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Feifei Cheng Department of Medicine and Therapeutics The Chinese University of Hong Kong, Hong Kong, Hong Kong

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Noel Yat Hey Ng Department of Medicine and Therapeutics The Chinese University of Hong Kong, Hong Kong, Hong Kong

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Claudia Ha Ting Tam Department of Medicine and Therapeutics The Chinese University of Hong Kong, Hong Kong, Hong Kong
Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong, Hong Kong

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Yuying Zhang Department of Medicine and Therapeutics The Chinese University of Hong Kong, Hong Kong, Hong Kong
Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong, Hong Kong

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Cadmon King Poo Lim Department of Medicine and Therapeutics The Chinese University of Hong Kong, Hong Kong, Hong Kong
Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong

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Guozhi Jiang Department of Medicine and Therapeutics The Chinese University of Hong Kong, Hong Kong, Hong Kong
Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong, Hong Kong

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Alex Chi Wai Ng Department of Medicine and Therapeutics The Chinese University of Hong Kong, Hong Kong, Hong Kong

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Tiffany Tse Ling Yau Department of Medicine and Therapeutics The Chinese University of Hong Kong, Hong Kong, Hong Kong

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Lai Ping Cheung Department of Obstetrics and Gynaecology, The Chinese University of Hong Kong, Hong Kong, Hong Kong

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Aimin Xu Department of Medicine, Li Ka Shing (LKS) Faculty of Medicine, University of Hong Kong, Hong Kong, Hong Kong
State Key Laboratory of Pharmaceutical Biotechnology, University of Hong Kong, Hong Kong, Hong Kong
Department of Pharmacy and Pharmacology, LKS Faculty of Medicine, University of Hong Kong, Hong Kong, Hong Kong

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Juliana C N Chan Department of Medicine and Therapeutics The Chinese University of Hong Kong, Hong Kong, Hong Kong
Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Chinese University of Hong Kong-Shanghai Jiao Tong University Joint Research Centre in Diabetes Genomics and Precision Medicine, Hong Kong, Hong Kong

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Ronald C W Ma Department of Medicine and Therapeutics The Chinese University of Hong Kong, Hong Kong, Hong Kong
Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Chinese University of Hong Kong-Shanghai Jiao Tong University Joint Research Centre in Diabetes Genomics and Precision Medicine, Hong Kong, Hong Kong

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Women with polycystic ovary syndrome (PCOS) have an increased risk of developing type 2 diabetes. FGF19, FGF21 and lipocalin-2 have emerged as important markers of metabolic risk. This study aims to compare the levels of FGF19, FGF21 and lipocalin-2 between subjects with or without PCOS, and to investigate the relationship between proteins and diabetes progression. In this nested case–control cohort study, 128 Chinese PCOS women and 128 controls were recruited and followed-up. All subjects underwent the oral glucose tolerance test for the evaluation of glycaemic status. Baseline serum protein levels were measured using ELISA. Compared with controls, PCOS subjects had higher levels of FGF19 (P < 0.001) and FGF21 (P = 0.022), but had lower lipocalin-2 (P < 0.001). In total, 20.8% of PCOS and 9.2% of controls developed diabetes over a mean duration of 10.4 ± 1.2 and 11.3 ± 0.5 years, respectively. Logistic regression analyses suggested FGF19 was positively associated with diabetes progression in controls, after adjusting for age, follow-up duration, waist and fasting glucose (P = 0.026, odds ratio (OR) (95% CI): 7.4 (1.3–43.6)), and the positive relationship between FGF21 and diabetes progression in controls was attenuated by adjusting for age and follow-up duration (P = 0.183). Lipocalin-2 was positively correlated with diabetes progression in PCOS group (P = 0.026, OR (95% CI)): 2.5 (1.1–5.6)); however, this became attenuated after adjusting for waist and fasting glucose (P = 0.081). In conclusion, there is differential expression of FGF19, FGF21, and lipocalin-2 in PCOS. The serum level of FGF19, and FGF21 is associated with diabetes progression in women without PCOS, while lipocalin-2 was related to diabetes progression in PCOS women.

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