Reduced Oxidant Stress and Extended Lifespan in Mice Exposed to a Low Glycotoxin Diet

Cai, Weiping; He, John Cijiang; Zhu, Li; Xue, Chen; Wallenstein, Sylvan; Striker, Gary E.; Vlassara, Helen

doi:10.2353/ajpath.2007.061281

Cited by 167 publications

(198 citation statements)

References 64 publications

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“…Furthermore, one study found that reducing dietary exposure to preformed AGEs (achieved by reducing the exposure of the diet to heat during processing) extended both mean and maximum life span of mice (49). Even more intriguingly, a study of CR in rats reported reduced AGE accumulation in the animals with restricted food intake (50), and more recently, a study looking at the relationship between CR, AGE accumulation, and life span found that feeding mice a diet high in AGEs blocked CR's ability to extend mean or maximum life span (51).…”

Section: Advanced Glycation End Productsmentioning

confidence: 99%

Dietary Interventions to Extend Life Span and Health Span Based on Calorie Restriction

Minor

Allard

Younts

et al. 2010

The Journals of Gerontology Series A: Biological Sciences and M

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The societal impact of obesity, diabetes, and other metabolic disorders continues to rise despite increasing evidence of their negative long-term consequences on health span, longevity, and aging. Unfortunately, dietary management and exercise frequently fail as remedies, underscoring the need for the development of alternative interventions to successfully treat metabolic disorders and enhance life span and health span. Using calorie restriction (CR)-which is well known to improve both health and longevity in controlled studies-as their benchmark, gerontologists are coming closer to identifying dietary and pharmacological therapies that may be applicable to aging humans. This review covers some of the more promising interventions targeted to affect pathways implicated in the aging process as well as variations on classical CR that may be better suited to human adaptation.

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Section: Advanced Glycation End Productsmentioning

confidence: 99%

Dietary Interventions to Extend Life Span and Health Span Based on Calorie Restriction

Minor

Allard

Younts

et al. 2010

The Journals of Gerontology Series A: Biological Sciences and M

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“…Recent studies in mice have shown that decreased intake, or formation, of protein-AGEs can make major contributions to lifespan extension in mice (Cai et al, 2007;Uribarri et al, 2007a and2007b). MG, a spontaneously-generated glycolytic by-product, induces senescence in cultured fibroblasts (Sejersen and Rattan, 2008), and is a primary source of intracellular glycation in both yeast (Gomes et al, 2008) and mice (Morcos et al, 2008).…”

Section: Carnosine and Post-synthetic Protein Modificationmentioning

confidence: 99%

On the enigma of carnosine’s anti-ageing actions

Hipkiss¹

2009

Experimental Gerontology

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Carnosine ( -alanyl-L-histidine) has described as a forgotten and enigmatic dipeptide. Carnosine's enigma is particularly exemplified by its apparent anti-ageing actions; it suppresses cultured human fibroblast senescence and delays ageing in senescence-accelerated mice and Drosophila, but the mechanisms reponsible remain uncertain. In addition to carnosine's well-documented anti-oxidant, anti-glycating, aldehyde-scavenging and toxic metal-ion chelating properties, its ability to influence the metabolism of altered polypeptides, whose accumulation characterises the senescent phenotype, should also be considered. When added to cultured cells, carnosine was found in a recent study to suppress phosphorylation of the translational initiation factor eIF4E resulting in decreased translation frequency of certain mRNA species. Mutations in the gene coding for eIF4E in nemtodes extend organism lifespan, hence carnosine's anti-ageing effects may be a consequence of decreased error-protein synthesis which in turn lowers formation of protein carbonyls and increases protease availability for degradation of polypeptides altered postsynthetically. Other studies have revealed carnosine-induced upregulation of stress protein expression and nitric oxide synthesis, both of which may stimulate proteasomal elimination of altered proteins. Some anti-convulsants can enhance nematode longevity and suppress the effects of a protein repair defect in mice, and as carnosine exerts anti-convulsant effects in rodents, it is speculated that the dipeptide may participate in the repair of protein isoaspartyl groups. These new observations only add to the enigma of carnosine's real in vivo functions. More experimentation is clearly required. ACCEPTED MANUSCRIPT 3 Carnosine and ageing.The naturally-occurring dipeptide carnosine ( -alanyl-L-histidine) has been described as forgotten and enigmatic (Bauer, 2005): the present paper is an attempt to rectify the former opinion, but, however only adds to the latter view. Amongst carnosine's enigmatic properties are its apparent anti-ageing actions; the dipeptide is one of a very few naturally-occurring compounds which suppresses cell senescence, induces rejuvenating effects Holliday, 1994 and, and protects against telomere shortening (Shao et al., 2004) in cultured human fibroblasts. The dipeptide also extends the life-span of senescence-accelerated mice (Yuneva et al., 1999) and Drosophila (Yuneva et al., 2002). There are many possible mechanisms by which carnosine exerts these anti-ageing actions however, some of which were summarized a decade ago (Hipkiss, 1998). Meanwhile there have been a number of publications suggesting further possible routes by which carnosine could suppress

