Hyperandrogenemia in early adulthood is an independent risk factor for abnormal glucose metabolism in middle age |
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Author: | Tuorila, Katri1; Ollila, Meri-Maija1; Järvelin, Marjo-Riitta2,3,4,5; |
Organizations: |
1Department of Obstetrics and Gynecology, University of Oulu and Oulu University Hospital, Medical Research Center, PEDEGO Research Unit, Oulu, Finland 2MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK 3Center for Life Course Health Research, Faculty of Medicine, University of Oulu, Oulu, Finland
4Unit of Primary Health Care, Oulu University Hospital, OYS, Oulu, Finland
5Department of Life Sciences, College of Health and Life Sciences, Brunel University London, London, UK 6Department of Obstetrics and Gynecology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland 7Institute of Reproductive and Developmental Biology, Imperial College London, London, UK 8NordLab Oulu, Department of Clinical Chemistry, University of Oulu and Oulu University Hospital, Medical Research Center Oulu, Oulu, Finland |
Format: | article |
Version: | published version |
Access: | open |
Online Access: | PDF Full Text (PDF, 0.4 MB) |
Persistent link: | http://urn.fi/urn:nbn:fi-fe2022013111513 |
Language: | English |
Published: |
Endocrine society,
2021
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Publish Date: | 2022-01-31 |
Description: |
AbstractContext: The role of androgen excess as a contributing factor to abnormal glucose metabolism (AGM) and insulin resistance in women remains controversial. Objectives: To investigate whether hyperandrogenemia (HA) estimated by serum testosterone (T) level and free androgen index (FAI) at ages 31 and 46 years is associated with insulin resistance, insulin secretion and AGM by age 46. Design: Prospective study including 5889 females followed at ages 31 and 46 years. Setting: General community. Participants: Women with HA were compared with normoandrogenic women at ages 31 and 46 years. Intervention: None. Main outcome measurements: AGM, including prediabetes and type 2 diabetes mellitus, homeostatic model assessments of insulin resistance (HOMA–IR) and of pancreatic β-cell function (HOMA–B). Results: At age 31 years, HA women displayed increased HOMA–IR (P = 0.002), HOMA–B (P = 0.007), and higher fasting insulin (P = 0.03) than normoandrogenic women after adjusting for body mass index (BMI). At age 46 years, there was a nonsignificant trend toward higher fasting glucose (P = 0.07) and glycated hemoglobin A1 (P = 0.07) levels in HA women. Women in the highest T quartile (odds ratio [OR] = 1.80; 95%CI, 1.15–2.82) at age 31 years and in the 2 highest FAI quartiles at ages 31 (Q4: OR = 3.76; 95% CI, 2.24–6.32) and 46 (Q4: OR = 2.79; 95% CI, 1.74–4.46) years had increased risk for AGM, independently of BMI, when compared with women in Q1. SHBG was inversely associated with AGM (at age 31 years: Q4: OR = 0.37; 95% CI, 0.23–0.60, at age 46 years: Q4: OR = 0.28; 95% CI, 0.17–0.44). Conclusions: Hyperandrogenemia and low SHBG in early and middle age associates with AGM independently of BMI. see all
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Series: |
Journal of clinical endocrinology & metabolism |
ISSN: | 0021-972X |
ISSN-E: | 1945-7197 |
ISSN-L: | 0021-972X |
Volume: | 106 |
Issue: | 11 |
Pages: | e4621 - e4633 |
DOI: | 10.1210/clinem/dgab456 |
OADOI: | https://oadoi.org/10.1210/clinem/dgab456 |
Type of Publication: |
A1 Journal article – refereed |
Field of Science: |
3123 Gynaecology and paediatrics 3121 General medicine, internal medicine and other clinical medicine |
Subjects: | |
Funding: |
NFBC1966 received financial support from University of Oulu Grant no. 65354 and no. 24000692, Oulu University Hospital Grant no. 2/97, 8/97 and no. 24301140, Ministry of Health and Social Affairs Grant no. 23/251/97, 160/97, 190/97, National Institute for Health and Welfare, Helsinki Grant no. 54121, Regional Institute of Occupational Health, Oulu, Finland Grant no. 50621, 54231, ERDF European Regional Development Fund Grant no. 539/2010 A31592, National Institute for Health Research (UK), Medical Research Council (UK) (Program Grant G0802782) and Genesis Research Trust (UK) Grant no. P58199. This work was also supported by grants from the Finnish Medical Foundation, the North Ostrobothnia Regional Fund, Academy of Finland (315921, 321763, 104781, 120315, 129269, 1114194, 24300796, 295760), the Sigrid Juselius Foundation and Medical Research Center Oulu. The study is not supported or sponsored by any commercial organization, grant, or fund. |
Academy of Finland Grant Number: |
315921 321763 295760 114194 129269 |
Detailed Information: |
315921 (Academy of Finland Funding decision) 321763 (Academy of Finland Funding decision) 295760 (Academy of Finland Funding decision) 114194 (Academy of Finland Funding decision) 129269 (Academy of Finland Funding decision) |
Copyright information: |
© The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium,
provided the original work is properly cited. |
https://creativecommons.org/licenses/by/4.0/ |