Increased transforming growth factor-beta1 plasma concentration is associated with high plasma 3,3',5'-tri-iodothyronine in elderly patients with nonthyroidal illnesses

Corica, Francesco; Allegra, Alessandro; Corsonello, Andrea; Buemi, Michele; Rubino, Federico Maria; Bonanzinga, S; Ruello, Antonella; Ceruso, D

doi:10.1530/eje.0.1380047

Cited by 7 publications

(5 citation statements)

References 21 publications

(30 reference statements)

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“…This finding led the authors to propose that this factor might play a role in the induction of thyroid changes in nonthyroid illness (106). These results agree with the demonstration that TGF-b1 stimulates the expression of type III dehalogenase and inhibits T 4 to T 3 conversion (67).…”

Section: Tgf-b1 and Nonthyroidal Illnesssupporting

confidence: 71%

Role of Transforming Growth Factor Beta in the Regulation of Thyroid Function and Growth

Pisarev

Thomasz

Juvenal

2009

Thyroid

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Transforming growth factor beta (TGF-beta) exists in nature as three isoforms. They exert their effects by binding to a type II receptor located at the cell membrane. The TGF-beta-type II receptor complex then recruits type I receptor, and this new complex stimulates the phosphorylation of Smads 2 and 3, which are subsequently transferred to the nucleus, where they regulate gene transcription. The thyroid gland expresses the TGF-beta1 gene mRNA and synthesizes the protein, which under physiologic conditions regulates thyroid growth and function. Different studies have demonstrated that TGF-beta1 inhibits cell proliferation and a number of functional parameters. These include cyclic adenosine monophosphate (AMP) formation, iodine uptake and organification, hormone secretion, and the expression of thyroglobulin, thyroid peroxidase, and Na(+)/I(-) symporter. The expression of the TGF-beta1 gene and protein may be stimulated by iodine under normal conditions. Since TGF-beta1 mimics some of the inhibitory actions of iodine, its participation in thyroid autoregulation has been proposed; however, this concept is still debated. In thyroid tumors, the inhibitory action of TGF-beta1 on cell proliferation is progressively lost as the tumor becomes more undifferentiated. The alterations in the signaling pathway of TGF-beta1 are not the same in tumors from different species. Even within the same species, such as the pig thyroid, the results may be different depending on whether monolayers or follicular suspensions are employed. The data suggest that it is not entirely possible to apply the results obtained in animal studies to normal or pathological human thyroid tissue. More studies are required to provide the information needed to develop treatments, based on targeting the signaling pathway of TGF-beta1, for undifferentiated thyroid cancer and other thyroid diseases.

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Section: Tgf-b1 and Nonthyroidal Illnesssupporting

confidence: 71%

Role of Transforming Growth Factor Beta in the Regulation of Thyroid Function and Growth

Pisarev

Thomasz

Juvenal

2009

Thyroid

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“…These changes in thyroid hormone metabolism are referred to as the 'sick euthyroid syndrome' and several authors have indicated cytokines (e.g. TNF-·, IL-1, IL-6, IL-2, FGF, and TGF-ß 1 ) as putative mediators of this syndrome [1][2][3][4][5][6]. Although the pathophysiological implications of this condition are not well understood, it seems to represent a mechanism leading to a reduction of catabolic processes and oxygen consumption in the course of chronic diseases [7,8].…”

Section: Introductionmentioning

confidence: 99%

Plasma Leptin Concentrations in Relation to Sick Euthyroid Syndrome in Elderly Patients with Nonthyroidal Illnesses

Corsonello

Buemi²,

Artemisia³

et al. 2000

Gerontology

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Background: Leptin, the ob gene product, seems to be involved in regulating energy expenditure in humans, but its role in the pathophysiology of the energy imbalance in chronically ill patients is largely unknown. Objective: To evaluate plasma leptin concentrations and thyroid function in elderly patients with nonthyroidal illnesses (NTI). Methods: Sixty-four NTI elderly patients (75.0 ± 6.3 years, 27 males and 37 females) and 21 age- and sex-matched healthy controls (73.0 ± 5.5 years, 9 males and 12 females) were enrolled in the study. In all subjects tri-iodothyronine (T₃), thyroxine (T₄), reverse T₃ (rT₃), free T₃ (fT₃), free T₄ (fT₄), TSH, and plasma leptin concentrations were measured. Nutritional status was also evaluated in all subjects studied by the measurement of body mass index (BMI), lymphocytes, serum iron, hemoglobin, plasma albumin, transferrin and total cholesterol. Results: The data on thyroid hormones enabled us to identify three groups: group A, subjects (15 patients) with T₃ and fT₃ levels comparable to those of controls; group B, subjects (25 patients) with T₃ and fT₃ levels lower than controls and rT₃ levels comparable to those of controls; group C, subjects (24 patients) with T₃ and fT₃ levels lower than those of controls and high rT₃ levels. The patients of group C showed lower plasma leptin levels than the controls, 6.6 (5.5–14.2) and 16.3 (7.2–23.7) ng/ml (median with interquartile range in parentheses, p < 0.05), respectively. Females also showed higher plasma leptin levels than males in the controls, group A and group B, but not in group C. Moreover, plasma leptin concentrations were directly correlated to BMI in all the groups studied, while a negative correlation between leptin and rT₃ was detectable in group C (r = –0.44, p < 0.05), also after adjusting for BMI and sex. Conclusions: The concurrence of modifications in plasma leptin and thyroid hormones concentrations found in elderly NTI patients with a sick euthyroid syndrome could reflect a particular neuroendocrine status, leading to a reduction in the catabolic processes in the course of chronic diseases.

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“…Transforming growth factor‐β (TGF‐β) is a multifunctional polypeptide, produced mainly by lymphoid cells and involved in embryonic development, tumorigenesis, fibrosis, wound healing, hematopoiesis, and immunoregulation . Among the three known isoforms of TGF‐β present in human serum, TGF‐β1 is the isoform most commonly found in human tissues . Maternal plasma TGF‐β concentrations are greater during pregnancy than in non‐pregnant state but there is no consensus on its quantitative evolution during pregnancy and postpartum …”

Section: Introductionmentioning

confidence: 99%

“…[14][15][16] Among the three known isoforms of TGFβ present in human serum, TGF-β1 is the isoform most commonly found in human tissues. 17,18 Maternal plasma TGFβ concentrations are greater during pregnancy than in non-pregnant state but there is no consensus on its quantitative evolution during pregnancy and postpartum. [19][20][21][22] Increased oestradiol concentrations during pregnancy enhance Th2 responses.…”

Section: Introductionmentioning

confidence: 99%

Associations of maternal oestradiol, cortisol, and TGF‐β1 plasma concentrations with thyroid autoantibodies during pregnancy and postpartum

Sakkas

Paltoglou

Linardi

et al. 2018

Clinical Endocrinology

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Increased transforming growth factor-beta1 plasma concentration is associated with high plasma 3,3',5'-tri-iodothyronine in elderly patients with nonthyroidal illnesses

Cited by 7 publications

References 21 publications

Role of Transforming Growth Factor Beta in the Regulation of Thyroid Function and Growth

Role of Transforming Growth Factor Beta in the Regulation of Thyroid Function and Growth

Plasma Leptin Concentrations in Relation to Sick Euthyroid Syndrome in Elderly Patients with Nonthyroidal Illnesses

Associations of maternal oestradiol, cortisol, and TGF‐β1 plasma concentrations with thyroid autoantibodies during pregnancy and postpartum

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