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Metabolic programming in the offspring after gestational overfeeding in the mother: toward neonatal rescuing with metformin in a swine model

内科学 内分泌学 二甲双胍 脂肪组织 体重增加 后代 医学 脂联素 妊娠期 脂肪细胞 背景(考古学) 出生体重 代谢综合征 生物 怀孕 胰岛素抵抗 胰岛素 肥胖 古生物学 体重 遗传学
作者
Sílvia Xargay‐Torrent,Berta Mas‐Parés,Gemma Carreras‐Badosa,Esther Lizárraga-Mollinedo,J. Tibau,J. Reixach,Estíbaliz Platero-Gutierrez,Anna Prats‐Puig,Francis de Zegher,Lourdes Ibáñez,Judit Bassols,Abel López‐Bermejo
出处
期刊:International Journal of Obesity [Springer Nature]
卷期号:46 (5): 1018-1026 被引量:3
标识
DOI:10.1038/s41366-022-01076-5
摘要

Maternal overfeeding during gestation may lead to adverse metabolic programming in the offspring mediated by epigenetic alterations. Potential reversal, in early life, of these alterations may help in the prevention of future cardio-metabolic conditions. In this context, our aims were: (1) to study the effects of maternal overfeeding on the metabolic and epigenetic programming of offspring's adipose tissue; and (2) to test the potential of postnatal metformin treatment to reverse these changes.We used a swine animal model where commercial production sows were either overfed or kept under standard diet during gestation, and piglets at birth were randomly assigned to metformin (n = 16 per group) or vehicle treatment during lactation (n = 16 per group).Piglets born to overfed sows showed a worse metabolic profile (higher weight, weight gain from birth and abdominal circumference; all p < 0.05) together with altered serological markers (increased HOMA-IR, fructosamine, total cholesterol, C-Reactive Protein and lower HMW adiponectin; all p < 0.05). The visceral adipose tissue also showed altered morphology (increased adipocyte area, perimeter and diameter; all p < 0.05), as well as changes in gene expression (higher CCL2 and INSR, lower DLK1; all p < 0.05), and in DNA methylation (96 hypermethylated and 99 hypomethylated CpG sites; FDR < 0.05). Metformin treatment significantly ameliorated the abnormal metabolic profile, decreasing piglets' weight, weight gain from birth, abdominal circumference and fructosamine (all p < 0.05) and reduced adipocyte area, perimeter, and diameter in visceral adipose tissue (all p < 0.05). In addition, metformin treatment potentiated several associations between gene expression in visceral adipose tissue and the altered metabolic markers.Maternal overfeeding during gestation leads to metabolic abnormalities in the offspring, including adipose tissue alterations. Early metformin treatment mitigates these effects and could help rescue the offspring's metabolic health.
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