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“…Furthermore, data obtained from humans and experimental animals indicate that exogenous food-ingested AGEs, present in highly thermolyzed fat-containing Westernized diets, result in elevated serum levels and increased tissue deposition of AGEs that can provoke the initiation or progression of insulin resistance and other endocrine abnormalities (Diamanti-Kandarakis et al 2007a, Cai et al 2008, de Assis et al 2009). Similarly, low-glycotoxin dietfed mice exhibit extended lifespan and reduced oxidative stress, while restriction of AGEs improves insulin resistance in T2DM patients (Cai et al 2007, Uribarri et al 2011.…”

Section: Introductionmentioning

confidence: 99%

Dietary glycotoxins affect scavenger receptor expression and the hormonal profile of female rats

Chatzigeorgiou¹,

Kandaraki²,

Piperi³

et al. 2013

Journal of Endocrinology

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The levels of advanced glycation end products (AGEs) are increased under conditions of impaired glucose metabolism and/or oxidative stress, promoting insulin resistance and other endocrine abnormalities. AGEs play a major role in the pathogenesis of several diseases such as diabetes, atherosclerosis, polycystic ovary syndrome and Alzheimer's disease, contributing to progressive ageing. Receptor-based clearance of AGEs by the receptor for AGE (RAGE) and/or the macrophage scavenger receptor A (SR-A) is considered as a main factor for the regulation of the concentration of AGEs under these conditions. This study aimed to investigate the expression of RAGE (AGER) and SR-A (MSR1) under high/low-dietary AGE conditions in vivo and their potential contribution to the metabolic and sex hormonal profile of female rats. Female Wistar rats were fed a low-AGE or high-AGE diet for 3 months. Serum samples were collected at baseline and at the completion of the 3-month period for the measurements of metabolic and hormonal parameters. Peripheral blood mononuclear cells (PBMCs) were isolated for the determination of the expression of RAGE and SR-A. The high-AGE diet-fed rats exhibited increased glucose, insulin and testosterone levels as well as decreased oestradiol and progesterone levels compared with the low-AGE diet-fed ones, thus indicating a metabolic and hormonal dysregulation attributed to high-AGE dietary exposure. The expression of RAGE was significantly down-regulated in the PBMCs of the high-AGE diet-fed rats (PZ0.041), and it was correlated negatively with insulin and testosterone levels and positively with progesterone levels. The expression of SR-A was also decreased in the high-AGE diet-fed rats to marginal significance. Decreased monocytic expression of scavenger receptors such as RAGE and SR-A may result in a higher deposition of AGEs in peripheral endocrine tissues, thus promoting endocrine-related abnormalities and diseases.

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Reduced Oxidant Stress and Extended Lifespan in Mice Exposed to a Low Glycotoxin Diet

Cited by 167 publications

References 64 publications

Dietary Interventions to Extend Life Span and Health Span Based on Calorie Restriction

Dietary Interventions to Extend Life Span and Health Span Based on Calorie Restriction

On the enigma of carnosine’s anti-ageing actions

Dietary glycotoxins affect scavenger receptor expression and the hormonal profile of female rats

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