Increased intestinal permeability to oral chromium (51Cr) -EDTA in human Type 2 diabetes

Objective In animal models of obesity and Type 2 diabetes, permeability of the intestine is increased because of impairment of tight junction proteins, allowing translocation of bacterial endotoxin and resulting in low‐grade systemic inflammation. This has yet to be demonstrated in humans. The objec...

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Published inDiabetic medicine Vol. 31; no. 5; pp. 559 - 563
Main Authors Horton, F., Wright, J., Smith, L., Hinton, P. J., Robertson, M. D.
Format Journal Article
LanguageEnglish
Published Oxford Blackwell Publishing Ltd 01.05.2014
Blackwell
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Abstract Objective In animal models of obesity and Type 2 diabetes, permeability of the intestine is increased because of impairment of tight junction proteins, allowing translocation of bacterial endotoxin and resulting in low‐grade systemic inflammation. This has yet to be demonstrated in humans. The objective of this study was the demonstration of increased intestinal permeability in human Type 2 diabetes. Methods We examined intestinal permeability using chromium (51Cr)‐EDTA urinary recovery in twenty well‐controlled men with Type 2 diabetes compared with control subjects matched for age, gender and BMI. Results Intestinal permeability was significantly increased (P = 0.002) in the diabetic group and was correlated to increased levels of systemic inflammatory markers high‐sensitivity C‐reactive protein (r = 0.694, P = 0.001), interleukin 6 (r = 0.548, P = 0.012) and tumour necrosis factor alpha (r = 0.564, P = 0.010). Conclusion This is the first demonstration that increased intestinal permeability may be a feature of human Type 2 diabetes. What's new? There is increasing evidence linking an inflammatory cascade originating in the gut with systemic inflammation and the development of metabolic disease. An early and key feature of this cascade is an increase in intestinal permeability, although this has yet to be demonstrated in human diabetes. In this proof of concept study, we demonstrate for the first time an increase in intestinal permeability in people with Type 2 diabetes.
AbstractList There is increasing evidence linking an inflammatory cascade originating in the gut with systemic inflammation and the development of metabolic disease. An early and key feature of this cascade is an increase in intestinal permeability, although this has yet to be demonstrated in human diabetes. In this proof of concept study, we demonstrate for the first time an increase in intestinal permeability in people with Type 2 diabetes.
Objective In animal models of obesity and Type 2 diabetes, permeability of the intestine is increased because of impairment of tight junction proteins, allowing translocation of bacterial endotoxin and resulting in low-grade systemic inflammation. This has yet to be demonstrated in humans. The objective of this study was the demonstration of increased intestinal permeability in human Type 2 diabetes. Methods We examined intestinal permeability using chromium (51Cr)-EDTA urinary recovery in twenty well-controlled men with Type 2 diabetes compared with control subjects matched for age, gender and BMI. Results Intestinal permeability was significantly increased (P = 0.002) in the diabetic group and was correlated to increased levels of systemic inflammatory markers high-sensitivity C-reactive protein (r = 0.694, P = 0.001), interleukin 6 (r = 0.548, P = 0.012) and tumour necrosis factor alpha (r = 0.564, P = 0.010). Conclusion This is the first demonstration that increased intestinal permeability may be a feature of human Type 2 diabetes. What's new? There is increasing evidence linking an inflammatory cascade originating in the gut with systemic inflammation and the development of metabolic disease. An early and key feature of this cascade is an increase in intestinal permeability, although this has yet to be demonstrated in human diabetes. In this proof of concept study, we demonstrate for the first time an increase in intestinal permeability in people with Type 2 diabetes. [PUBLICATION ABSTRACT]
In animal models of obesity and Type 2 diabetes, permeability of the intestine is increased because of impairment of tight junction proteins, allowing translocation of bacterial endotoxin and resulting in low-grade systemic inflammation. This has yet to be demonstrated in humans. The objective of this study was the demonstration of increased intestinal permeability in human Type 2 diabetes. We examined intestinal permeability using chromium ((51) Cr)-EDTA urinary recovery in twenty well-controlled men with Type 2 diabetes compared with control subjects matched for age, gender and BMI. Intestinal permeability was significantly increased (P = 0.002) in the diabetic group and was correlated to increased levels of systemic inflammatory markers high-sensitivity C-reactive protein (r = 0.694, P = 0.001), interleukin 6 (r = 0.548, P = 0.012) and tumour necrosis factor alpha (r = 0.564, P = 0.010). This is the first demonstration that increased intestinal permeability may be a feature of human Type 2 diabetes.
