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Insulin resistance is related to impaired lung function in morbidly obese women: a case–control study
Author(s) -
Lecube Albert,
Sampol Gabriel,
Muñoz Xavier,
Lloberes Patricia,
Hernández Cristina,
Simó Rafael
Publication year - 2010
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/dmrr.1131
Subject(s) - medicine , insulin resistance , vital capacity , spirometry , pulmonary function testing , body mass index , confidence interval , outpatient clinic , homeostatic model assessment , cardiology , diabetes mellitus , type 2 diabetes , obesity , gastroenterology , endocrinology , lung , lung function , asthma , diffusing capacity
Background There is growing evidence suggesting an association between type 2 diabetes and impaired pulmonary function. However, the role of insulin resistance itself remains to be elucidated. The aim of the study is to determine whether obese patients with insulin resistance without diabetes have reduced pulmonary function in comparison with non‐diabetic obese subjects without insulin resistance. Methods Seventy‐five morbidly obese non‐diabetic women [50 with an insulin resistance index (homeostasis model assessment, HOMA‐IR) ≥ 3.8—cases—and 25 with HOMA‐IR < 3.8—controls—] with a history of not smoking and without prior cardiovascular or respiratory disease were prospectively recruited in the outpatient Obesity Unit of a university hospital. Both groups were closely matched by age, body mass index and waist circumference. Pulmonary function test included a forced spirometry and static pulmonary volume measurements. Results Patients with HOMA‐IR ≥ 3.8 showed lower forced expiratory volume at 1 s [mean difference − 7.6% of predicted (95% confidence interval − 14.2 to − 0.9); p = 0.025], and also a lower maximum midexpiratory flow [mean difference − 16.4% of predicted (95% confidence interval − 30.9 to − 2.0); p = 0.026] in comparison with those with HOMA‐IR < 3.8. Significant negative correlations between HOMA‐IR and forced expiratory volume at 1 s, maximum midexpiratory flow and forced vital capacity were detected. Multiple linear regression analysis showed that HOMA‐IR (β = − 0.323, p = 0.002) and total lung capacity (β = 0.468, p < 0.001) were independently associated with forced expiratory volume at 1 s ( r 2 = 0.358). Conclusions Insulin resistance is related to respiratory function impairment in morbidly obese women. Our results strongly suggest that the metabolic pathways related to insulin resistance are crucial in initiating lung abnormalities previously described in type 2 diabetic patients. Copyright © 2010 John Wiley & Sons, Ltd.