3,5,3′‐triiodothyronine (T3) is a survival factor for pancreatic β‐cells undergoing apoptosis

Falzacappa, Cecilia Verga; Panacchia, Laura; Bucci, Barbara; Stigliano, Antonio; Cavallo, Maria Gisella; Brunetti, Ercole; Toscano, Vincenzo; Misiti, Silvia

doi:10.1002/jcp.20460

Cited by 80 publications

(84 citation statements)

References 51 publications

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“…Our evidence suggested the involvement of the PI3K pathway in mediating this novel survival action of T 3 ; in particular, we have shown that T 3 is able to induce the phosphorylation of Akt in the islet cells hCM and rRINm5F (Verga Falzacappa et al 2006). Additionally, Cao et al (2005) have demonstrated that T 3 is specifically able to activate Akt in a non-genomic manner.…”

Section: Introductionsupporting

confidence: 51%

Thyroid hormone receptor TRβ1 mediates Akt activation by T3 in pancreatic β cells

Falzacappa

Petrucci²,

Patriarca³

et al. 2007

Journal of Molecular Endocrinology

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It has recently been recognized that thyroid hormones may rapidly generate biological responses by non-genomic mechanisms that are unaffected by inhibitors of transcription and translation. The signal transduction pathways underlying these effects are just beginning to be defined. We demonstrated that thyroid hormone T 3 rapidly induces Akt activation in pancreatic b cells rRINm5F and hCM via thyroid hormone receptor (TR) b1. The phosphorylation of Akt was T 3 specific and dependent. Coimmunoprecipitation and colocalization experiments revealed that the phosphatidylinositol 3 kinase (PI3K) p85a subunit and the thyroid receptor b1 were able to form a complex at the cytoplasmic level in both the cell lines, suggesting that a 'cytoplasmic TRb1' was implicated. Moreover, we evidenced that T 3 treatment was able to induce kinase activity of the TRb1-associated PI3K. The silencing of TRb1 expression through RNAi confirmed this receptor to be crucial for the T 3 -induced activation of Akt. This action involved a T 3 -induced nuclear translocation of activated Akt, as demonstrated by confocal immunofluorescence. In summary, T 3 is able to specifically activate Akt in the islet b cells rRINm5F and hCM through the interaction between TRb1 and PI3K p85a, demonstrating the involvement of TRb1 in this novel T 3 non-genomic action in islet b cells.

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Section: Introductionsupporting

confidence: 51%

Thyroid hormone receptor TRβ1 mediates Akt activation by T3 in pancreatic β cells

Falzacappa

Petrucci²,

Patriarca³

et al. 2007

Journal of Molecular Endocrinology

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“…Thyroid hormone replacement is associated with a decrease in HbA1c level, which is influenced by increased erythropoiesis rather than by changes in glucose level. The observation of negative correlation between T3 and HbA1c is supported by the views of various authors [17,20,21] who state a derangement of glycemic control in type 2 diabetes which influences the thyroid hormone levels. Furthermore, significant negative correlations were noted between parameters of glycemic control and serum T3 levels respectively.…”

Section: Discussionmentioning

confidence: 73%

“…Therefore, the study demonstrated that serum T3 may be a reliable index of glycemic control in diabetes mellitus. It has recently been reported that T3 has an anti-apoptotic and protective effect on the pancreatic beta cells [20,21]. T3 activates the PI-3 kinase pathway via thyroid hormone receptor on the beta cell, and stimulates insulin secretion.…”

Section: Discussionmentioning

confidence: 99%

Thyroid Disorders in Patients of Type 2 Diabetes Mellitus

et al. 2013

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The study was planned to assess the prevalence of thyroid disorders in type 2 diabetes in North Indian population and to correlate the serum insulin and glycosylated haemoglobin levels with thyroid hormones. It is a case control study. One hundred and twenty patients of type 2 diabetes were included in the study along with 117 adults of the same age group and normal glucose levels as controls. All blood samples were taken from subjects who fasted for at least 12 h before the blood collection. Glycosylated hemoglobin was determined by ion exchange chromatography and serum insulin and thyroid hormones were assessed through enzyme linked immunosorbent assay. Fasting blood glucose and glycosylated haemoglobin levels were significantly higher in diabetics showing a poor glucose control. Serum tri-iodothyronine values were significantly lower in diabetics. There was a significant correlation between glycosylated haemoglobin and thyroid hormones. There was no correlation between serum insulin and thyroid hormones.

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“…In addition, thyroid hormones are crucial for myocardial development and they may promote myocardial cell survival. Lack of thyroid hormones in the embryonic stage may induce myocardial cell apoptosis and downregulate the mRNA expressions of functional thyroid hormones receptors (Alisi et al 2005, Verga et al 2006.…”

Section: Discussionmentioning

confidence: 99%

Effects of hyper- and hypothyroid on expression of thyroid hormone receptor mRNA in rat myocardium

Liu

Li²,

Shi³

et al. 2007

Journal of Endocrinology

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Thyroid dysfunction is classified into hyperthyroidism and congenital hypothyroidism (CH). Both hyperthyroidism and CH can cause heart lesions; however, the mechanisms involved remain unclear. The left ventricle was collected from eu-, hyper-, and hypothyroid rat. RNAwas extracted and reverse-transcripted to cDNA. Real-time fluorescence quantitation-PCR was used to quantify the differential expression of thyroid hormone receptor (TR) subtype mRNA among eu-, hyper-, and hypothyroid rat myocardium. Here, we show that compared with the normal myocardium, TRa1 mRNA expression was upregulated by 51% (P!0 . 01), TRa2 mRNA expression was downregulated by 58% (P!0 . 01), and TRb1 mRNA expression remained unchanged in hyperthyroid rat myocardium (PO0 . 05). TRa1, TRa2, and TRb1 were expressed in normal and hypothyroid rat myocardium throughout the developmental process. In hypothyroid rats, myocardial TRa1 mRNA expression was generally downregulated and the expression peak appeared late. Myocardial TRa2 mRNA expression was generally upregulated and the expression peak appeared late. Myocardial TRb1 mRNA expression was generally downregulated and changed similarly with the control group. In addition, the hypogenetic myocardium can be seen in the hypothyroid rat by pathology study. Taken together, the abnormal expression of TR subtype mRNA may have a close relationship with the pathogenesis of CH and hyperthyroidism heart disease.

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3,5,3′‐triiodothyronine (T3) is a survival factor for pancreatic β‐cells undergoing apoptosis

Cited by 80 publications

References 51 publications

Thyroid hormone receptor TRβ1 mediates Akt activation by T3 in pancreatic β cells

Thyroid hormone receptor TRβ1 mediates Akt activation by T3 in pancreatic β cells

Thyroid Disorders in Patients of Type 2 Diabetes Mellitus

Effects of hyper- and hypothyroid on expression of thyroid hormone receptor mRNA in rat myocardium

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