nonHDLc. Explanation of these phenomena will require additional studies.

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Section: Discussionmentioning

confidence: 99%

Effect of rhTSH on Lipids

Delitala

Scuteri

Maioli

et al. 2020

JCM

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“…Whether rhTSH effect on serum leptin persists beyond the length of this study cannot be established at this time, since blood sampling was stopped at 96 h after the first rhTSH administration, according to the standard protocol for thyroglobulin measurement in thyroid cancer patients. In a recent study, no significant variations in serum leptin concentrations after in vivo stimulation with rhTSH were reported (26). The small number of subjects and different times of observation of TSH effects might explain the lack of significant changes in serum leptin observed in that study.…”

Section: Discussionmentioning

confidence: 54%

Acute exogenous TSH administration stimulates leptin secretion in vivo

Santini¹,

Galli²,

Maffei

et al. 2010

European Journal of Endocrinology

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TSH-receptor (TSHR) has been found in a variety of cell types, including preadipocytes and adipocytes. In vitro, TSH-mediated preadipocyte and adipocyte responses include proliferation, differentiation, survival, and lipolysis. Objective: To measure the response of serum leptin to exogenous administration of recombinant human TSH (rhTSH) in vivo. Patients: One hundred patients with differentiated thyroid cancer already treated by total thyroidectomy and 131 I remnant ablation were enrolled. Mean (GS.E.M.) body mass index (BMI) was 26.9G0.6 kg/m 2 . Methods: Patients received a standard dose of rhTSH for measurement of thyroglobulin in the follow-up of their disease. Blood samples were taken for the assay of TSH and leptin before the first administration of rhTSH (time 0), and 24 h (time 1), 48 h (time 2), 72 h (time 3), and 96 h (time 4) after the first administration of rhTSH. Results: Significant mean serum leptin increments, with respect to basal value, were 16, 13, 18, and 11% at times 1, 2, 3, and 4 respectively. Significant positive correlations of leptin-area under the curve with respect to basal leptin levels (rZ0.43; P!0.0001) and BMI (rZ0.32; P!0.005) were observed. Conclusions: Acute rhTSH administration in hypothyroid subjects under L-thyroxine therapy produces a rise in serum leptin. This increase is proportional to the adipose mass suggesting that a functioning TSHR is expressed on the surface of adipocytes. The role that TSHR activation in adipocytes might play in physiological and pathological conditions remains a matter of investigation.

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