Clinical Investigations

The Effect of Continuous Positive Airway Pressure Treatment on Insulin Sensitivity in Patients with Obstructive Sleep Apnoea Syndrome and Type 2 Diabetes
Igor Alexander Harsch^a, Simin Pour Schahin^a, Kerstin Brückner^a, Martin Radespiel-Tröger^b, Florian S. Fuchs^a, Eckhart Georg Hahn^a, Peter Christopher Konturek^a, Tobias Lohmann^a, Joachim Hans Ficker<sup>a

a</sup>1st Department of Medicine,
^bDepartment of Medical Informatics, Biometrics and Epidemiology, Friedrich Alexander University Erlangen-Nürnberg, Erlangen, Germany

Address of Corresponding Author

Respiration 2004;71:252-259 (DOI: 10.1159/000077423)

  Key Words

• Insulin resistance
• Continuous positive airwaypressure treatment
• Diabetes mellitus
• Obstructivesleep apnoea
• Leptin
• Obesity

  Abstract

Background: The obstructive sleep apnoea syndrome (OSA) is a frequent condition, as well as type 2 diabetes mellitus. Both diseases are characterized by insulin resistance. Objectives: The aim of this study was to establish whether OSA is an independent risk factor for increased insulin resistance in diabetics. For this purpose, we tested the hypothesis that the insulin sensitivity in patients with type 2 diabetes and OSA can be improved by 2 days or 3 months of continuous positive airway pressure (CPAP) treatment. Methods: In 9 obese patients with type 2 diabetes and OSA [apnoea/hypopnoea index 43.1 ± 21.3; body mass index (BMI) 37.3 ± 5.6 kg/m²] and good glycaemic control on oral antidiabetics or on diet alone (HbA1c 6.4 ± 0.7%), the insulin sensitivity index (ISI) was established by euglycaemic hyperinsulinaemic clamp tests at baseline, after 2 days and after 3 months of effective CPAP treatment. Results: ISI was unchanged after 2 days of CPAP treatment, but was significantly improved after 3 months (4.38 ± 2.94 vs. 2.74 ± 2.25 at baseline; p = 0.021), without any significant changes in BMI. Glycaemic control was unaffected after 3 months (HbA1c 6.3 ± 0.6%; not significant). Fasting leptin levels showed no significant changes. Conclusions: These results indicate that OSA itself is an independent risk factor for insulin resistance. This effect may be explained by the elevated sympathetic activity in OSA.

Copyright © 2004 S. Karger AG, Basel

  Author Contacts

Dr. med. Igor Alexander Harsch, 1st Dept. of Medicine, Friedrich Alexander University
Division of Respiratory Medicine and Division of Endocrinology and Metabolism
Ulmenweg 18, DE-91054 Erlangen (Germany)
Tel. +49 9131 85 35000, Fax +49 9131 85 35231
E-Mail igor.harsch@med1.imed.uni-erlangen.de

  Article Information

Received: August 21, 2003
Accepted: November 11, 2003
Number of Print Pages : 8
Number of Figures : 2, Number of Tables : 2, Number of References : 44