Metabolic Determinants of Impaired Pulmonary Function in Patients with Newly Diagnosed Type 2 Diabetes Mellitus

Röhling, Martin; Pesta, Dominik; Markgraf, Daniel F.; Straßburger, Klaus; Knebel, Birgit; Burkart, Volker; Szendroedi, Julia; Müssig, Karsten; Roden, Michael

doi:10.1055/a-0653-7135

Cited by 19 publications

(22 citation statements)

References 37 publications

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“…Decline In Lung Volumes, FEV1, FVC and Diffusion capacity ensue with aging as well as in obese subjects with further exaggeration in presence of diabetes leading to worsening restrictive pulmonary disease frequently resulting in onset of Cor pulmonale [120] [121] [122] [123] These manifestations may be attributed to unifying mechanism; lack of entry of Glucose into alveolar cells and respiratory Muscles of Chest, Diaphragm secondary to insulin resistance as well as a relative or absolute decline in insulin secretion [104].…”

Section: Pulmonary Dysfunctionmentioning

confidence: 99%

Diabetes Mellitus: Disorder of Cellular Dysfunction Due to Lack of Entry into Cell of Glucose. The Most Efficient Fuel for Cellular Function*

Kabadi¹

2021

OJEMD

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Background: Diabetes Mellitus is established to be a chronic hyperglycemic disorder secondary to altered glucose metabolism. Alternatively, hyperglycemia may be one of several manifestations in subjects with type 1 and type 2 diabetes Mellitus. Most tissues require insulin for entry of glucose, exceptions being red blood cells, renal medulla and nervous system. Hyperglycemia in intravascular compartment and other extra cellular milieu may be attributed to impaired glucose entry into endothelial cells of the vessel wall and cells in other tissues due to absence of insulin in type 1 and both insulin resistance and decline in insulin secretion in type 2 Diabetes. Objective: Hypothesis is proposed that Diabetes mellitus is a disorder of cellular dysfunction due to lack of entry of glucose, the most efficient fuel. Literature review was conducted to establish the perspective. Results: Declines in both phases of insulin secretion are induced by lack of glucose entry into pancreatic beta cells. Hyperglycemia is perpetuated by increased hepatic glucose production caused by sustained hyperglucagonemia secondary to lack of glucose entry into the pancreatic alpha cells. Moreover, decline in insulin secretion by beta cells and rise in glucagon release by alpha cells are enhanced by fall in GLP1 and GIP caused by dysfunction of L cells and K cells secondary to lack of glucose entry in both types of diabetes. Increased prevalence of infections and thromboembolic events may be attributed to dysfunction of leukocytes and platelets due to impaired glucose entry. Finally, alterations in metabolemics including Adiponectin, TNF alpha, Plasminogen inhibitor factor 1, Homocysteine, CRP, Lipids etc. as

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Section: Pulmonary Dysfunctionmentioning

confidence: 99%

Diabetes Mellitus: Disorder of Cellular Dysfunction Due to Lack of Entry into Cell of Glucose. The Most Efficient Fuel for Cellular Function*

Kabadi¹

2021

OJEMD

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“…5,6 Studies conducted in patients with type 2 diabetes mellitus demonstrated that hs-CRP associates negatively with lung function. 6,7 Insulin resistance and hyperinsulinemia Insulin resistance, especially seen in type 2 diabetes, contributes to increased insulin levels which leads to increased airway smooth muscle (ASM) mass and contractility that decreases muscle strength in the long run. Increased respiratory smooth muscle mass also leads to airway hypersensitivity and activation of epithelial mesenchymal trophic unit leading to airway remodeling.…”

Section: Chronic Inflammationmentioning

confidence: 99%

“…5,6 Studies conducted in patients with type 2 diabetes mellitus demonstrated that hs-CRP associates negatively with lung function. 6,7…”

