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Published online May 20, 2008
Diabetes Care 31:1596-1601, 2008
DOI: 10.2337/dc07-2323
© 2008 by the American Diabetes Association
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Pathophysiology/Complications
Original Research

Diminished Alveolar Microvascular Reserves in Type 2 Diabetes Reflect Systemic Microangiopathy

William W. Chance, MSEE, Chanhaeng Rhee, MD, Cuneyt Yilmaz, PHD, D. Merrill Dane, MS, M. Lourdes Pruneda, MSN, Philip Raskin, MD and Connie C.W. Hsia, MD

From the Department of Internal Medicine, University of Texas Southwestern, Dallas, Texas

Corresponding author: Connie C.W. Hsia, connie.hsia{at}utsouthwestern.edu

OBJECTIVE—Alveolar microvascular function is moderately impaired in type 1 diabetes, as manifested by restriction of lung volume and diffusing capacity (DLCO). We examined whether similar impairment develops in type 2 diabetes and defined the physiologic sources of impairment as well as the relationships to glycemia and systemic microangiopathy.

RESEARCH DESIGN AND METHODS—A cross-sectional study was conducted at a university-affiliated diabetes treatment center and outpatient diabetes clinic, involving 69 nonsmoking type 2 diabetic patients without overt cardiopulmonary disease. Lung volume, pulmonary blood flow (Q), DLCO, membrane diffusing capacity (measured from nitric oxide uptake [DLNO]), and pulmonary capillary blood volume (VC) were determined at rest and exercise for comparison with those in 45 healthy nonsmokers as well as with normal reference values.

RESULTS—In type 2 diabetic patients, peak levels of oxygen uptake, Q and DLCO, DLNO, and VC at exercise were 10–25% lower compared with those in control subjects. In nonobese patients (BMI <30 kg/m2), reductions in DLCO, DLNO, and VC were fully explained by the lower lung volume and peak Q, but these factors did not fully explain the impairment in obese patients (BMI >30 kg/m2). The slope of the increase in VC with respect to Q was reduced ~20% in patients regardless of BMI, consistent with impaired alveolar-capillary recruitment. Functional impairment was directly related to A1C level, retinopathy, neuropathy, and microalbuminuria in a sex-specific manner.

CONCLUSIONS—Alveolar microvascular reserves are reduced in type 2 diabetes, reflecting restriction of lung volume, alveolar perfusion, and capillary recruitment. This reduction correlates with glycemic control and extrapulmonary microangiopathy and is aggravated by obesity.


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