The Low AGE Diet: A Neglected Aspect of Clinical Nephrology Practice?

Uribarri, Jaime; He, John Cijiang

doi:10.1159/000381315

Cited by 17 publications

(13 citation statements)

References 40 publications

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“…Undoubtedly, MG is not absorbed in the free form but as amino acid adducts, which are at least in part absorbed and accumulate in different tissues. If confirmed, this could contradict the current theory of a simple association among hyperglycemia, MG formation, and AGE accumulation and alert for the hidden risks of MG‐enriched diets (revised by). The recent studies from Uribarri et al.…”

Section: Discussionmentioning

confidence: 90%

“…Since then, several studies have correlated elevated MG levels in plasma of diabetic patients with the accelerated progression of diabetes complications . Moreover, the accumulation of MG‐derived advanced glycation end products (AGE) was correlated with the development of diabetic nephropathy, retinopathy, neuropathy, declined cognitive function, and atherosclerosis in adult and pediatric populations . Additionally, recent studies support the thesis that MG‐derived AGE deposition may occur since early stages of disease such as prediabetes, being involved in mechanisms that contribute to the onset of type 2 diabetes, namely insulin resistance and β‐cell damage .…”

Section: From Methylglyoxal Discovery To Clinical Relevancementioning

confidence: 94%

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Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

Matafome

Rodrigues

Sena

et al. 2016

Medicinal Research Reviews

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Glucose and fructose metabolism originates the highly reactive byproduct methylglyoxal (MG), which is a strong precursor of advanced glycation end products (AGE). The MG has been implicated in classical diabetic complications such as retinopathy, nephropathy, and neuropathy, but has also been recently associated with cardiovascular diseases and central nervous system disorders such as cerebrovascular diseases and dementia. Recent studies even suggested its involvement in insulin resistance and beta-cell dysfunction, contributing to the early development of type 2 diabetes and creating a vicious circle between glycation and hyperglycemia. Despite several drugs and natural compounds have been identified in the last years in order to scavenge MG and inhibit AGE formation, we are still far from having an effective strategy to prevent MG-induced mechanisms. This review summarizes the endogenous and exogenous sources of MG, also addressing the current controversy about the importance of exogenous MG sources. The mechanisms by which MG changes cell behavior and its involvement in type 2 diabetes development and complications and the pathophysiological implication are also summarized. Particular emphasis will be given to pathophysiological relevance of studies using higher MG doses, which may have produced biased results. Finally, we also overview the current knowledge about detoxification strategies, including modulation of endogenous enzymatic systems and exogenous compounds able to inhibit MG effects on biological systems.

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Section: Discussionmentioning

confidence: 90%

Section: From Methylglyoxal Discovery To Clinical Relevancementioning

confidence: 94%

Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

Matafome

Rodrigues

Sena

et al. 2016

Medicinal Research Reviews

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“…The endogenous production of AGE is thought to be important, but dietary AGE are also of interest, although we did not focus on them in the present study. However, the concentration of MG in patients on peritoneal dialysis reportedly decreases by dietary restriction of AGE . It is possible that such an effect might improve the outcome for patients with CKD by reducing oxidative stress and inflammation …”

Section: Discussionmentioning

confidence: 97%

“…However, the concentration of MG in patients on peritoneal dialysis reportedly decreases by dietary restriction of AGE. 22,23 It is possible that such an effect might improve the outcome for patients with CKD by reducing oxidative stress and inflammation. 24 In CKD, it has been reported that renal tubular damage is correlated with a decrease in the activity of glyoxalase I in proximal tubule cells.…”

