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Prenatal androgen excess impairs beta-cell function by decreased sirtuin 3 expression.

Yu Zhou1,2, Min Gong2, Yingfei Lu1

  • 1Central Laboratory, Translational Medicine Research Center, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.

The Journal of Endocrinology
|August 9, 2021
PubMed
Summary

Prenatal testosterone exposure causes obesity and glucose intolerance in aged female offspring. This metabolic disturbance is linked to reduced sirtuin 3 (SIRT3) expression and increased oxidative stress in pancreatic beta cells.

Keywords:
Sirt3agingbeta cell functionoxidative stressprenatal androgen excess

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Area of Science:

  • Endocrinology
  • Metabolic Research
  • Reproductive Biology

Background:

  • Prenatal androgen excess is linked to metabolic disorders in female offspring.
  • Long-term effects on glucose metabolism and pancreatic beta-cell function remain under-investigated.

Purpose of the Study:

  • To investigate the long-term impact of prenatal testosterone exposure on glucose metabolism and pancreatic beta-cell function in aged female offspring.
  • To elucidate the underlying molecular mechanisms involving sirtuin 3 (SIRT3) and oxidative stress.

Main Methods:

  • Utilized a mouse model with maternal testosterone excess and their female offspring.
  • Assessed glucose metabolism, insulin levels, lipid profiles, and testosterone concentrations in aged offspring.
  • Investigated pancreatic beta-cell function, SIRT3 expression, oxidative stress markers, and cellular energy levels (cAMP, ATP).

Main Results:

  • Prenatal androgen treatment induced obesity, glucose intolerance, and altered insulin/triglyceride levels in aged female offspring.
  • Testosterone excess downregulated SIRT3 expression, activated oxidative stress, and impaired beta-cell function.
  • Overexpression of SIRT3 in isolated islets normalized oxidative stress, restored energy levels, and improved glucose-stimulated insulin secretion.

Conclusions:

  • Prenatal testosterone exposure leads to lasting metabolic dysfunction in aged female offspring.
  • Suppression of SIRT3 and activation of oxidative stress in pancreatic beta cells are key mechanisms driving this dysfunction.
  • SIRT3 upregulation presents a potential therapeutic target for mitigating these adverse effects.