Quantitative assessment of organ distribution of dietary protein‐bound <sup>13</sup>C‐labeled N<sup>ɛ</sup>‐carboxymethyllysine after a chronic oral exposure in mice

Tessier, Frédéric J.; Niquet-Léridon, Céline; Jacolot, Philippe; Jouquand, Céline; Génin, Michaël; Schmidt, Ann‐Marie; Grossin, Nicolas; Boulanger, Éric

doi:10.1002/mnfr.201600140

Cited by 114 publications

(108 citation statements)

References 35 publications

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“…The ME‐3 treatment significantly reduced dCML accumulation only in those organs we have already shown to predominantly accumulate this exogenous AGE. [ 38 ] The probiotic significantly reduced the levels of free CML in the kidneys (−32%) and lungs (−18%) of diabetic mice ( db/db 43.8 ± 11.0 vs db/db Lf 33.1 ± 8.3 mmol g −1 kidneys; db/db 35.8 ± 7.2 vs db/db Lf 29.1 ± 6.4 mmol g −1 lungs; Figure 4A,B), and tended to reduce free CML in the kidneys of WT mice ( db/+ 30.5±7.4 vs db/+ Lf 25.0±8.0 mmol g −1 kidneys; Figure 4A). ME‐3 treatment had no effect on the accumulation of free CML in the hearts or livers of either genotype (Figure 4C,D).…”

Section: Resultsmentioning

confidence: 99%

The Effect of Lactobacillus fermentum ME‐3 Treatment on Glycation and Diabetes Complications

Guilbaud

Howsam

Niquet-Léridon

et al. 2020

Molecular Nutrition Food Res

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Scope Type 2 diabetes (T2D) induces organ damage associated with glycation, among other metabolic pathways. While therapeutic strategies have been tested to reduce the formation and impact of glycation products, results remain equivocal. Anti‐diabetic therapies using probiotics have been proposed, but their effect upon glycation has not been reported. Here, the effects of the bacterial strain Lactobacillus fermentum ME‐3 on glycation and T2D‐related complications in a mouse model of T2D are investigated. Methods & Results Wild‐type LepRdb/+ and diabetic LepRdb/db littermates receive a daily gavage of either water or the probiotic ME‐3 strain (1010 CFU). Glycation markers, fructoselysine‐derived furosine (FL‐furosine) and carboxymethyllysine (CML), are quantified in four major organs and plasma using stable‐isotope dilution LC–MS/MS. After 12 weeks of ME‐3 treatment, diabetic mice gain less weight and exhibit an apparently improved glucose tolerance. The ME‐3 treatment reduces median renal levels of FL‐furosine in both genotypes by 12–15%, and renal and pulmonary free‐CML in diabetic mice by 30% and 18%, respectively. Attenuated hepatic steatosis and an improved plasma lipid profile are also observed with treatment in both genotypes, while the gut microbiota profile is unchanged. Conclusion L. fermentum ME‐3 has therapeutic potential for reducing the formation/accumulation of some glycation products in kidneys and attenuating some common diabetes‐related complications.

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Section: Resultsmentioning

confidence: 99%

The Effect of Lactobacillus fermentum ME‐3 Treatment on Glycation and Diabetes Complications

Guilbaud

Howsam

Niquet-Léridon

et al. 2020

Molecular Nutrition Food Res

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“…We recently demonstrated that dCML accumulates in most organs but particularly in kidneys and lungs . Hence, the level of free CML in vivo is highly influenced by exposure to dCML.…”

Section: Discussionmentioning

confidence: 99%

“…The Amadori product formation was measured indirectly by quantifying furosine, which is the major breakdown product of fructoselysine during acid hydrolysis. We also developed a method to separately analyse free and protein‐bound CML, following recent work in our laboratory showing that this latter form of CML accumulates in organs as a function of dietary exposure …”