Section: Discussionmentioning

confidence: 99%

Methylglyoxal as a prognostic factor in patients with chronic kidney disease

et al. 2019

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Aim Advanced glycation end products and their precursors cause vascular damage through oxidative stress. We investigated the hypothesis that methylglyoxal (MG), 3‐deoxyglucosone (3‐DG) and pentosidine influence outcomes of chronic kidney disease (CKD) patients. Methods We conducted a 3 years prospective observational study involving 150 outpatients at CKD stages 3–5. At enrolment, MG, 3‐DG and pentosidine plasma concentrations were measured; patients were divided into tertiles according to the concentration of each substance. The primary endpoint was death, a cardiovascular event or end‐stage renal disease. Survival analysis was performed using the Cox regression model. Results The patients’ mean age was 62 ± 12 years, 97 were men, and 20 had diabetic nephropathy. The mean estimated glomerular filtration rate was 25.0 ± 12.1 mL/min per 1.73 m2, which negatively correlated with MG but not with 3‐DG and pentosidine. Forty‐eight patients reached the primary endpoint. Compared with the lowest MG tertile, the hazard ratio for the primary endpoint was 7.57 (95% confidence interval (CI): 1.71–33.54) in the middle tertile and 27.00 (CI: 6.46–112.82) in the highest tertile. When adjusted for characteristics at baseline, the corresponding hazard ratio decreased to 2.09 (CI: 0.37–11.96) and 6.13 (CI: 0.97–38.82), but MG tertile remained an independent risk factor for the primary endpoint. However, 3‐DG and pentosidine were not related to the primary outcome. Conclusion Methylglyoxal has a close clinical association with CKD. Higher MG concentrations may contribute renal function deterioration in CKD. In CKD patients, MG concentration might be useful when determining the prognosis.

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“…UV AGE-specific fluorescence could potentially be used to monitor interventions to lower the concentration of AGEs: e.g., a low AGE diet [37]. AGEs in food generally have a low biological availability when ingested: only 10-30% of the total amount of AGEs in a meal is absorbed.…”

Section: Discussionmentioning

confidence: 99%

UV Fluorescence-Based Determination of Urinary Advanced Glycation End Products in Patients with Chronic Kidney Disease

Steenbeke

Bruyne

Aken³

et al. 2020

Diagnostics

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Advanced glycation end products (AGEs) are a class of proteins or lipids that are non-enzymatically glycated and oxidized after contact with aldose sugars. The accumulation of AGEs results in carbonyl stress, which is characteristic for diabetes mellitus, uremia, atherosclerosis and vascular dysfunction. In recent decades, several innovative methods have been developed to measure the concentration of AGEs in blood or urine. In the present study, we evaluated the use of UV fluorescence as an alternative tool to detect urinary AGEs in four groups of well characterized chronic kidney disease (CKD) patients over a wide range of kidney insufficiency and in a group of healthy subjects. Using an excitation wavelength of 365 nm, the fluorescence spectra of urinary AGEs were recorded in the 400–620 nm emission range. When considering the emission peaks at 440 nm and 490 nm, a significantly higher AGE-specific fluorescence intensity was detected in CKD patients compared to healthy subjects (p < 0.0001 and p = 0.0001, respectively). The urinary creatinine adjusted fluorescence emission spectra in the group of CKD patients with diabetes mellitus were comparable with those of CKD patients without diabetes mellitus. Creatinine-adjusted fluorescence emission spectra were highest in CKD patients with proteinuria, moderate in CKD patients without proteinuria and lowest in healthy controls (p < 0.0001 at both emission wavelengths). In a multiple regression analysis, age, CRP and insulin treatment were predictors of fluorescence intensity at the emission wavelength of 440 nm. Age and insulin treatment were predictors at 490 nm. The presented method is a simple, cheap, alternative method to monitor the AGE-load in the CKD population.

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The Low AGE Diet: A Neglected Aspect of Clinical Nephrology Practice?

Cited by 17 publications

References 40 publications

Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

Methylglyoxal as a prognostic factor in patients with chronic kidney disease

UV Fluorescence-Based Determination of Urinary Advanced Glycation End Products in Patients with Chronic Kidney Disease

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