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Leptin Signalling in the Ovary of Diet-Induced Obese Mice Regulates Activation of Nod-Like Receptor Protein 3 Inflammasome

Marek Adamowski, Karolina Wołodko, Joana Oliveira, Juan Castillo-Fernandez, Daniel Murta, Gavin Kelsey, António M. Galvão
doi: https://doi.org/10.1101/2021.08.16.456479
Marek Adamowski
1Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research of Polish Academy of Sciences, Olsztyn, Poland
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Karolina Wołodko
1Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research of Polish Academy of Sciences, Olsztyn, Poland
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Joana Oliveira
2Centro de Investigação em Ciências Veterinárias, Lusófona University, Lisbon, Portugal
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Juan Castillo-Fernandez
3Epigenetics Programme, The Babraham Institute, Cambridge, CB22 3AT, UK
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Daniel Murta
4Centro de Investigação Interdisciplinar Egas Moniz (CiiEM), Escola Superior de Saúde Egas Moniz, Campus Universitário, Quinta da Granja, Monte de Caparica, Portugal
5C.I.I.S.A., Faculty of Veterinary Medicine, University of Lisbon, Lisbon, Portugal
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Gavin Kelsey
3Epigenetics Programme, The Babraham Institute, Cambridge, CB22 3AT, UK
6Centre for Trophoblast Research, University of Cambridge, Cambridge, CB2 3EG, UK
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António M. Galvão
1Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research of Polish Academy of Sciences, Olsztyn, Poland
3Epigenetics Programme, The Babraham Institute, Cambridge, CB22 3AT, UK
6Centre for Trophoblast Research, University of Cambridge, Cambridge, CB2 3EG, UK
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  • For correspondence: antonio.galvao@babraham.ac.uk
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1 Abstract

Obesity leads to ovarian dysfunction and the establishment of local leptin resistance. The aim of our study was to characterise levels of Nod-Like Receptor Protein 3 (NLRP3) inflammasome activation during obesity progression in the mouse ovaries and liver and test the putative role of leptin on its regulation. C57BL/6J mice were treated with equine chorionic gonadotropin (eCG) or human chorionic gonadotropin (hCG) for oestrous cycle synchronisation and ovaries collection. In diet-induced obesity (DIO) model, mice were fed chow diet (CD) or high fat diet (HFD) for 4 or 16 weeks (wk), whereas in hyperleptinemic model (LEPT), mice were injected with leptin for 16 days (16L) or saline (16C) and in the genetic obese leptin-deficient ob/ob (+/? and -/-) animals were fed CD for 4wk. Either ovaries and liver were collected, as well as cumulus cells (CCs) after superovulation from DIO and LEPT. In DIO protocol, protein expression of NLRP3 inflammasome components was increased in 4wk HFD, but decreased in 16wk HFD. Moreover LEPT and ob/ob models revealed NLRP3 and IL-1β upregulation in 16L and downregulation in ob/ob. Transcriptome analysis of CC showed common genes between LEPT and 4wk HFD modulating NLRP3 inflammasome. Moreover analysis in the liver showed upregulation of NLRP3 protein only after 16wk HFD, but also the downregulation of NLRP3 protein in ob/ob-/-. We showed the link between leptin signalling and NLRP3 inflammasome activation in the ovary throughout obesity progression in mice, elucidating the molecular mechanisms underpinning ovarian failure in maternal obesity.

Competing Interest Statement

The authors have declared no competing interest.

Footnotes

  • https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE180300

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Leptin Signalling in the Ovary of Diet-Induced Obese Mice Regulates Activation of Nod-Like Receptor Protein 3 Inflammasome
Marek Adamowski, Karolina Wołodko, Joana Oliveira, Juan Castillo-Fernandez, Daniel Murta, Gavin Kelsey, António M. Galvão
bioRxiv 2021.08.16.456479; doi: https://doi.org/10.1101/2021.08.16.456479
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Leptin Signalling in the Ovary of Diet-Induced Obese Mice Regulates Activation of Nod-Like Receptor Protein 3 Inflammasome
Marek Adamowski, Karolina Wołodko, Joana Oliveira, Juan Castillo-Fernandez, Daniel Murta, Gavin Kelsey, António M. Galvão
bioRxiv 2021.08.16.456479; doi: https://doi.org/10.1101/2021.08.16.456479

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