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Elevated circulating adiponectin levels do not prevent anxiety-like behavior in a PCOS-like mouse model
Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden ; Institute of Veterinary Pharmacology and Toxicology, University of Zürich-VetSuisse, Zürich, Switzerland.
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2024 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 14, no 1, article id 563Article in journal (Refereed) Published
Abstract [en]

Polycystic ovary syndrome (PCOS) is associated with symptoms of moderate to severe anxiety and depression. Hyperandrogenism is a key feature together with lower levels of the adipocyte hormone adiponectin. Androgen exposure leads to anxiety-like behavior in female offspring while adiponectin is reported to be anxiolytic. Here we test the hypothesis that elevated adiponectin levels protect against the development of androgen-induced anxiety-like behavior. Pregnant mice overexpressing adiponectin (APNtg) and wildtypes were injected with vehicle or dihydrotestosterone to induce prenatal androgenization (PNA) in the offspring. Metabolic profiling and behavioral tests were performed in 4-month-old female offspring. PNA offspring spent more time in the closed arms of the elevated plus maze, indicating anxiety-like behavior. Intriguingly, neither maternal nor offspring adiponectin overexpression prevented an anxiety-like behavior in PNA-exposed offspring. However, adiponectin overexpression in dams had metabolic imprinting effects, shown as lower fat mass and glucose levels in their offspring. While serum adiponectin levels were elevated in APNtg mice, cerebrospinal fluid levels were similar between genotypes. Adiponectin overexpression improved metabolic functions but did not elicit anxiolytic effects in PNA-exposed offspring. These observations might be attributed to increased circulating but unchanged cerebrospinal fluid adiponectin levels in APNtg mice. Thus, increased adiponectin levels in the brain are likely needed to stimulate anxiolytic effects. 

Place, publisher, year, edition, pages
Springer Nature, 2024. Vol. 14, no 1, article id 563
Keywords [en]
Adiponectin, Androgens, Animals, Anti-Anxiety Agents, Anxiety, Female, Humans, Mice, Polycystic Ovary Syndrome, Pregnancy, Prenatal Exposure Delayed Effects, androgen, anxiolytic agent, animal, human, metabolism, mouse, ovary polycystic disease, prenatal exposure
National Category
Physiology Endocrinology and Diabetes Neurosciences Obstetrics, Gynecology and Reproductive Medicine
Research subject
Translational Medicine TRIM
Identifiers
URN: urn:nbn:se:his:diva-23545DOI: 10.1038/s41598-023-50503-8ISI: 001136960700018PubMedID: 38177175Scopus ID: 2-s2.0-85181457736OAI: oai:DiVA.org:his-23545DiVA, id: diva2:1829242
Funder
University of GothenburgSwedish Research Council, 2020-02485Magnus Bergvall Foundation, 2022-082Hjalmar Svensson's Research Foundation, 2022-291Swedish Research Council, 2021-01549Swedish Research Council, 2022-00550Novo Nordisk Foundation, NNF22OC0072904Swedish Research Council, 2018-00660NIH (National Institutes of Health), R01DK129321Swedish Research Council, 2020-01463Insamlingsstiftelsen Diabetes Wellness
Note

CC BY 4.0 DEED

© 2024, The Author(s)

Correspondence Address: A. Benrick; Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Box 423, 40530, Sweden; email: anna.benrick@gu.se

Open access funding provided by University of Gothenburg. AB holds funding from the Swedish Research Council (2020-02485), Magnus Bergvalls Foundation (2022-082), Tore Nilssons Foundation (2022-033), and Hjalmars Svenssons Foundation (2022-291). JPK holds funding from the Swedish Research Council (2021-01549), the Swiss Cancer Research Foundation (KFS-5745-02-2023-R), and Boehringer Ingelheim. ESV holds funding from the Swedish Research Council (2022-00550), the Novo Nordisk Foundation (NNF22OC0072904), KPS is funded by the Swedish Research Council (2018-00660), and the National Institutes of Health R01DK129321, and IWA. holds funding from the Swedish Research Council (2020-01463), Mary von Sydow Foundation (5022), EFSD//European Research Program on ‘New Targets for Diabetes or Obesity-related Metabolic Diseases’ supported by MSD 2022, and Diabetes Wellness Sverige. The funding bodies did not have a role in the study design and had no role in the implementation of the study.

Available from: 2024-01-18 Created: 2024-01-18 Last updated: 2024-04-15Bibliographically approved

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