Maternal hypothyroidism in mice influences glucose metabolism in adult offspring

Yasmine Kemkem, Daniela Nasteska, Annie De Bray, Paula Bargi-Souza, Rodrigo Peliciari-Garcia, Anne Guillou, Patrice Mollard, David Hodson, Marie Schaeffer

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)
175 Downloads (Pure)


During pregnancy, maternal metabolic disease and hormonal imbalance may alter fetal beta cell development and/or proliferation, thus leading to an increased risk for developing type 2 diabetes in adulthood. Although thyroid hormones play an important role in fetal endocrine pancreas development, the impact of maternal hypothyroidism on glucose homeostasis in adult offspring remains poorly understood.

We investigated this using a mouse model of hypothyroidism, induced by administration of an iodine-deficient diet supplemented with propylthiouracil during gestation.

Here, we show that, when fed normal chow, adult mice born to hypothyroid mothers were more glucose-tolerant due to beta cell hyperproliferation (two- to threefold increase in Ki67-positive beta cells) and increased insulin sensitivity. However, following 8 weeks of high-fat feeding, these offspring gained 20% more body weight, became profoundly hyperinsulinaemic (with a 50% increase in fasting insulin concentration), insulin-resistant and glucose-intolerant compared with controls from euthyroid mothers. Furthermore, altered glucose metabolism was maintained in a second generation of animals.

Therefore, gestational hypothyroidism induces long-term alterations in endocrine pancreas function, which may have implications for type 2 diabetes prevention in affected individuals.

Original languageEnglish
Pages (from-to)1822-1835
Issue number9
Early online date30 May 2020
Publication statusE-pub ahead of print - 30 May 2020


  • Beta cell function
  • calcium imaging
  • diabetes
  • hypothyroidism
  • pancreas


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