Diminished alveolar microvascular reserves in type 2 diabetes reflect systemic microangiopathy

William W. Chance, Chanhaeng Rhee, Cuneyt Yilmaz, D. Merrill Dane, M. Lourdes Pruneda, Philip Raskin, Connie C W Hsia

Research output: Contribution to journalArticle

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Abstract

OBJECTIVE -Alveolar microvascular function is moderately impaired in type 1 diabetes, as manifested by restriction of lung volume and diffusing capacity (DL CO). 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), DL CO, membrane diffusing capacity (measured from nitric oxide uptake [DL NO]), and pulmonary capillary blood volume (V C) 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 DL CO,DL NO, and V C at exercise were 10-25% lower compared with those in control subjects. In nonobese patients (BMI <30 kg/m 2), reductions in DL CO,DL NO, and V C 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/m 2). The slope of the increase in V C 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.

Original languageEnglish (US)
Pages (from-to)1596-1601
Number of pages6
JournalDiabetes Care
Volume31
Issue number8
DOIs
StatePublished - Aug 2008

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Type 2 Diabetes Mellitus
Carbon Monoxide
Lung
Blood Volume
Reference Values
Exercise
Ambulatory Care Facilities
Type 1 Diabetes Mellitus
Nitric Oxide
Research Design
Perfusion
Obesity
Cross-Sectional Studies
Oxygen
Membranes
Therapeutics

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Advanced and Specialized Nursing

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Diminished alveolar microvascular reserves in type 2 diabetes reflect systemic microangiopathy. / Chance, William W.; Rhee, Chanhaeng; Yilmaz, Cuneyt; Dane, D. Merrill; Pruneda, M. Lourdes; Raskin, Philip; Hsia, Connie C W.

In: Diabetes Care, Vol. 31, No. 8, 08.2008, p. 1596-1601.

Research output: Contribution to journalArticle

Chance, William W. ; Rhee, Chanhaeng ; Yilmaz, Cuneyt ; Dane, D. Merrill ; Pruneda, M. Lourdes ; Raskin, Philip ; Hsia, Connie C W. / Diminished alveolar microvascular reserves in type 2 diabetes reflect systemic microangiopathy. In: Diabetes Care. 2008 ; Vol. 31, No. 8. pp. 1596-1601.
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AU - Rhee, Chanhaeng

AU - Yilmaz, Cuneyt

AU - Dane, D. Merrill

AU - Pruneda, M. Lourdes

AU - Raskin, Philip

AU - Hsia, Connie C W

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N2 - OBJECTIVE -Alveolar microvascular function is moderately impaired in type 1 diabetes, as manifested by restriction of lung volume and diffusing capacity (DL CO). 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), DL CO, membrane diffusing capacity (measured from nitric oxide uptake [DL NO]), and pulmonary capillary blood volume (V C) 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 DL CO,DL NO, and V C at exercise were 10-25% lower compared with those in control subjects. In nonobese patients (BMI <30 kg/m 2), reductions in DL CO,DL NO, and V C 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/m 2). The slope of the increase in V C 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.

AB - OBJECTIVE -Alveolar microvascular function is moderately impaired in type 1 diabetes, as manifested by restriction of lung volume and diffusing capacity (DL CO). 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), DL CO, membrane diffusing capacity (measured from nitric oxide uptake [DL NO]), and pulmonary capillary blood volume (V C) 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 DL CO,DL NO, and V C at exercise were 10-25% lower compared with those in control subjects. In nonobese patients (BMI <30 kg/m 2), reductions in DL CO,DL NO, and V C 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/m 2). The slope of the increase in V C 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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