98%
921
2 minutes
20
Thyroid stimulating hormone (TSH) stimulates the secretion of thyroid hormones by binding the TSH receptor (TSHR). TSHR is well-known to be expressed in thyroid tissue, excepting it, TSHR has also been expressed in many other tissues. In this study, we have examined the expression of TSHR in rat pancreatic islets and evaluated the role of TSH in regulating pancreas-specific gene expression. TSHR was confirmed to be expressed in rodent pancreatic islets and its cell line, INS-1 cells. TSH directly affected the glucose uptake in INS cells by up-regulating the expression of GLUT2, and furthermore this process was blocked by SB203580, the specific inhibitor of the p38 MAPK signaling pathway. Similarly, TSH stimulated GLUT2 promoter activity, while both a dominant-negative p38MAPK α isoform (p38MAPK α-DN) and the specific inhibitor for p38MAPK α abolished the stimulatory effect of TSH on GLUT2 promoter activity. Finally, INS-1 cells treated with TSH showed increased protein level of glucokinase and enhanced glucose-stimulated insulin secretion. Together, these results confirm that TSHR is expressed in INS-1 cells and rat pancreatic islets, and suggest that activation of the p38MAPK α might be required for TSH-induced GLUT2 gene transcription in pancreatic β cells.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5792451 | PMC |
http://dx.doi.org/10.1038/s41598-018-20449-3 | DOI Listing |
Front Endocrinol (Lausanne)
September 2025
Department of Biological Sciences, University of Denver, Denver, CO, United States.
The ability to quantify protein secretion is critical for studying the secretory pathway. This is particularly important in endocrine cells where dysregulated hormone secretion is associated with the development of diseases such as type 2 diabetes. To measure protein secretion, researchers have previously relied on techniques such as ELISA, RIA and Western blot, which all present limitations, including cost and time consumption.
View Article and Find Full Text PDFJ Mater Chem B
September 2025
Nanostructured Materials Laboratory, University of Georgia, Athens, GA, 30602, USA.
Three-dimensional cell cultures on biomimetic scaffolds have gained significant attention in tissue engineering, drug delivery, and scalable cell production. Current challenges in creating an ideal scaffold are providing maximum space for cells to grow while ensuring efficient nutrient, metabolite, and gas exchange to prevent the formation of necrotic or apoptotic regions. In our work, we grow insulin-producing INS-1 cells on touch-spun polycaprolactone (PCL) fiber scaffolds.
View Article and Find Full Text PDFEndocrine
August 2025
Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Xuzhou, Jiangsu Province, China.
Aims: This study investigated the protective role of Perilipin 5 (PLIN5) in pancreatic β-cell dysfunction under diabetic conditions, focusing on its regulatory effects on lipid metabolism and mitochondrial dynamics.
Materials And Methods: Diabetic db/db mice and pancreatic beta cell line INS-1 were employed to investigate the role of PLIN5 in insulin secretion and lipid metabolism under high glucose (HG) conditions. The phenotypic changes were evaluated by staining and measurement of biochemical indexes.
Sci Rep
August 2025
Medicinal Plant Innovation Center of Mae Fah Luang University, Mae Fah Luang University, Chiang Rai, 57100, Thailand.
Traditional herbal formulations offer promising avenues for diabetes management by targeting multiple molecular pathways. Mathurameha (MT), a polyherbal preparation, has been historically used for its antidiabetic potential. However, its molecular mechanisms remain largely unexplored.
View Article and Find Full Text PDFAdv Sci (Weinh)
August 2025
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, 100191, China.
Although leucine-rich repeat-containing G protein-coupled receptor 4 (LGR4) is abundantly expressed in the pancreas, it is currently unknown whether LGR4 impacts pancreatic endocrine cells. Here, a critical role of LGR4 is demonstrated in islet β cell mass using a group of transgenic mice with LGR4 deficiency. Knock-out of Lgr4 in the pancreas and islet β cells significantly reduced islet β cell mass, and subsequently impaired glucose metabolism upon the challenge of a high-fat diet.
View Article and Find Full Text PDF