Insulin improves alveolar-capillary membrane gas conductance in type 2 diabetes

Marco Guazzi, Iacopo Oreglia, Maurizio D. Guazzi

Research output: Contribution to journalArticle

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Abstract

OBJECTIVE - In type 1 diabetes, lung diffusing capacity for carbon monoxide (DL CO) may be impaired, and insulin has been shown to be beneficial in cases in which near-normal metabolic control is achieved. An influence of insulin, per se, on the alveolar-capillary membrane conductance is unexplored. We aimed at testing this possibility. RESEARCH DESIGN AND METHODS - We studied 19 life-long nonsmoking, asymptomatic patients with type 2 diabetes and normal cardiac function, whose GHb averaged 6.2 ± 0.3% with diet and hypoglycemic drugs. DL CO and its subcomponents (alveolar capillary membrane conductance [D M] and pulmonary capillary blood volume available for gas exchange [Vc]), vital capacity (VC), forced expiratory volume 1 s (FEV 1), cardiac output (CO), ejection fraction (EF), pulmonary wedge pressure (WPP), and pulmonary arteriolar resistance (PAR) were determined before and within 60 min after infusion of 50 ml saline + 10 IU of regular insulin or after saline alone on 2 consecutive days (random block design). Glycemia was kept at baseline levels during experiments by dextrose infusion. RESULTS - Percent of normal predicted DL CO averaged 84.2 ± 7.9% and in 14 patients was <100%. Insulin infusion, not saline alone, improved (P <0.01) DL CO (12%) and D M (14%) and raised DL CO to 98% of the normal predicted value. There were no variations in VC, FEV 1 CO, EF, WPP, or PAR, suggesting that the influences of the hormone on gas transfer were not mediated by changes in spirometry, volumes, and hemodynamics of the lung. CONCLUSIONS - Several cases of type 2 diabetes present with increased impedance to gas transfer across the alveolar-capillary membrane, and hypoglycemic drugs do not prevent this inconvenience. Insulin, independently of the metabolic effects, acutely improves gas exchange, possibly through a facilitation of the alveolar-capillary interface conductance.

Original languageEnglish
Pages (from-to)1802-1806
Number of pages5
JournalDiabetes Care
Volume25
Issue number10
DOIs
Publication statusPublished - Oct 2002

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Cardiac Output
Type 2 Diabetes Mellitus
Gases
Insulin
Membranes
Lung
Vital Capacity
Forced Expiratory Volume
Hypoglycemic Agents
Lung Volume Measurements
Pulmonary Wedge Pressure
Spirometry
Carbon Monoxide
Blood Volume
Electric Impedance
Type 1 Diabetes Mellitus
Reference Values
Research Design
Hemodynamics
Hormones

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Insulin improves alveolar-capillary membrane gas conductance in type 2 diabetes. / Guazzi, Marco; Oreglia, Iacopo; Guazzi, Maurizio D.

In: Diabetes Care, Vol. 25, No. 10, 10.2002, p. 1802-1806.

Research output: Contribution to journalArticle

Guazzi, Marco ; Oreglia, Iacopo ; Guazzi, Maurizio D. / Insulin improves alveolar-capillary membrane gas conductance in type 2 diabetes. In: Diabetes Care. 2002 ; Vol. 25, No. 10. pp. 1802-1806.
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abstract = "OBJECTIVE - In type 1 diabetes, lung diffusing capacity for carbon monoxide (DL CO) may be impaired, and insulin has been shown to be beneficial in cases in which near-normal metabolic control is achieved. An influence of insulin, per se, on the alveolar-capillary membrane conductance is unexplored. We aimed at testing this possibility. RESEARCH DESIGN AND METHODS - We studied 19 life-long nonsmoking, asymptomatic patients with type 2 diabetes and normal cardiac function, whose GHb averaged 6.2 ± 0.3{\%} with diet and hypoglycemic drugs. DL CO and its subcomponents (alveolar capillary membrane conductance [D M] and pulmonary capillary blood volume available for gas exchange [Vc]), vital capacity (VC), forced expiratory volume 1 s (FEV 1), cardiac output (CO), ejection fraction (EF), pulmonary wedge pressure (WPP), and pulmonary arteriolar resistance (PAR) were determined before and within 60 min after infusion of 50 ml saline + 10 IU of regular insulin or after saline alone on 2 consecutive days (random block design). Glycemia was kept at baseline levels during experiments by dextrose infusion. RESULTS - Percent of normal predicted DL CO averaged 84.2 ± 7.9{\%} and in 14 patients was <100{\%}. Insulin infusion, not saline alone, improved (P <0.01) DL CO (12{\%}) and D M (14{\%}) and raised DL CO to 98{\%} of the normal predicted value. There were no variations in VC, FEV 1 CO, EF, WPP, or PAR, suggesting that the influences of the hormone on gas transfer were not mediated by changes in spirometry, volumes, and hemodynamics of the lung. CONCLUSIONS - Several cases of type 2 diabetes present with increased impedance to gas transfer across the alveolar-capillary membrane, and hypoglycemic drugs do not prevent this inconvenience. Insulin, independently of the metabolic effects, acutely improves gas exchange, possibly through a facilitation of the alveolar-capillary interface conductance.",
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