Insulin resistance is related to impaired lung function in morbidly obese women: a case-control study

Diabetes Metab Res Rev. 2010 Nov;26(8):639-45. doi: 10.1002/dmrr.1131. Epub 2010 Sep 29.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Case-Control Studies
  • Diabetes Mellitus, Type 2 / etiology
  • Female
  • Forced Expiratory Flow Rates / physiology
  • Forced Expiratory Volume / physiology
  • Humans
  • Insulin Resistance / physiology*
  • Lung / physiopathology*
  • Middle Aged
  • Obesity, Morbid / complications*
  • Pulmonary Diffusing Capacity / physiology