Food-advanced glycation end products aggravate the diabetic vascular complications via modulating the AGEs/RAGE pathway

Lv, Xing; Lv, Gaohong; Guoying, Dai; Sun, Hongmei; Xu, Hao

doi:10.1016/s1875-5364(16)30101-7

Cited by 26 publications

(20 citation statements)

References 59 publications

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“…MG-H1 is the major AGE in proteins of tissues and body fluids [ 24 ]. It increases in DM and is associated with vascular complications, renal failure, arthritis (OA and rheumatic arthritis) and ageing [ 25 – 28 ]. In the current study, SF levels of both MG and MG-H1 were higher in OA with DM than that in OA without DM, presenting evidence in support of a putative mechanism explaining the relationship between OA and DM in epidemiological studies.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia-related advanced glycation end-products is associated with the altered phosphatidylcholine metabolism in osteoarthritis patients with diabetes

et al. 2017

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To test whether type 2 diabetic patients have an elevated level of advanced glycation end-products (AGEs) and responsible for altered phosphatidylcholine metabolism, which we recently found to be associated with osteoarthritis (OA) and diabetes mellitus (DM), synovial fluid (SF) and plasma samples were collected from OA patients with and without DM. Hyperglycemia-related AGEs including methylglyoxal (MG), free methylglyoxal-derived hydroimidazolone (MG-H1), and protein bound N-(Carboxymethyl)lysine (CML) and N-(Carboxyethyl)lysine (CEL) levels were measured in both SF and plasma samples using liquid chromatography coupled tandem mass spectrometry methodology. The correlation between these AGEs and phosphatidylcholine acyl-alkyl C34:3 (PC ae C34:3) and C36:3 (PC ae C36:3) were examined. Eighty four patients with knee OA, including 46 with DM and 38 without DM, were included in the study. There was no significant difference in plasma levels of MG, MG-H1, CML, and CEL between OA patients with and without DM. However, the levels of MG and MG-H1, but not CML and CEL in SF were significantly higher in OA patients with DM than in those without (all p ≤0.04). This association strengthened after adjustment for age, body mass index (BMI), sex and hexose level (p<0.02). Moreover, the levels of MG-H1 in SF was negatively and significantly correlated with PC ae C34:3 (ρ = -0.34; p = 0.02) and PC ae C36:3 (ρ = -0.39; P = 0.03) after the adjustment of age, BMI, sex and hexose level. Our data indicated that the production of non-protein bound AGEs was increased within the OA-affected joint of DM patients. This is associated with changes in phosphatidylcholine metabolism and might be responsible for the observed epidemiological association between OA and DM.

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Section: Discussionmentioning

confidence: 99%

Hyperglycemia-related advanced glycation end-products is associated with the altered phosphatidylcholine metabolism in osteoarthritis patients with diabetes

et al. 2017

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“…Direct role for AGEs has been shown in mice by administering synthetic AGEs (derived from MGO treatment of BSA) that enhanced the accumulation of triglycerides and premature development of insulin resistance due to the reduction in anti-AGE receptor 1 (AGER1) and sirtuin 1 (SIRT1) in various tissues (Cai et al, 2012). Diet-derived AGEs has also been shown to exacerbate conditions of diabetic complications resulting in accumulation of pro-inflammatory factors such as tumor necrosis factor- α (TNF- α ) and interleukin-6 (IL-6) in the serum of streptozotocin-induced diabetic mice (LV et al, 2016). AGEs also lead to significant vascular complications and damage to organs such as the heart and kidney (LV et al, 2016).…”

Section: The Maillard Reaction: Initiators Propagators and Chemistrymentioning

confidence: 99%

“…Diet-derived AGEs has also been shown to exacerbate conditions of diabetic complications resulting in accumulation of pro-inflammatory factors such as tumor necrosis factor- α (TNF- α ) and interleukin-6 (IL-6) in the serum of streptozotocin-induced diabetic mice (LV et al, 2016). AGEs also lead to significant vascular complications and damage to organs such as the heart and kidney (LV et al, 2016). These studies provide evidence behind the direct involvement of α-DCs such as MGO in mediating a variety of age-related disease complications.…”

