Prevention of diabetic nephropathy in mice by a diet low in glycoxidation products

Zhao, Feng; He, Cijiang; Cai, Weiping; Hattori, Masao; Steffes, Michael W.; Vlassara, Helen

doi:10.1002/dmrr.283

Cited by 200 publications

(171 citation statements)

References 49 publications

Supporting

Mentioning

151

Contrasting

Unclassified

Order By: Relevance

“…Positive correlation between dAGE content and serum/tissue AGE levels have been also confirmed by several animal study [17,27,28]. For example Peppa et al [29] to assess the role of dAGEs on type 1 diabetes, exposed the genetically susceptible NOD mice to a high-AGE diet and to a nutritionally similar diet with approximate fivefold-lower levels of CML and MG and demonstrated that after 44 weeks of treatment, NOD mice fed with Low-AGE diet showed almost half of serum AGE levels respect to High-AGE diet fed NOD mice.…”

Section: Dages Intestinal Absorptionsupporting

confidence: 55%

Advanced Glycation End Products (Ages) in Food: Focusing on Mediterranean Pasta

Abate¹,

Delbarba²,

Marziano³

et al. 2015

J Nutr Food Sci

View full text Add to dashboard Cite

Advanced glycation end products, also known as glycotoxins, are a diverse group of highly oxidant compounds with pathogenic significance in aged-chronic disease, including diabetes, cardiovascular disease and neurodegenerative disease. They are produced physiologically in the body when reducing sugar binds to a free amino acid group of macromolecules. Thus conditions such as hyperglycemia and/or oxidative stress can favor AGE product formation, contributing to ageing processes and the exacerbation of pathological states. Beside endogenous AGEs, dietary AGE intake contributes significantly to the body AGE pool. It assumes that if dietary AGE intake gets lower, any chronic disease, such as diabetes and cardiovascular disease can be ameliorated, and even cured. For this reason, recently great attention has been made on the identification and quantification of AGE products in the consumed foods. Here we reviewed some knowledge, found in literature, concerning the formation of AGEs in food, their gastrointestinal absorption, and their toxic effects. In addition original data on AGE content in the Mediterranean pasta was discussed in relation to their production processes and cooking time.

show abstract

Section: Dages Intestinal Absorptionsupporting

confidence: 55%

Advanced Glycation End Products (Ages) in Food: Focusing on Mediterranean Pasta

Abate¹,

Delbarba²,

Marziano³

et al. 2015

J Nutr Food Sci

View full text Add to dashboard Cite

show abstract

“…The structural and functional LDL changes found in the present studies were consistent with the differences in AGE content of the diet, with AGE levels in serum as reflected in CML and MG derivatives, but also with levels of the circulating inflammatory markers C-reactive protein, tumor necrosis factor-␣, and VCAM-1 reported previously. 18 These findings supported the postulated relationship between exogenous AGE and diabetic cardiovascular disease 18,28,29 and opened a new window into the mechanisms involved in these events.…”

Section: Discussionmentioning

confidence: 54%

High Levels of Dietary Advanced Glycation End Products Transform Low-Dersity Lipoprotein Into a Potent Redox-Sensitive Mitogen-Activated Protein Kinase Stimulant in Diabetic Patients

et al. 2004

Self Cite

View full text Add to dashboard Cite

Background-LDL modification by endogenous advanced glycation end products (AGEs) is thought to contribute to cardiovascular disease of diabetes. It remains unclear, however, whether exogenous (diet-derived) AGEs influence glycoxidation and endothelial cell toxicity of diabetic LDL. Methods and Results-Twenty-four diabetic subjects were randomized to either a standard diet (here called high-AGE, HAGE) or a diet 5-fold lower in AGE (LAGE diet) for 6 weeks. LDL pooled from patients on HAGE diet (Db-HAGE-LDL) was more glycated than LDL from the LAGE diet group (

show abstract

“…Human studies confirmed that about 10% of exogenous AGEs are absorbed and correlate with circulating and tissue AGEs levels, exceeding their endogenous production [11]. Data in humans and experimental animals favor that exogenous food-ingested AGEs result in elevated serum levels and increased tissue deposition [12,13]. Specifically, ingestion of a meal rich in AGEs has led to increased serum levels of AGEs in diabetic patients, which were compared with controls, and tissue deposition was enhanced when the AGE meals were rich in fat [11].…”

Section: Introductionmentioning

confidence: 92%

Accumulation of dietary glycotoxins in the reproductive system of normal female rats

et al. 2007

View full text Add to dashboard Cite

The aim of the present study was to investigate whether dietary advanced glycation end-products (AGEs) can be detected in the ovarian tissue of normal female rats and whether they can affect their metabolic or hormonal profile. Sixty normal rats (20 animals in each group) were randomly assigned to regular diet, either high (H-AGE) or low (L-AGE) in AGE content for 6 months. H-AGE rats demonstrated higher levels of fasting glucose (P<0.001), insulin (P< 0.069), and serum AGEs (P< 0.001) than control and L-AGE rats. Additionally, the H-AGE group showed increased AGE localization in the theca interna cells of the ovarian tissue compared to control/L-AGE rats (P= 0.003). Furthermore, increased receptor for AGE (RAGE) staining was also observed in granulosa cells compared to control/L-AGE samples (P=0.038). In the H-AGE group, plasma testosterone was higher than in control rats (P<0.001) and in the L-AGE group (P<0.001). However, H-AGE rats did not exhibit higher body weight compared with normal (P=0.118) and L-AGE-fed rats (P= 0.35). These results demonstrate for the first time that administration of high AGE diet in female rats for a prolonged period is associated with increased deposition of AGEs in the theca cells and of RAGE in the granulosa and theca interna cells of the ovarian tissue compared with the corresponding ovarian compartments of the control and

show abstract

Prevention of diabetic nephropathy in mice by a diet low in glycoxidation products

Abstract: Intake of high-level, food-derived AGEs is a major contributor to DN in T1D and T2D mice. Avoidance of dietary AGEs provides sustained protection against DN in mice; providing the rationale for similar studies in human diabetic patients.

Cited by 200 publications

References 49 publications

Advanced Glycation End Products (Ages) in Food: Focusing on Mediterranean Pasta

Advanced Glycation End Products (Ages) in Food: Focusing on Mediterranean Pasta

High Levels of Dietary Advanced Glycation End Products Transform Low-Dersity Lipoprotein Into a Potent Redox-Sensitive Mitogen-Activated Protein Kinase Stimulant in Diabetic Patients

Accumulation of dietary glycotoxins in the reproductive system of normal female rats

Contact Info

Product

Resources

About