Prenatal nicotine exposure induces poor articular cartilage quality in female adult offspring fed a high-fat diet and the intrauterine programming mechanisms

Reproductive Toxicology
Kai TieHui Wang

Abstract

Prenatal nicotine exposure (PNE) induces skeletal growth retardation and dyslipidemia in offspring displaying intrauterine growth retardation (IUGR). Cholesterol accumulation resulting from cholesterol efflux dysfunction may reduce the quality of articular cartilage through fetal programming. This study evaluated the quality of articular cartilage of female adult offspring fed a high-fat diet and explored the mechanisms using a rat IUGR model established by the administration of 2.0mg/kg/d of subcutaneous nicotine from gestational days 11-20. The results demonstrated an increased OARSI (Osteoarthritis Research Society International) score and total cholesterol content, decreased serum corticosterone, and increased IGF1 and dyslipidemia with catch-up growth in PNE adult offspring. Cartilage matrix, IGF1 and cholesterol efflux pathway expression were reduced in PNE fetuses and adult offspring. Therefore, PNE induced poor articular cartilage quality in female adult offspring fed a high-fat diet via a dual programming mechanism.

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Citations

Aug 17, 2018·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Jin ZhouHui Wang
Dec 1, 2020·Frontiers in Veterinary Science·Emma L WeatherallCristina L Esteves
Jul 4, 2020·Biochimica Et Biophysica Acta. Molecular Cell Research·Yi-Zhong WangHui Wang

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