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Related Experiment Video

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Developmental androgenization programs metabolic dysfunction in adult mice: Clinical implications.

Franck Mauvais-Jarvis1

  • 1Division of Endocrinology & Metabolism; Department of Medicine; Tulane University Health Sciences Center; School of Medicine; New Orleans, LA USA.

Adipocyte
|April 11, 2014
PubMed
Summary

Neonatal androgen exposure in mice programs features of metabolic syndrome, including insulin resistance and hypertension, mirroring polycystic ovary syndrome (PCOS) in women. This mouse model offers insights into developmental origins of metabolic disease.

Keywords:
adipose tissue dysfunctionandrogen excessdevelopmentmetabolic syndromeobesity

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Area of Science:

  • Endocrinology
  • Developmental Biology
  • Metabolic Research

Background:

  • Polycystic ovary syndrome (PCOS) is linked to a developmental origin of metabolic syndrome.
  • Fetal programming by androgens may underlie reproductive and metabolic abnormalities in adulthood.

Purpose of the Study:

  • To investigate the role of developmental androgen excess in programming adult metabolic dysfunction.
  • To establish and characterize a mouse model of neonatal androgenization.

Main Methods:

  • Neonatal female mice were exposed to testosterone (NTF) and compared to controls (CF).
  • Male mice with neonatal testosterone exposure (NTM) were also studied alongside control males (CM).
  • Phenotypic analyses included food intake, body composition, adipocyte size, hormone levels, insulin sensitivity, and blood pressure.

Main Results:

  • NTF mice exhibited increased food intake, lean mass, visceral adiposity, insulin resistance, pre-diabetes, and hypertension.
  • NTF mice showed hypoadiponectinemia, decreased osteocalcin, and a novel leptin resistance.
  • NTM mice displayed hypogonadotropic hypogonadism, reduced lean mass, and subcutaneous adiposity without cardiometabolic issues.

Conclusions:

  • Neonatal androgen excess in females programs key features of metabolic syndrome relevant to PCOS.
  • This mouse model elucidates the developmental programming of metabolic dysfunction.
  • Findings have implications for understanding and treating human metabolic diseases linked to early-life androgen exposure.