Fonction pulmonaire du patient diabétique

Fontaine-Delaruelle, C.; Viart-Ferber, C.; Luyton, Cédric; Couraud, S.

doi:10.1016/j.pneumo.2015.03.010

Cited by 19 publications

(15 citation statements)

References 18 publications

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“…Diabetic patients exhibit a high risk of pulmonary disorders that are often associated with restrictive impairment of lung function. Many cross-sectional studies have consistently shown that when compared with healthy subjects, patients with diabetes have significant decreases in many parameters including lower vital capacity, medium expiratory flow, expiratory residual volume, the total lung capacity (TLC), forced vital capacity (FVC), and forced expiratory volume in one second (FEV1) [ 38 - 41 ][ 26 , 27 ]. It has also been reported that the restrictive, but not the obstructive ventilatory dysfunction, is associated with development of prediabetes and precedes the development of type 2 diabetes [ 42 ].…”

Section: Pulmonary Dysfunction In Diabetic Lung Injurymentioning

confidence: 99%

“…It has been demonstrated that there is a significant decrease in the ratio between DLCO and alveolar ventilation in pulmonary gas exchange in the diabetic group when compared with that in healthy controls [ 54 ]. DLCO is predominantly due to a low membrane diffusing capacity (DMCO) [ 55 ] while in type 2 diabetes both DMCO and capillary blood volume are reduced [ 38 ]. Interestingly, at peak exercise, type 1 diabetic subjects demonstrated a decreased DLCO when corrected for cardiac output (DLCO/Q) [ 56 ].…”

Section: Pulmonary Dysfunction In Diabetic Lung Injurymentioning

confidence: 99%

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Potential Biochemical Mechanisms of Lung Injury in Diabetes

Zheng¹,

Wu²,

Jin³

et al. 2017

Aging and disease

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Accumulating evidence has shown that the lung is one of the target organs for microangiopathy in patients with either type 1 or type 2 diabetes mellitus (DM). Diabetes is associated with physiological and structural abnormalities in the diabetic lung concurrent with attenuated lung function. Despite intensive investigations in recent years, the pathogenic mechanisms of diabetic lung injury remain largely elusive. In this review, we summarize currently postulated mechanisms of diabetic lung injury. We mainly focus on the pathogenesis of diabetic lung injury that implicates key pathways, including oxidative stress, non-enzymatic protein glycosylation, polyol pathway, NF-κB pathway, and protein kinase c pathway. We also highlight that while numerous studies have mainly focused on tissue or cell damage in the lung, studies focusing on mitochondrial dysfunction in the diabetic lung have remained sketchy. Hence, further understanding of mitochondrial mechanisms of diabetic lung injury should provide invaluable insights into future therapeutic approaches for diabetic lung injury.

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Section: Pulmonary Dysfunction In Diabetic Lung Injurymentioning

confidence: 99%

Section: Pulmonary Dysfunction In Diabetic Lung Injurymentioning

confidence: 99%

Potential Biochemical Mechanisms of Lung Injury in Diabetes

Zheng¹,

Wu²,

Jin³

et al. 2017

Aging and disease

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“…In diabetes patients with or without poor glycemic control or microangiopathic complications, but without lung disease, studies revealed a reduction of CO diffusing capacity and a restrictive pattern of spirometric parameters [6, 18, 20], but no correlation with the duration of diabetes [20]. The potential role of obesity was addressed by comparing diabetes with obese non-diabetes patients [21]; TLCO was reduced in diabetes. In addition, diabetic neuropathy, macrovascular complications, impaired renal function and insulin treatment were linked to low TLCO [21].…”

Section: Discussionmentioning

confidence: 99%

“…The potential role of obesity was addressed by comparing diabetes with obese non-diabetes patients [21]; TLCO was reduced in diabetes. In addition, diabetic neuropathy, macrovascular complications, impaired renal function and insulin treatment were linked to low TLCO [21]. A meta-analysis summarized the association between diabetes and a restrictive lung function pattern in terms of FEV 1 , FVC and CO diffusing capacity, irrespective of BMI, smoking, diabetes duration and HbA1c levels in lung-healthy subjects [22].…”