Section: Introductionmentioning

confidence: 99%

The LepR^db/db mice model for studying glycation in the context of diabetes

Guilbaud

Howsam

Niquet-Léridon³

et al. 2019

Diabetes Metabolism Res

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Background Early (furosine) and advanced (carboxymethyllysine, CML) products of glycation (AGEs) have been reported as increased in plasma, tissues, and organs of diabetic people, indicating a direct link between glycation and type 2 diabetes (T2D). While murine models present some of the characteristics observed in diabetic humans, their pertinence as models of glycation, particularly for T2D, remains poorly described. The aim of this study was to characterize and compare glycation in several organs of two commonly studied murine models of T2D using stable isotope dilution liquid chromatography tandem mass spectrometry (LC‐MS/MS). Methods Defining parameters of type 2 diabetes including body weight, fasting glycaemia, and glucose intolerance were measured in three different C57BL6 mouse models of T2D—the genetic LepRdb/db (db/db) model and two diet‐induced obesity (DIO) models—and their respective controls. Furosine, free, and protein‐bound CML were quantified in kidneys, lungs, heart, and liver by LC‐MS/MS. Results The obesity, hyperglycaemia, and glucose intolerance in db/db mice was accompanied by an increase of furosine and protein‐bound CML levels in all organs relative to controls. The DIO models took several months to become obese, exhibited less severe hyperglycaemia and glucose intolerance, while glycation products were not significantly different between these groups (with the exception of furosine in liver and CML in lungs). Conclusions The db/db model better reflected the characteristics of human T2D compared with the DIO models and exhibited greater formation and accumulation of both furosine and protein‐bound CML in all of the organs tested here.

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“…Tessier et al . () also reported that mice exposed to dietary CML showed accumulation of CML in the ileum and colon, and the amount of CML in the ileum was greater than in the colon, which indicated that CML accumulation mainly occurred in the ileum. We speculate that the high CML accumulation detected in the GI tract may be due to the high hydrophilicity of CML (Hellwig et al ., ) and that CML can be trapped in intestinal epithelial cells and reach the circulatory system.…”

Section: Resultsmentioning

confidence: 85%

“…Previous studies have focused on oxidative damage in the kidneys (Elmhiri et al ., ), liver (Liu et al ., ) and spleen (Cai et al ., ), mainly due to extensive CML accumulation in these tissues. The most recent research has suggested that the majority of the dietary protein‐bound CML accumulates in the ileum and colon (Tessier et al ., ), but the downstream effects of the AGE‐RAGE interaction in the GI tract are largely unexplored. Only a few studies have investigated the effects of AGEs on the colon, and their results are the subject of some controversy.…”

Section: Introductionmentioning

confidence: 99%

Accumulation and effects of dietary advanced glycation end products on the gastrointestinal tract in rats

Yuan

Zhao

et al. 2018

Int J of Food Sci Tech

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Summary The gastrointestinal (GI) tract represents the first barrier against the penetration of organisms by dietary advanced glycation end products (AGEs), but the tissue accumulation of AGEs and AGE‐induced effects on the GI tract have yet to be completely elucidated. This study aimed to investigate the tissue accumulation of AGEs and AGE‐induced oxidative stress and inflammation in the GI tract of rats after long‐term consumption of AGEs from bread crust (BC). The GI tract was then removed to analyse carboxymethyllysine (CML) and malondialdehyde (MDA) contents, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH‐Px) and the levels of tumour necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6). This study demonstrates that the oral intake of AGEs promotes their accumulation in the GI tract, and AGEs attenuate the first‐line antioxidant defence and stimulate the inflammatory response of the GI tract by downregulating enzymatic antioxidative pathways and increasing inflammatory cytokine levels.

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Quantitative assessment of organ distribution of dietary protein‐bound ¹³C‐labeled N^ɛ‐carboxymethyllysine after a chronic oral exposure in mice

Abstract: The kidney is not the only organ affected by the accumulation of dCML. Its high accumulation in other tissues and organs may also, however, have important physiological consequences.

Cited by 114 publications

References 35 publications

The Effect of Lactobacillus fermentum ME‐3 Treatment on Glycation and Diabetes Complications

The Effect of Lactobacillus fermentum ME‐3 Treatment on Glycation and Diabetes Complications

The LepR^db/db mice model for studying glycation in the context of diabetes

Accumulation and effects of dietary advanced glycation end products on the gastrointestinal tract in rats

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Quantitative assessment of organ distribution of dietary protein‐bound 13C‐labeled Nɛ‐carboxymethyllysine after a chronic oral exposure in mice

Abstract: The kidney is not the only organ affected by the accumulation of dCML. Its high accumulation in other tissues and organs may also, however, have important physiological consequences.

Cited by 114 publications

References 35 publications

The Effect of Lactobacillus fermentum ME‐3 Treatment on Glycation and Diabetes Complications

The Effect of Lactobacillus fermentum ME‐3 Treatment on Glycation and Diabetes Complications

The LepRdb/db mice model for studying glycation in the context of diabetes

Accumulation and effects of dietary advanced glycation end products on the gastrointestinal tract in rats

Contact Info

Product

Resources

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Quantitative assessment of organ distribution of dietary protein‐bound ¹³C‐labeled N^ɛ‐carboxymethyllysine after a chronic oral exposure in mice

The LepR^db/db mice model for studying glycation in the context of diabetes