Objective In animal models of obesity and Type 2 diabetes, permeability of the intestine is increased because of impairment of tight junction proteins, allowing translocation of bacterial endotoxin and resulting in low‐grade systemic inflammation. This has yet to be demonstrated in humans. The objective of this study was the demonstration of increased intestinal permeability in human Type 2 diabetes. Methods We examined intestinal permeability using chromium (51Cr)‐EDTA urinary recovery in twenty well‐controlled men with Type 2 diabetes compared with control subjects matched for age, gender and BMI. Results Intestinal permeability was significantly increased (P = 0.002) in the diabetic group and was correlated to increased levels of systemic inflammatory markers high‐sensitivity C‐reactive protein (r = 0.694, P = 0.001), interleukin 6 (r = 0.548, P = 0.012) and tumour necrosis factor alpha (r = 0.564, P = 0.010). Conclusion This is the first demonstration that increased intestinal permeability may be a feature of human Type 2 diabetes. What's new? There is increasing evidence linking an inflammatory cascade originating in the gut with systemic inflammation and the development of metabolic disease. An early and key feature of this cascade is an increase in intestinal permeability, although this has yet to be demonstrated in human diabetes. In this proof of concept study, we demonstrate for the first time an increase in intestinal permeability in people with Type 2 diabetes.
In animal models of obesity and Type 2 diabetes, permeability of the intestine is increased because of impairment of tight junction proteins, allowing translocation of bacterial endotoxin and resulting in low-grade systemic inflammation. This has yet to be demonstrated in humans. The objective of this study was the demonstration of increased intestinal permeability in human Type 2 diabetes.OBJECTIVEIn animal models of obesity and Type 2 diabetes, permeability of the intestine is increased because of impairment of tight junction proteins, allowing translocation of bacterial endotoxin and resulting in low-grade systemic inflammation. This has yet to be demonstrated in humans. The objective of this study was the demonstration of increased intestinal permeability in human Type 2 diabetes.We examined intestinal permeability using chromium ((51) Cr)-EDTA urinary recovery in twenty well-controlled men with Type 2 diabetes compared with control subjects matched for age, gender and BMI.METHODSWe examined intestinal permeability using chromium ((51) Cr)-EDTA urinary recovery in twenty well-controlled men with Type 2 diabetes compared with control subjects matched for age, gender and BMI.Intestinal permeability was significantly increased (P = 0.002) in the diabetic group and was correlated to increased levels of systemic inflammatory markers high-sensitivity C-reactive protein (r = 0.694, P = 0.001), interleukin 6 (r = 0.548, P = 0.012) and tumour necrosis factor alpha (r = 0.564, P = 0.010).RESULTSIntestinal permeability was significantly increased (P = 0.002) in the diabetic group and was correlated to increased levels of systemic inflammatory markers high-sensitivity C-reactive protein (r = 0.694, P = 0.001), interleukin 6 (r = 0.548, P = 0.012) and tumour necrosis factor alpha (r = 0.564, P = 0.010).This is the first demonstration that increased intestinal permeability may be a feature of human Type 2 diabetes.CONCLUSIONThis is the first demonstration that increased intestinal permeability may be a feature of human Type 2 diabetes.
Author Robertson, M. D.
Horton, F.
Wright, J.
Hinton, P. J.
Smith, L.
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Issue 5
Keywords Endocrinopathy
Type 2 diabetes
Human
Obesity
Nutrition
Digestive system
Nutrition disorder
Gut
Oral administration
Metabolic diseases
Permeability
EDTA
Chromium
Endocrinology
Nutritional status
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2013 The Authors. Diabetic Medicine © 2013 Diabetes UK.
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Snippet Objective In animal models of obesity and Type 2 diabetes, permeability of the intestine is increased because of impairment of tight junction proteins,...
There is increasing evidence linking an inflammatory cascade originating in the gut with systemic inflammation and the development of metabolic disease. An...
In animal models of obesity and Type 2 diabetes, permeability of the intestine is increased because of impairment of tight junction proteins, allowing...
Objective In animal models of obesity and Type 2 diabetes, permeability of the intestine is increased because of impairment of tight junction proteins,...
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SubjectTerms Administration, Oral
Biological and medical sciences
Biomarkers - metabolism
C-Reactive Protein - metabolism
Case-Control Studies
Cell Membrane Permeability - physiology
Chromium Radioisotopes - administration & dosage
Chromium Radioisotopes - urine
Diabetes
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - urine
Diabetes. Impaired glucose tolerance
Edetic Acid - administration & dosage
Edetic Acid - urine
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Feeding. Feeding behavior
Fundamental and applied biological sciences. Psychology
Humans
Interleukin-6 - blood
Intestinal Absorption - physiology
Intestinal Mucosa - metabolism
Intestines - cytology
Male
Medical sciences
Middle Aged
Tumor Necrosis Factor-alpha - blood
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Vertebrates: endocrinology
Title Increased intestinal permeability to oral chromium (51Cr) -EDTA in human Type 2 diabetes
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https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fdme.12360
https://www.ncbi.nlm.nih.gov/pubmed/24236770
https://www.proquest.com/docview/1515629272
https://www.proquest.com/docview/1516395800
Volume 31
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