Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice.
about
Advanced glycation end products in foods and a practical guide to their reduction in the dietCirculating glycotoxins and dietary advanced glycation endproducts: two links to inflammatory response, oxidative stress, and agingAdvanced glycation end-products: modifiable environmental factors profoundly mediate insulin resistanceRole of nutritional factors at the early life stages in the pathogenesis and clinical course of type 1 diabetesLifestyle and Advanced Glycation End Products (AGEs) Burden: Its Relevance to Healthy AgingMaternally transmitted and food-derived glycotoxins: a factor preconditioning the young to diabetes?Advanced glycation in health and disease: role of the modern environment.Advanced glycation end products are direct modulators of β-cell function.Regulation of RAGE for attenuating progression of diabetic vascular complications.Dietary advanced glycation end products and aging.Relationship of Soluble RAGE with Insulin Resistance and Beta Cell Function during Development of Type 2 Diabetes Mellitus.Glycotoxin and autoantibodies are additive environmentally determined predictors of type 1 diabetes: a twin and population study.Meat consumption and its association with C-reactive protein and incident type 2 diabetes: the Rotterdam StudyDiet-derived advanced glycation end products are major contributors to the body's AGE pool and induce inflammation in healthy subjects.Oral glycotoxins determine the effects of calorie restriction on oxidant stress, age-related diseases, and lifespan.Dietary Advanced Glycation End Products and Their Potential Role in Cardiometabolic Disease in Children.AGE restriction in diabetes mellitus: a paradigm shift.Diabetic threesome (hyperglycaemia, renal function and nutrition) and advanced glycation end products: evidence for the multiple-hit agent?Advanced glycation end products inhibit glucose-stimulated insulin secretion through nitric oxide-dependent inhibition of cytochrome c oxidase and adenosine triphosphate synthesisSuppression of native defense mechanisms, SIRT1 and PPARγ, by dietary glycoxidants precedes disease in adult humans; relevance to lifestyle-engendered chronic diseases.Advanced glycation end product receptor-1 transgenic mice are resistant to inflammation, oxidative stress, and post-injury intimal hyperplasia.Advanced glycation end products (AGE) and diabetes: cause, effect, or both?Anti-inflammatory therapy in type 1 diabetes.Advanced glycation End-products (AGEs): an emerging concern for processed food industries.Dietary factors in the development of type 1 diabetes.Receptor for Advanced Glycation End Products (RAGE) in Type 1 Diabetes Pathogenesis.A1 beta-casein milk protein and other environmental pre-disposing factors for type 1 diabetesDisparate effects on renal and oxidative parameters following RAGE deletion, AGE accumulation inhibition, or dietary AGE control in experimental diabetic nephropathy.Renal effects of oral maillard reaction product load in the form of bread crusts in healthy and subtotally nephrectomized rats.Digestibility of extruded proteins and metabolic transit of N ε -carboxymethyllysine in rats.Dietary habits and their relationship with hormones and metabolism in overweight and obese women with polycystic ovary syndrome.[The role of advanced glycation end-products (AGEs) in the development of vascular diabetic complications].Perinatal exposure to high dietary advanced glycation end products in transgenic NOD8.3 mice leads to pancreatic beta cell dysfunction.Impact of Maillard reaction products on nutrition and health: Current knowledge and need to understand their fate in the human digestive system.Potential involvement of dietary advanced glycation end products in impairment of skeletal muscle growth and muscle contractile function in mice.Advanced glycation end products downregulate glucokinase in mice.Receptor for advanced glycation end-products (RAGE) provides a link between genetic susceptibility and environmental factors in type 1 diabetes.Adverse effects of Hif1a mutation and maternal diabetes on the offspring heart.Short-term effects of dietary advanced glycation end products in ratsRole of advanced glycation end products in mobility and considerations in possible dietary and nutritional intervention strategies
P2860
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P2860
Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice.
@en
Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice.
@nl
type
label
Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice.
@en
Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice.
@nl
prefLabel
Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice.
@en
Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice.
@nl
P2093
P1433
P1476
Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice.
@en
P2093
Cijiang He
Feng Zheng
Helen Vlassara
Masakazu Hattori
Melpomeni Peppa
Robert McEvoy
P304
P356
10.2337/DIABETES.52.6.1441
P407
P577
2003-06-01T00:00:00Z