TY - JOUR
T1 - Insulin resistance in transgender individuals correlates with android fat mass
AU - Bretherton, Ingrid
AU - Spanos, Cassandra
AU - Leemaqz, Shalem Y.
AU - Premaratne, Gehan
AU - Grossmann, Mathis
AU - Zajac, Jeffrey D.
AU - Cheung, Ada S.
N1 - Funding Information:
The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: IB is supported by an Australian Government Research Training Program Scholarship and a Rowden White Scholarship (# 184409), The University of Melbourne. AC is supported by an Australian Government National Health and Medical Research Council Early Career Fellowship (#1143333) and receives research support by the Viertel Charitable Foundation Clinical Investigator Award, Endocrine Society of Australia Postdoctoral Award, Austin Medical Research Foundation and the Royal Australasian College of Physicians Vincent Fairfax Family Foundation.
Funding Information:
The authors would like to acknowledge contribution of the participants who volunteered their time for this study. The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: IB is supported by an Australian Government Research Training Program Scholarship and a Rowden White Scholarship (# 184409), The University of Melbourne. AC is supported by an Australian Government National Health and Medical Research Council Early Career Fellowship (#1143333) and receives research support by the Viertel Charitable Foundation Clinical Investigator Award, Endocrine Society of Australia Postdoctoral Award, Austin Medical Research Foundation and the Royal Australasian College of Physicians Vincent Fairfax Family Foundation.
Funding Information:
AC has received speaker’s honoraria from Astra Zeneca and Merck Sharp & Dohme. MG has received research funding from Bayer, Weight Watchers, Lilly Otzuka, and speaker’s honoraria from Besins Health Care and Novartis. All other authors have no conflicts of interest to declare.
Publisher Copyright:
© The Author(s), 2021.
PY - 2021
Y1 - 2021
N2 - Background: Transgender individuals receiving gender-affirming hormone therapy (GAHT) are at increased risk of adverse cardiovascular outcomes. This may be related to effects on body composition and insulin resistance. Aims: To examine relationships between body fat distribution and insulin resistance in transgender individuals on established GAHT. Methods: Comparisons of body composition (dual energy X-ray absorptiometry) and insulin resistance [Homeostasis Model of Insulin Resistance (HOMA2-IR)] were made between transgender individuals (43 trans men and 41 trans women) on established GAHT (>12 months) and age-matched cisgender controls (30 males and 48 females). Multiple linear regressions were used to examine the relationship between HOMA2-IR and fat mass with gender, adjusting for age and total duration of GAHT and Pearson correlation coefficients are reported. Results: Compared with control cisgender women, trans men had mean difference of +7.8 kg (4.0, 11.5), p < 0.001 in lean mass and higher android:gynoid fat ratio [0.2 (0.1, 0.3), p < 0.001], but no difference in overall fat mass or insulin resistance. Compared with control cisgender men, trans women had median difference in lean mass of −6.9 kg (–10.6, –3.1), p < 0.001, fat mass of +9.8 kg (3.9, 14.5), p = 0.001, lower android:gynoid fat ratio −0.1 (–0.2,–0.0), p < 0.05), and higher insulin resistance 1.6 (1.3–1.9), p < 0.001). Higher HOMA2-IR correlated with higher android (r2 = 0.712, p < 0.001) and gynoid (r2 = 0.572, p < 0.001) fat mass in both trans men and trans women. Conclusion: Android fat more strongly correlates with insulin resistance than gynoid fat in transgender individuals. Higher fat mass and insulin resistance in trans women may predispose to increased cardiovascular risk. Despite adverse fat distribution, insulin resistance was not higher in trans men.
AB - Background: Transgender individuals receiving gender-affirming hormone therapy (GAHT) are at increased risk of adverse cardiovascular outcomes. This may be related to effects on body composition and insulin resistance. Aims: To examine relationships between body fat distribution and insulin resistance in transgender individuals on established GAHT. Methods: Comparisons of body composition (dual energy X-ray absorptiometry) and insulin resistance [Homeostasis Model of Insulin Resistance (HOMA2-IR)] were made between transgender individuals (43 trans men and 41 trans women) on established GAHT (>12 months) and age-matched cisgender controls (30 males and 48 females). Multiple linear regressions were used to examine the relationship between HOMA2-IR and fat mass with gender, adjusting for age and total duration of GAHT and Pearson correlation coefficients are reported. Results: Compared with control cisgender women, trans men had mean difference of +7.8 kg (4.0, 11.5), p < 0.001 in lean mass and higher android:gynoid fat ratio [0.2 (0.1, 0.3), p < 0.001], but no difference in overall fat mass or insulin resistance. Compared with control cisgender men, trans women had median difference in lean mass of −6.9 kg (–10.6, –3.1), p < 0.001, fat mass of +9.8 kg (3.9, 14.5), p = 0.001, lower android:gynoid fat ratio −0.1 (–0.2,–0.0), p < 0.05), and higher insulin resistance 1.6 (1.3–1.9), p < 0.001). Higher HOMA2-IR correlated with higher android (r2 = 0.712, p < 0.001) and gynoid (r2 = 0.572, p < 0.001) fat mass in both trans men and trans women. Conclusion: Android fat more strongly correlates with insulin resistance than gynoid fat in transgender individuals. Higher fat mass and insulin resistance in trans women may predispose to increased cardiovascular risk. Despite adverse fat distribution, insulin resistance was not higher in trans men.
KW - body composition
KW - gender dysphoria
KW - gender identity
KW - insulin resistance
KW - transgender persons
KW - transsexualism
UR - https://www.scopus.com/pages/publications/85099797716
U2 - 10.1177/2042018820985681
DO - 10.1177/2042018820985681
M3 - Article
AN - SCOPUS:85099797716
SN - 2042-0188
VL - 12
JO - Therapeutic Advances in Endocrinology and Metabolism
JF - Therapeutic Advances in Endocrinology and Metabolism
ER -