Thyroid stimulating hormone stimulates the expression of glucose transporter 2 via its receptor in pancreatic β cell line, INS-1 cells

Lyu, Jingya; Imachi, Hitomi; Yoshimoto, Takuo; Fukunaga, Kohji; Sato, Seisuke; Ibata, Tomohiro; Kobayashi, Toshihiro; Dong, Tao; Yonezaki, Kazuko; Yamaji, Nao; Kikuchi, Fumi; Iwama, Hisakazu; Ishikawa, Ryou; Haba, Reiji; Sugiyama, Yasunori; Zhang, Huanxiang; Murao, Koji

doi:10.1038/s41598-018-20449-3

Cited by 16 publications

(14 citation statements)

References 53 publications

(52 reference statements)

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“…Findings from different laboratories present an ambiguous picture of the role of p38α in browning and thermogenesis [173,176,177]. Similar to adipocytes, p38 isoforms present various functions in pancreatic β-cells and skeletal muscle [186][187][188][189]207,208]. In pancreatic β-cells, p38δ/γ suppress insulin secretion [186,187,189], whereas p38α promotes glucose uptake [188].…”

Section: Discussionmentioning

confidence: 99%

“…However, the exact molecular mechanisms by which the p38δ-PDK1 pathway is regulated remain to be defined. Furthermore, p38α directly affects the glucose uptake in pancreatic β-cells through TSH signaling by up-regulating the expression of GLUT2 gene [188]. Finally, p38γ may have an important role in TNFα-mediated downregulation of ATP-binding cassette transporter A1 (ABCA1) expression, leading to suppression of insulin secretion [189].…”

Section: The Role Of P38s In Pancreatic β-Cellsmentioning

confidence: 99%

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Impact of Conventional and Atypical MAPKs on the Development of Metabolic Diseases

Kassouf

Sumara

2020

Biomolecules

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The family of mitogen-activated protein kinases (MAPKs) consists of fourteen members and has been implicated in regulation of virtually all cellular processes. MAPKs are divided into two groups, conventional and atypical MAPKs. Conventional MAPKs are further classified into four sub-families: extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK1, 2 and 3), p38 (α, β, γ, δ), and extracellular signal-regulated kinase 5 (ERK5). Four kinases, extracellular signal-regulated kinase 3, 4, and 7 (ERK3, 4 and 7) as well as Nemo-like kinase (NLK) build a group of atypical MAPKs, which are activated by different upstream mechanisms than conventional MAPKs. Early studies identified JNK1/2 and ERK1/2 as well as p38α as a central mediators of inflammation-evoked insulin resistance. These kinases have been also implicated in the development of obesity and diabetes. Recently, other members of conventional MAPKs emerged as important mediators of liver, skeletal muscle, adipose tissue, and pancreatic β-cell metabolism. Moreover, latest studies indicate that atypical members of MAPK family play a central role in the regulation of adipose tissue function. In this review, we summarize early studies on conventional MAPKs as well as recent findings implicating previously ignored members of the MAPK family. Finally, we discuss the therapeutic potential of drugs targeting specific members of the MAPK family.

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Section: Discussionmentioning

confidence: 99%

Section: The Role Of P38s In Pancreatic β-Cellsmentioning

confidence: 99%

Impact of Conventional and Atypical MAPKs on the Development of Metabolic Diseases

Kassouf

Sumara

2020

Biomolecules

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“…More investigations are needed in order to reveal the detailed effect of TRH on the pancreas [ 34 ]. About TSH, there is only one report that shows that TSH can stimulate GLUT2 gene transcription by activating the p38 MAPK signal pathway [ 35 ].…”

Section: Thyroid Hormone Receptors and Transporters In Pancreasmentioning

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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“…TSHR may induce different effects depending on the tissue where it is expressed. In rodent pancreatic islets binding of TSH to its receptor stimulates the activity of glucose transporter 2 (GLUT2) promoter [35]. The lack of TSHR expression in the liver disrupts hepatic lipid metabolism.…”

Section: Prace Poglądowementioning

confidence: 99%

“…Receptor hormonu tyreotropowego może indukować różne efekty w zależności od tkanki, w której ulega ekspresji. W wysepkach trzustkowych u gryzoni wiązanie TSH z receptorem stymuluje aktywność promotora transportera glukozy 2 (GLUT2, glucose transporter 2) [35]. Hepatocyty bez ekspresji TSHR wykazują zaburzenia wątrobowego metabolizmu lipidów.…”

Section: Prace Poglądoweunclassified

Glycosylation of thyroid-stimulating hormone receptor

Korta

Pocheć

2019

Endokrynologia Polska

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Thyroid-stimulating hormone receptor (TSHR) is a typical membrane receptor with 7-transmembrane helix domain (7TMR), coupled to the G protein. The mature receptor, present in the cell membrane, is composed of the A subunit comprising a large extracellular domain, and the B subunit, which consists of a short extracellular fragment anchored in the cell membrane and an intracellular part. The TSH receptor is subject to numerous post-translational modifications that determine its final structure and significantly affect its activity. One of them is glycosylation. TSHR is abundantly N-glycosylated, due to the presence of six N-glycosylation sites in the extracellular domain (Asn77, Asn99, Asn113, Asn177, Asn198, Asn302), mostly evolutionarily conserved. N-glycans constitute 30-40% of the receptor molecular weight. The glycans are necessary for the receptor trafficking to the plasma membrane and binding of TSH to the receptor. Fucosylated and sialylated N-oligosaccharides were found on TSHR molecules. The increased sialylation of TSHR glycans correlates positively with the receptor binding ability and prolongs the time of receptor incorporation into the cell membrane. TSHR is the main autoantigen in Graves' disease (GD), one of the thyroid autoimmune diseases. One hypothesis assumes that the higher N-glycosylation of THSR in human compared to animals influences the breaking of autotolerance and GD development. N-oligosaccharides are the important part of THSR molecule, necessary for the proper functioning of receptors and probably involved in thyroid autoimmunity in GD.

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Thyroid stimulating hormone stimulates the expression of glucose transporter 2 via its receptor in pancreatic β cell line, INS-1 cells

Cited by 16 publications

References 53 publications

Impact of Conventional and Atypical MAPKs on the Development of Metabolic Diseases

Impact of Conventional and Atypical MAPKs on the Development of Metabolic Diseases

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

Glycosylation of thyroid-stimulating hormone receptor

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