The Adverse Effects of Thyrotropin Absence on Pancreatic β Cell Function in Mice.

Abstract	Thyrotropin (TSH) is a modulator of glucose metabolism by binding to its receptor on pancreatic cells. We used thyrotropin receptor (TSHR) knockout mice (Tshr -/-) as a model of TSH deletion to study its function in pancreatic β cells. Tshr -/- mice had a similar body weight at birth compared with Tshr +/+ mice, but grew at a significantly slower rate until adulthood with adequate thyroxine supplementation. TSH deletion led to lower fasting and postprandial blood glucose, insulin secretion impairment, and atrophy of islets in adult mice. Transcription factors and markers of pancreatic β cell maturation, Pdx1, Nkx6.1, Glut2, and insulin, together with cell proliferation marker Ki67 showed no differences at the mRNA level between the two groups. However, the Bax/Bcl-2 ratio was remarkably elevated in Tshr -/- mice at both mRNA and protein levels. We hypothesized that pancreatic cell apoptosis, rather than abnormal cell proliferation and maturation, is associated with pancreatic dysfunction and glucose intolerance in the absence of TSH modulation.
Authors	Yu Yang, Yu Chen, Jie Chen, Danyu Zhang, Jianhua Wang, Xiaodong Mao, Xiao Wei, Xingjia Li, Xianghua Ma, Chao Liu, Kun Wang
Journal	Journal of diabetes research (J Diabetes Res) Vol. 2019 Pg. 9536032 ( 2019) ISSN: 2314-6753 [Electronic] England
PMID	31179344 (Publication Type: Journal Article)
Chemical References	Glucose Transporter Type 2 Homeodomain Proteins Insulin Nkx6-1 protein, mouse Receptors, Thyrotropin Slc2a2 protein, mouse Trans-Activators pancreatic and duodenal homeobox 1 protein Thyrotropin Glucose Thyroxine
Topics	Animals Apoptosis Body Weight Cell Proliferation Female Gene Deletion Gene Expression Profiling Glucose (metabolism) Glucose Tolerance Test Glucose Transporter Type 2 (metabolism) Heterozygote Homeodomain Proteins (metabolism) Homeostasis Insulin (metabolism) Insulin-Secreting Cells (pathology) Male Mice Mice, Knockout Organ Size Pancreas (physiopathology) Receptors, Thyrotropin (genetics) Thyrotropin (physiology) Thyroxine (therapeutic use) Trans-Activators (metabolism)

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