Section: The Maillard Reaction: Initiators Propagators and Chemistrymentioning

confidence: 99%

The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality

et al. 2018

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Accumulation of advanced glycation end products (AGEs) on nucleotides, lipids, and peptides/proteins are an inevitable component of the aging process in all eukaryotic organisms, including humans. To date, a substantial body of evidence shows that AGEs and their functionally compromised adducts are linked to and perhaps responsible for changes seen during aging and for the development of many age-related morbidities. However, much remains to be learned about the biology of AGE formation, causal nature of these associations, and whether new interventions might be developed that will prevent or reduce the negative impact of AGEs-related damage. To facilitate achieving these latter ends, we show how invertebrate models, notably Drosophila melanogaster and Caenorhabditis elegans, can be used to explore AGE-related pathways in depth and to identify and assess drugs that will mitigate against the detrimental effects of AGE-adduct development.

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“…Diabetic mice on a high‐AGE diet have been shown to have fibrous caps and signs that indicated progression of atherosclerosis (Lin et al., ). Compared to diabetic mice on a control diet, a high‐AGE diet was observed to exacerbate diabetic characteristics, such as high‐blood‐glucose and low‐serum‐insulin levels (Lv, Lv, Dai, Sun, & Xu, ). The high‐AGE diet also deteriorated the microanatomy of the pancreas, heart, and kidneys, including altering the structure of endothelial cells, mesangial cells, and podocytes along with increased damage to cardiac muscle and to the fibrous tissue of the heart (Lv et al., ).…”

Section: Ages and Their Association With Diseasementioning

confidence: 99%

“…Compared to diabetic mice on a control diet, a high‐AGE diet was observed to exacerbate diabetic characteristics, such as high‐blood‐glucose and low‐serum‐insulin levels (Lv, Lv, Dai, Sun, & Xu, ). The high‐AGE diet also deteriorated the microanatomy of the pancreas, heart, and kidneys, including altering the structure of endothelial cells, mesangial cells, and podocytes along with increased damage to cardiac muscle and to the fibrous tissue of the heart (Lv et al., ). Alzheimer's disease model mice fed a high‐AGE diet showed a decrease in spatial learning, an increase in oxidative stress, and an increase in AGE depositions in the vasculature and hippocampus (Lubitz et al., ).…”

Section: Ages and Their Association With Diseasementioning

confidence: 99%

The Inhibition of Advanced Glycation End Products by Carnosine and Other Natural Dipeptides to Reduce Diabetic and Age‐Related Complications

Freund

Chen

Decker

2018

Comp Rev Food Sci Food Safe

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As people age they are at a greater risk for many disorders including cardiovascular, renal, and neurodegenerative diseases, and these conditions are exacerbated by diabetes. An important cause of the maladies associated with both age and diabetes is the formation of advanced glycation end products (AGEs). AGE formation is initiated by glycation reactions between reducing sugars and free amine groups. A cascade of other reactions follows, leading to alterations in membrane function and damage to the proteome, such as protein crosslinking. Compounds that prevent these reactions are currently being researched, but peptides hold great potential as they tend to lack toxicity, are absorbed intact, are easily produced, and are cheaper than other options. Of the peptides researched, carnosine is the most promising. Research suggests that carnosine is absorbed into the plasma unaltered and intact. Carnosine has been shown to prevent AGE formations through reduction of blood glucose, prevention of early glycation, and even reversing previously formed AGEs. Other promising peptides and amino acids include β-alanine, L-histidine, homocarnosine, anserine, and glutathione. If bioactive peptides and amino acids can minimize the formation of AGEs, foods containing these peptides could be used to improve health.

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Food-advanced glycation end products aggravate the diabetic vascular complications via modulating the AGEs/RAGE pathway

Cited by 26 publications

References 59 publications

Hyperglycemia-related advanced glycation end-products is associated with the altered phosphatidylcholine metabolism in osteoarthritis patients with diabetes

Hyperglycemia-related advanced glycation end-products is associated with the altered phosphatidylcholine metabolism in osteoarthritis patients with diabetes

The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality

The Inhibition of Advanced Glycation End Products by Carnosine and Other Natural Dipeptides to Reduce Diabetic and Age‐Related Complications

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