ECE2022 Poster Presentations Reproductive and Developmental Endocrinology (61 abstracts)
Is there a link between polycystic ovary syndrome and transgenerational transmission of a reproductive and metabolic function in male offspring?
Sanjiv Risal 1 , Congru Li 2 , Qing Luo 2 , Romina Fornes 2 , Maria Manti 2 , Haojiang Lu 2 , Gustaw Eriksson 2 , Claes Ohlsson 3 , Eva Lindgren 2 , Nicolas Crisosto 4 , Manuel Maliqueo 5 , Barbara Echiburú 5 , Sergio Recabarren 5 , Teresa Sir Petermann 5 , Anna Benrick 6 , Nele Brusselaers 7 , Jie Qiao 8 , Qiaolin Deng 9 & Elisabet Stener-Victorin 9
1Karolinska Institute, Department of Physiology and Pharmacology, Stockholm, Sweden; 1Karolinska Institute, Department of Physiology and Pharmacology, Stockholm, Sweden; 3University of Gothenburg, Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy; 4University of Chile, Endocrinology and Metabolism Laboratory, West Division, School of Medicine, University of Chile, Carlos Schachtebeck 299, Interior Quinta Normal, Santiago, Chile; 5Laboratory of Animal Physiology and Endocrinology, Faculty of Veterinary Sciences, University of Concepción, Chillán, Chile; 6Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; 7Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; 8Center of Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, China; 9Karolinska Institute, Department of Physiology and Pharmacology, Sweden
Our previous study showed that polycystic ovary syndrome (PCOS)-like reproductive and metabolic phenotypes induced by maternal dihydrotestosterone (DHT)-exposure, can be passed on in mice from mothers (F0) to daughters (F1), granddaughters (F2), and even to great-granddaughters (F3). The female transmission is independent of diet-induced obesity and is mediated by transcriptional and mitochondrial perturbations of oocytes accompany. How maternal DHT-exposure and obesity affect their male progeny across generations is less known. Based on two clinical studies: a Swedish nationwide register and a Chilean case-control study, we found that sons of mothers with PCOS are more obese and have dyslipidemia. Next, we investigated whether diet-induced maternal obesity and/or prenatal DHT-exposure in mice, mimicking both the lean and the obese PCOS phenotype, result in transgenerational transmission of a PCOS-like phenotype in male offspring via male germline. We find a transmission of reproductive and metabolic dysfunction in F1 and F3 male offspring in both androgenized and obese lineages, respectively, but with stronger phenotype in the obese lineage. Small non-coding RNAs (sncRNAs) sequencing of sperm from F1 and F3 male offspring revealed common differential expressed sncRNAs (DEsncRNAs) across generations in androgenized, obese, and obese and androgenized lineages, with distinct regulatory patterns among lineages. Three of the predicted targets of PIWI-interacting RNA and micro RNAs were also differentially expressed in serum from sons of PCOS mothers. Our results reveal a previously unknown risk of reproductive and metabolic dysfunction in male progeny of PCOS mothers, which is likely caused by epigenetic germline changes by sncRNAs.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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