Section: Discussionmentioning

confidence: 99%

Transfer factor for carbon monoxide in patients with COPD and diabetes: results from the German COSYCONET cohort

et al. 2017

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BackgroundAn impairment of CO diffusing capacity has been shown in diabetic patients without lung disease. We analyzed how diffusing capacity in patients with COPD is affected by the concurrent diagnosis of diabetes.MethodsData from the initial visit of the German COPD cohort COSYCONET were used for analysis. 2575 patients with complete lung function data were included, among them 358 defined as diabetics with a reported physician diagnosis of diabetes and/or specific medication. Pairwise comparisons between groups and multivariate regression models were used to identify variables predicting the CO transfer factor (TLCO%pred) and the transfer coefficient (KCO%pred).ResultsCOPD patients with diabetes differed from those without diabetes regarding lung function, anthropometric, clinical and laboratory parameters. Moreover, gender was an important covariate. After correction for lung function, gender and body mass index (BMI), TLCO%pred did not significantly differ between patients with and without diabetes. The results for the transfer coefficient KCO were similar, demonstrating an important role of the confounding factors RV%pred, TLC%pred, ITGV%pred, FEV1%pred, FEV1/FVC, age, packyears, creatinine and BMI. There was not even a tendency towards lower values in diabetes.ConclusionThe analysis of data from a COPD cohort showed no significant differences of CO transport parameters between COPD patients with and without diabetes, if BMI, gender and the reduction in lung volumes were taken into account. This result is in contrast to observations in lung-healthy subjects with diabetes and raises the question which factors, among them potential anti-inflammatory effects of anti-diabetes medication are responsible for this finding.

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“…Patients with T2DM exhibit pulmonary system alterations that likely contribute to reduced exercise capacity and would be expected to increase the work of the respiratory muscles and thus blood flow (BF) requirement to these muscles during exercise. For example, compared to healthy controls, T2DM patients exhibit a reduced vital capacity and total lung volume (Anandhalakshmi et al, 2013;Fontaine-Delaruelle et al, 2016), loss of elastic properties of the lung and respiratory muscle strength (Anandhalakshmi et al, 2013;Correa et al, 2011;Fuso et al, 2012;Zineldin et al, 2015), thickening of the alveolar epithelial and endothelial capillary basal lamina (Foster et al, 2010;Weynand et al, 1999), and impaired lung diffusion capacity at rest and during submaximal exercise (Anandhalakshmi et al, 2013;Chance et al, 2008;Saler et al, 2009). During exercise, T2DM patients, compared to healthy adults, have an exaggerated ventilatory response relative to CO 2 production (i.e.…”

Section: Introductionmentioning

confidence: 99%

Type II diabetes accentuates diaphragm blood flow increases during submaximal exercise in the rat

Butenas

Smith

Copp

et al. 2020

Respiratory Physiology & Neurobiology

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We investigated the effect of type 2 diabetes mellitus (T2DM) on respiratory muscle blood flow (BF) during exercise. Using the Goto-Kakizaki (GK) rat model of T2DM, we hypothesized that diaphragm, intercostal and transverse abdominis BFs (radiolabeled microspheres) would be higher in male GK rats (n=10) compared to healthy male Wistar controls (CON; n=8) during submaximal exercise (20 m/min, 10% grade). Blood glucose was significantly higher in GK (246±29 mg/dL) compared to CON (103±4 mg/dL; P<0.01). Respiratory muscle BFs were not different at rest (P>0.50). From rest to submaximal exercise, respiratory muscle BFs increased in both groups to all muscles (P<0.01). During submaximal exercise GK rats had higher diaphragm BFs (GK: 189±13; CON: 138±14 mL/min/100g, P<0.01), and vascular conductance (GK: 1.4±0.1; CON: 1.0±0.1 ml/min/mmHg/100g; P<0.01) compared to CON. There were no differences in intercostal or transverse abdominis BF or VC during exercise (P>0.15). These findings suggest that submaximal exercise requires a higher diaphragm BF and VC in T2DM compared to healthy counterparts.

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Fonction pulmonaire du patient diabétique

Cited by 19 publications

References 18 publications

Potential Biochemical Mechanisms of Lung Injury in Diabetes

Potential Biochemical Mechanisms of Lung Injury in Diabetes

Transfer factor for carbon monoxide in patients with COPD and diabetes: results from the German COSYCONET cohort

Type II diabetes accentuates diaphragm blood flow increases during submaximal exercise in the rat

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