Section: Chronic Inflammationmentioning

confidence: 99%

“…These changes and damages impair lung function. 7 AGE receptors are commonly found in membranes and cytoplasms of pneumocytes and macrophages in the lungs. When the AGE receptors are stimulated inflammatory response, cytokine production and endothelial vascular permeability increase and lungs' vascular network is damaged.…”

Section: Advanced Glycation End Productsmentioning

confidence: 99%

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Diabetes mellitus and the lungs

Ersoy

2020

Turkish Journal of Internal Medicine

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Diabetes mellitus is a chronic disease characterized by hyperglycemia causing damage to the vascular system. The lungs with a large vascular network are also predisposed to diabetes' vascular damage. Diabetes may lead to pulmonary parenchymal damage besides alterations in the vascular system and the alveolar-capillary membrane. Symptoms and damage caused by diabetes are usually underdiagnosed because of the large pulmonary reserves. Pulmonary involvement in diabetes is an area that draws attention in recent years. This attention increases especially with the new Coronavirus disease-2019 (COVID-19) pandemic when worse prognosis is detected in diabetics. In this review, possible mechanisms leading to pulmonary involvement and pulmonary function abnormalities in diabetes, interaction between COVID-19 and diabetes concerning lungs and the basic effects of antidiabetic drugs on the lungs are discussed in the view of the literature.

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“…Studien zeigen zwar eine Assoziation zwischen Lungenfunktionseinschränkungen und Blutglukoseauch bei Patienten ohne Diabetes mellitus. Dennoch gibt es keine Daten, die belegen, dass durch eine Verbesserung der Stoffwechselsituation auch eine Verbesserung der Lungenfunktion erreicht wird [23,24,38]. In einer Subgruppenanalyse von Patienten mit IPF und Diabetes mellitus konnte gezeigt werden, dass eine Metformintherapie ebenfalls keine positiven Effekte auf die Lungenfibrose hat [39].…”

Section: Therapeutische Ansätzeunclassified

Diabetische Pneumopathie

Kopf¹

2019

Diabetologie und Stoffwechsel

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Breathlessness or dyspnea is a frequent symptom in patients with diabetes and the first disease which has to be excluded is the coronary heart disease. However, previous epidemiological studies have shown that patients with diabetes mellitus have an increased risk for fibrotic pulmonary diseases, such as the idiopathic pulmonary fibrosis (IPF). Recent studies were able to show that patients with newly diagnosed type 2 diabetes have impaired pulmonary oxygen consumption and over 26 % of patients with long-term type 2 diabetes showed restrictive lung function with fibrotic interstitial lung diseases. Especially patients with type 2 diabetes and nephropathy had an 8-fold higher risk for lung diseases. This is not surprising since the pathomechanisms of pulmonary fibrosis and diabetic complications have much in common: reactive oxygen species induce DNA-damage with consecutive activation of inflammatory cytokines which induce fibrotic remodeling of the tissue. This leads us to the suggestion that patients with diabetes, albuminuria and breathlessness should be examined for interstitial lung disease on regular basis. However, data regarding the natural course of diabetic pneumopathy and therapeutic approaches are still missing. Small intervention studies with IPF-patients could show that sports and physical activity were able to stabilize the disease progression.

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Metabolic Determinants of Impaired Pulmonary Function in Patients with Newly Diagnosed Type 2 Diabetes Mellitus

Abstract: Recent-onset type 2 diabetes patients exhibit reductions in features of pulmonary function, which might be at least in part resulting from glucotoxicity.

Cited by 19 publications

References 37 publications

Diabetes Mellitus: Disorder of Cellular Dysfunction Due to Lack of Entry into Cell of Glucose. The Most Efficient Fuel for Cellular Function*

Diabetes Mellitus: Disorder of Cellular Dysfunction Due to Lack of Entry into Cell of Glucose. The Most Efficient Fuel for Cellular Function*

Diabetes mellitus and the lungs

Diabetische Pneumopathie

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