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

Yu Yang1, Yu Chen2, Jie Chen2

  • 1Department of Endocrinology, Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing 211100, China.

Journal of Diabetes Research
|June 11, 2019
PubMed

Insights

Thyrotropin (TSH) deletion impairs pancreatic beta cell function and glucose metabolism in mice. TSHR knockout mice exhibit reduced insulin secretion and islet atrophy, primarily due to increased apoptosis.

Area of Science:

  • Endocrinology
  • Metabolism
  • Cell Biology

Background:

  • Thyrotropin (TSH) plays a role in glucose metabolism by interacting with its receptor on pancreatic cells.
  • The specific function of TSH in pancreatic beta cells and its impact on glucose homeostasis remain incompletely understood.

Purpose of the Study:

  • To investigate the role of TSH in pancreatic beta cell function and glucose metabolism using a TSH receptor knockout (TSHR-/-) mouse model.
  • To elucidate the mechanisms underlying pancreatic dysfunction in the absence of TSH signaling.

Main Methods:

  • Utilized TSHR knockout (Tshr-/-) mice and compared them with wild-type (Tshr+/+) littermates.
  • Assessed body weight, glucose levels (fasting and postprandial), insulin secretion, islet morphology, and gene/protein expression of key beta cell markers and apoptosis regulators (Pdx1, Nkx6.1, Glut2, insulin, Ki67, Bax/Bcl-2 ratio).
  • Administered thyroxine supplementation to Tshr-/- mice to control for potential hypothyroidism.

Main Results:

  • Tshr-/- mice exhibited significantly slower growth rates and lower fasting/postprandial blood glucose levels compared to controls.
  • Impaired insulin secretion and atrophy of pancreatic islets were observed in adult Tshr-/- mice.
  • While beta cell maturation and proliferation markers were unchanged, the Bax/Bcl-2 ratio was significantly elevated, indicating increased apoptosis.

Conclusions:

  • TSH signaling is crucial for maintaining normal pancreatic beta cell function and glucose homeostasis.
  • The absence of TSH leads to pancreatic beta cell dysfunction and glucose intolerance, primarily mediated by enhanced apoptosis rather than impaired proliferation or maturation.
  • These findings highlight TSH as a potential therapeutic target for metabolic disorders.

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