Maternally Transmitted and Food-Derived Glycotoxins

Mericq, Verónica; Piccardo, Cecilia; Cai, Weiping; Xue, Chen; Zhu, Li; Striker, Gary E.; Vlassara, Helen; Uribarri, Jaime

doi:10.2337/dc10-1058

Cited by 72 publications

(59 citation statements)

References 26 publications

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“…In this context, clinical evidence indicates that circulating AGEs in healthy infants may closely correlate with, and even exceed, maternal or adult AGE levels within the first year of life, 163 which is in line with the above findings in mice. Furthermore, infants born to mothers with high serum AGEs had higher plasma insulin and lower adiponectin levels, findings which may be the result of the AGE content of heat-treated, commercial infant foods, which was found to be ~100-fold higher than in maternal breast milk.…”

Section: Ages and Diabetes Mellitus: A Paradigm Shiftsupporting

confidence: 81%

AGE restriction in diabetes mellitus: a paradigm shift

2011

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Persistently elevated oxidative stress and inflammation precede or occur during the development of type 1 or type 2 diabetes mellitus and precipitate devastating complications. Given the rapidly increasing incidence of diabetes mellitus and obesity in the space of a few decades, new genetic mutations are unlikely to be the cause, instead pointing to environmental initiators. A hallmark of contemporary culture is a preference for thermally processed foods, replete with pro-oxidant advanced glycation endproducts (AGEs). These molecules are appetite-increasing and, thus, efficient enhancers of overnutrition (which promotes obesity) and oxidant overload (which promotes inflammation). Studies of genetic and nongenetic animal models of diabetes mellitus suggest that suppression of host defenses, under sustained pressure from food-derived AGEs, may potentially shift homeostasis towards a higher basal level of oxidative stress, inflammation and injury of both insulin-producing and insulin-responsive cells. This sequence promotes both types of diabetes mellitus. Reducing basal oxidative stress by AGE restriction in mice, without energy or nutrient change, reinstates host defenses, alleviates inflammation, prevents diabetes mellitus, vascular and renal complications and extends normal lifespan. Studies in healthy humans and in those with diabetes mellitus show that consumption of high amounts of food-related AGEs is a determinant of insulin resistance and inflammation and that AGE restriction improves both. This Review focuses on AGEs as novel initiators of oxidative stress that precedes, rather than results from, diabetes mellitus. Therapeutic gains from AGE restriction constitute a paradigm shift.

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Section: Ages and Diabetes Mellitus: A Paradigm Shiftsupporting

confidence: 81%

AGE restriction in diabetes mellitus: a paradigm shift

2011

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“…Therefore, as the catch-up growth and nutrition are key elements in the development of metabolic diseases in children born SGA, and it being further proved that during pregnancy the concentration in maternal blood of diet-derived pro-oxidant advanced glycation end products affect the glycoxidants, inflammatory markers and insulin levels in infants up to 1 year of age [52], an adequate lifestyle program (appropriate diet during pregnancy and in the first year of life, fed formulas enriched with polyunsaturated fatty acids) might help to prevent MetS and NAFLD in these subjects.…”

Section: Discussionmentioning

confidence: 99%

Nonalcoholic Fatty Liver Disease in Prepubertal Children Born Small for Gestational Age: Influence of Rapid Weight Catch-Up Growth

Faienza¹,

Brunetti²,

Ventura³

et al. 2013

Horm Res Paediatr

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Background/Aims: We studied the association of low birth weight with ultrasound-assessed nonalcoholic fatty liver disease (NAFLD) to test the hypothesis that fetal growth retardation followed by a rapid weight catch-up growth might be an additional factor responsible for liver steatosis via insulin resistance (IR) and/or intra-abdominal fat. Methods: We enrolled 23 children born small for gestational age (SGA) with a rapid catch-up growth within the first 6-12 months, and 24 appropriate for gestational age (AGA) children as controls.All children underwent anthropometric, body composition measurements and evaluation of liver function tests, lipid profile, plasma glucose and insulin levels. Abdominal ultrasonography was performed in order to asses liver steatosis and thickness of subcutaneous and visceral adipose tissue. Results: NAFLD were observed in 8 out of the 23 SGA children (34.8%). IR and visceral fat were significantly increased in children with hepatic steatosis compared to those without. IR index was significantly related to liver steatosis, independently of body mass index standard deviation score and visceral fat. Conclusions: NAFLD should be recognized as an emerging problem in SGA prepubertal children who presented a rapid weight gain in postnatal life, and IR plays the key role. An appropriate diet during pregnancy and in the first year of life might prevent metabolic syndrome and NAFLD in these subjects.

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“…Future studies will be needed to elucidate mechanism underlying improved esRAGE level in response to vitamin E and its significance in the pathogenesis of hepatic steatosis. As mentioned previously, although not interventional in design, studies by Mericq and Boor et al (33, 35) have suggested effects of RAGE polymorphisms and AGEs in diet on glucose metabolism in infants.…”

Section: Human Studies Linking Dietary Ages and Diseasementioning

confidence: 88%

“…Further, introduction of processed infant foods increased dietary AGE consumption, which was also reflected in higher serum AGEs levels in the infants. In addition, levels of serum AGEs correlated inversely with levels of adiponectin, an antiinflammatory adipokine in the infants (33). A recent study by another research group confirmed differences in insulin sensitivity based on AGEs levels in breastfed versus formula fed infants although these differences disappeared at follow up at age 12–14 months (34).…”

Section: Human Studies Linking Dietary Ages and Diseasementioning

confidence: 99%

Dietary Advanced Glycation End Products and Their Potential Role in Cardiometabolic Disease in Children

Gupta

Uribarri²

2016

Horm Res Paediatr

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2,931

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The rising incidence of obesity and metabolic diseases such as diabetes mellitus and cardiovascular disease in adolescents and young adults is of grave concern. Recent studies favor a role of lifestyle factors over genetics in the perpetuation of inflammation, insulin resistance and oxidative stress, which are pathophysiologic processes common to the above diseases; furthermore, the importance of dietary factors in addition to calories and physical activity in these processes is being increasingly recognized. Advanced glycation end products (AGEs) belong to a category of dietary oxidants which have been implicated in the pathogenesis of inflammation, oxidative stress, insulin resistance, β-cell failure and endothelial dysfunction. This paper reviews the studies of AGEs with a focus on their role in cardiometabolic disease in children. A Medline search was performed using the key words ‘childhood obesity', ‘metabolic syndrome' and ‘advanced glycation end products'. Articles published in English between 1975 and 2015 and their references were reviewed. While most studies were performed in adults, a few studies also demonstrated a role of AGEs in obesity and associated cardiometabolic comorbidities in the younger population. Available evidence suggests an involvement of AGEs in the pathogenesis of adiposity and β-cell failure in children. Potential areas for further research to investigate underlying mechanisms are proposed.

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Maternally Transmitted and Food-Derived Glycotoxins

Cited by 72 publications

References 26 publications

AGE restriction in diabetes mellitus: a paradigm shift

AGE restriction in diabetes mellitus: a paradigm shift

Nonalcoholic Fatty Liver Disease in Prepubertal Children Born Small for Gestational Age: Influence of Rapid Weight Catch-Up Growth

Dietary Advanced Glycation End Products and Their Potential Role in Cardiometabolic Disease in Children

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