Hypothyroidism decreases proinsulin gene expression and the attachment of its mRNA and eEF1A protein to the actin cytoskeleton of INS-1E cells

Goulart-Silva, Francemilson; Serrano‐Nascimento, Caroline; Nunes, Maria Tereza

doi:10.1590/s0100-879x2011007500121

Cited by 5 publications

(2 citation statements)

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“…Glucokinase-specific activity and GLUT 2 protein expression were significantly decreased in isolated islets from hypothyroid rats, pointing out a possible mechanism for insulin secretion deficit [ 81 ]. Besides, TH deprival could decrease proinsulin gene expression and the attachment of eukaryotic translation elongation factor 1A (eEF1A) to the cytoskeleton in INS-1E cells, which is essential to attaching transcripts of proinsulin to the cytoskeleton and modulating their stability and translation rate [ 82 ]. Moreover, oxidative stress in hypothyroidism may directly cause pancreas injuries.…”

Section: Roles Of Thyroid and Thyroid Hormone In Pancreas Pathogenmentioning

confidence: 99%

The Roles of Thyroid and Thyroid Hormone in Pancreas: Physiology and Pathology

Chen

Xie

Shen

et al. 2018

International Journal of Endocrinology

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It is widely accepted that thyroid hormones (THs), secreted from the thyroid, play important roles in energy metabolism. It is also known that THs also alter the functioning of other endocrine glands; however, their effects on pancreatic function have not yet been reviewed. One of the main functions of the pancreas is insulin secretion, which is altered in diabetes. Diabetes, therefore, could be related to thyroid dysfunction. Earlier research on this subject focused on TH regulation of pancreas function (such as insulin secretion) or on insulin function through TH-mediated increase of energy metabolism. Afterwards, epidemiological investigations and animal test research found a link between autoimmune diseases, thyroid dysfunction, and pancreas pathology; however, the underlying mechanisms remain unknown. Furthermore, recent studies have shown that THs also play important roles in pancreas development and on islet pathology, both in diabetes and in pancreatic cancer. Therefore, an overview of the effects of thyroid and THs on pancreas physiology and pathology is presented. The topics contained in this review include a summary of the relationship between autoimmune thyroid dysfunction and autoimmune pancreas lesions and the effects of THs on pancreas development and pancreas pathology (diabetes and pancreatic cancer).

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Section: Roles Of Thyroid and Thyroid Hormone In Pancreas Pathogenmentioning

confidence: 99%

The Roles of Thyroid and Thyroid Hormone in Pancreas: Physiology and Pathology

Chen

Xie

Shen

et al. 2018

International Journal of Endocrinology

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“…A number of non-translational processes involving eEF1A are described suggesting that, due to its high abundancy, eEF1A may serve as an important hub protein which connects different cellular activities [3]. It contributes to cell cycle progression [4], chaperon-mediated autophagy [5], apoptosis [6], lypotoxic cell death [7], protein renaturation [8], endogenous proteolysis [9], lysosome biogenesis [10], spermatogenesis [11] and multiple cytoskeleton rearrangements [12][13][14].…”

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confidence: 99%

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2018

Biopolym. Cell

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To review mechanisms of regulation of expression and the functionality of two isoforms of translation elongation factor eEF1A in mammalian cells. Results. eEF1A1 and eEF1A2 proteins are regulated by post-translational modifications, protein-protein and protein-tRNA interactions as well as by controlling the amount of their mRNAs in human cells. Conclusions. EEF1A1 mRNA levels in cancer cells may depend on the allelic copy number while the level of EEF1A2 mRNA may be controlled by micro RNAs. eEF1A2 protein activity in different cellular processes may be determined, in part, by its increased affinity for tRNA and viral RNAs as compared to eEF1A1. eEF1A1 activity can be regulated by its increased susceptibility to post-translational modifications (PTM) and protein-protein interactions (PTI) as compared to eEF1A2.

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3,5-Diiodo-l-thyronine ameliorates diabetic nephropathy in streptozotocin-induced diabetic rats

Shang

Gao

Zhao

et al. 2013

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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3, 5-Diiodothyronine (T2), a natural metabolite of triiodothyronine (T3) from deiodination pathway, can mimic biologic effects of T3 without inducing thyrotoxic effects. Recent studies revealed T3 acted as a protective factor against diabetic nephropathy (DN). Nevertheless, little is known about the effect of T2 on DN. This study was designed to investigate whether and how T2 affects experimental models of DN in vivo and in vitro. Administration of T2 was found to prevent significant decrease in SIRT1 protein expression and activity as well as increases in blood glucose, urine albumin excretion, matrix expansion, transforming growth factor-β1 expression, fibronectin and type IV collagen deposition in the diabetic kidney. Concordantly, similar effects of T2 were exhibited in the cultured rat mesangial cells (RMC) exposed to high glucose and that could be abolished by a known SIRT1 inhibitor, sirtinol. Moreover, enhanced NF-κB acetylation and JNK phosphorylation present in both diabetic rats and high glucose-treated RMC were distinctly dampened by T2. Collectively, these results suggested that T2 was a protective agent against renal damage in diabetic nephropathy, whose action involved regulation of SIRT1.

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Hypothyroidism decreases proinsulin gene expression and the attachment of its mRNA and eEF1A protein to the actin cytoskeleton of INS-1E cells

Cited by 5 publications

References 35 publications

The Roles of Thyroid and Thyroid Hormone in Pancreas: Physiology and Pathology

The Roles of Thyroid and Thyroid Hormone in Pancreas: Physiology and Pathology

Untitled

3,5-Diiodo-l-thyronine ameliorates diabetic nephropathy in streptozotocin-induced diabetic rats

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