Open AccessPerturbed adipose tissue hydrogen peroxide metabolism in centrally obese men: Association with insulin resistance
Author(s) -
May G. Akl,
Eman Fawzy,
Maha M. Deif,
Ahmed Farouk,
Amany Elshorbagy
Publication year - 2017
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0177268
Subject(s) - medicine , endocrinology , insulin resistance , adipose tissue , obesity , catalase , glutathione peroxidase , homeostatic model assessment , body mass index , insulin , chemistry , overweight , oxidative stress
Objective Although adipose tissue hydrogen peroxide (H 2 O 2 ) and its metabolizing enzymes have been linked to obesity and insulin resistance in animal studies, this relation remains to be evaluated in humans. Methods Non-diabetic men (N = 43, median age, 49 (37, 54 y)) undergoing abdominal surgeries were studied. Participants were classified by body mass index (BMI) into normal-weight (N = 19), or overweight/obese (Ow/Ob; BMI ≥25; N = 24). Centrally obese men were identified by waist-height ratio ≥0.5. H 2 O 2 and activities of superoxide dismutase, catalase and glutathione peroxidase enzymes were assayed in subcutaneous fat samples, and visceral fat (available from N = 33), and their associations with anthropometric parameters, fasting serum lipids, and the homeostasis model of insulin resistance (HOMA-IR) were tested using correlations and multivariate linear regression. Results H 2 O 2 concentrations and catalase activity were increased in visceral fat from Ow/Ob men, compared to normal-weight subjects (+32%, P = 0.038 and +51%, P = 0.043 respectively). Centrally obese subjects had >2-fold higher superoxide dismutase activity (P = 0.005), 46% higher H 2 O 2 (P = 0.028), and 89% higher catalase activity (P = 0.009) in visceral fat, compared to lean subjects. Central obesity did not alter these markers in subcutaneous fat, apart from a 50% increase in catalase, and did not affect glutathione peroxidase in either fat depot. H 2 O 2 in visceral fat positively correlated with insulin resistance (r = 0.40, P = 0.032). Catalase activity in visceral fat was an independent determinant of HOMA-IR, explaining ~18% of the variance ( ß = 0.42, P = 0.016), after adjustment for age and BMI. Conclusion These findings suggest that adipose tissue catalase shows compensatory up-regulation in response to obesity-induced H 2 O 2 accumulation, and that perturbed H 2 O 2 metabolism in visceral fat is linked to insulin resistance in obese humans.