Abstract | BACKGROUND: METHODS: C57BL/6J female mice were provided with a control (Con) or obesogenic diet (Ob) to induce pre-conception obesity. Half the obese dams were treated orally with 300 mg/kg/d of metformin (Ob-Met) during pregnancy. Gonadal WAT depots from 8-week-old offspring were investigated for adipocyte size, macrophage infiltration and mRNA expression of pro-inflammatory genes using RT-PCR. RESULTS: Gestational metformin attenuated the adiposity in obese dams and increased the gestation length without correcting the offspring in utero growth restriction and catch-up growth caused by maternal obesity. Despite similar body weight, the Ob and Ob-Met offspring of both sexes showed adipocyte hypertrophy in young adulthood. Male Ob-Met offspring had increased WAT depot weight (p < 0.05), exaggerated adipocyte hyperplasia (p < 0.05 vs. Con and Ob offspring), increased macrophage infiltration measured via histology (p < 0.05) and the mRNA expression of F4/80 (p < 0.05). These changes were not observed in female Ob-Met offspring. CONCLUSIONS: Maternal metformin intervention during obese pregnancy causes excessive adiposity, adipocyte hyperplasia and WAT inflammation in male offspring, highlighting sex-specific effects of prenatal metformin exposure on offspring WAT.
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Authors | Josca M Schoonejans, Heather L Blackmore, Thomas J Ashmore, Catherine E Aiken, Denise S Fernandez-Twinn, Susan E Ozanne |
Journal | International journal of molecular sciences
(Int J Mol Sci)
Vol. 22
Issue 15
(Jul 28 2021)
ISSN: 1422-0067 [Electronic] Switzerland |
PMID | 34360870
(Publication Type: Journal Article)
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Chemical References |
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Topics |
- Adiposity
- Animals
- Animals, Newborn
(metabolism)
- Diabetes, Gestational
(drug therapy, metabolism)
- Female
- Male
- Metformin
(pharmacology)
- Mice
- Mice, Inbred C57BL
- Obesity, Maternal
(drug therapy, metabolism)
- Pregnancy
- Prenatal Exposure Delayed Effects
(metabolism, pathology)
- Sex Factors
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