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. 2022 Jan 10;20:12. doi: 10.1186/s12958-021-00878-y

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Altered molecular pathways of subcutaneous (SC) abdominal adipogenesis in polycystic ovary syndrome (PCOS) as a risk factor for lipotoxicity. In normal-weight PCOS women, exaggerated adipose stem cell (ASC) development to adipocytes occurs via androgen-independent mechanisms [23, 50]. Simultaneously, androgen excess inhibits early-stage adipogenesis, diminishes insulin-stimulated glucose uptake, promotes lipid storage and impairs catecholamine-stimulated lipolysis [31, 32, 35, 40, 47], favoring abdominal fat deposition and increased energy availability through hyperandrogenism and insulin resistance, respectively. These same traits are worsened in overweight/obese PCOS women who have greater preferential abdominal fat accumulation, hyperandrogenism, and systemic insulin resistance [2], along with impaired insulin suppression of lipolysis [2, 44], promoting ectopic lipid deposition and lipotoxicity [1]