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The cardiovascular complications of diabetes: a striking link through protein glycation.
Ahmad, MN, Farah, AI, Al-Qirim, TM
Romanian journal of internal medicine = Revue roumaine de medecine interne. 2020;(4):188-198
Abstract
Diabetes mellitus is a predominant cause of mortality and morbidity worldwide. One of its serious health problems is cardiovascular complications. Advanced glycation end products (AGEs) are a group of heterogeneous toxic oxidant compounds that are formed after a non-enzymatic reaction between monosaccharides and free amino groups of proteins, compound lipids, and nucleic acids. AGE interacts with various types of cells through a receptor for AGE (RAGE). The interaction between AGE and RAGE is responsible for a cascade of inflammation, oxidative stress, and disruption of calcium homeostasis in cardiac cells of diabetic patients. There is striking evidence that the AGE/RAGE axis with its consequences on inflammation and oxidative stress plays a major role in the development of cardiovascular complications. Therefore, considering AGE as a therapeutic target with foreseeable results would be a wise direction for future research. Interestingly, several studies on nutraceutical, pharmaceutical, and natural products have begun to reveal promising therapeutic results, and this could lead to better health outcomes for many diabetic patients worldwide. This article discusses the current literature addressing the connection between protein glycation and diabetes cardiovascular complications and suggests future avenues of research.
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Advanced glycation end products in diabetes, cancer and phytochemical therapy.
Dariya, B, Nagaraju, GP
Drug discovery today. 2020;(9):1614-1623
Abstract
The irreversible glycation and oxidation of proteins and lipids produces advanced glycation end products (AGEs). These modified AGEs are triggered to bind the receptor for AGE (RAGE), thereby activating its downstream signaling pathways, such as nuclear factor (NF)-κB and phosphoinositide 3-kinase (PI3K)/Akt, ultimately leading to diabetes and cancers. In this review, we focus on the interaction of AGE-RAGE and their associated pathways. We also consider the activity of phytochemicals, such as genistein and curcumin, that trap dicarbonyl compounds including methylglyoxal (MG) and glyoxalase that arise from multiple pathways to block AGE formation and prevent its interaction with RAGE.
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Functional and biological properties of Maillard conjugates and their potential application in medical and food: A review.
Nooshkam, M, Varidi, M, Verma, DK
Food research international (Ottawa, Ont.). 2020;:109003
Abstract
Protein and peptides are usually sensitive to environmental stresses, such as pH changes, high temperature, ionic strength, and digestive enzymes amongst other, which limit their food and medicinal applications. Maillard reaction (also called Maillard conjugation or glycation) occurs naturally without the addition of chemical agents and has been vastly applied to boost protein/peptide/amino acid functionalities and biological properties. Protein/peptide-saccharide conjugates are currently used as emulsifiers, antioxidants, antimicrobials, gelling agents, and anti-browning compounds in food model systems and products. The conjugates also possess the excellent stabilizing ability as a potent delivery system to enhance the stability and bioaccessibility of many bioactive compounds. Carbonyl scavengers such as polyphenols are able to significantly inhibit the formation of advanced glycation end products without a significant effect on early Maillard reaction products (MRPs) and melanoidins, which are currently applied as functional ingredients. This review paper highlights the technological functionality and biological properties of glycoconjugates in food model systems and products. Recent applications of MRPs in medical sciences are also presented.
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Inhibitory effect of phenolic compounds and plant extracts on the formation of advance glycation end products: A comprehensive review.
Khan, M, Liu, H, Wang, J, Sun, B
Food research international (Ottawa, Ont.). 2020;:108933
Abstract
Advance glycation end products (AGEs) are a diverse group of compounds formed through the non-enzymatic maillard reaction of reducing sugars with the free amino groups in proteins, lipids or nucleic acids. Accumulation of AGEs has been suggested to be a pathogenic mechanism of oxidative stress, inflammation and structural tissue damage leading to chronic vascular problems in many ailments including diabetes, atherosclerosis, neuropathy, retinopathy, nephropathy, aging, and chronic renal disease. Treatment with AGEs inhibitors is believed to be a potential strategy for preventing lifestyle-related diseases. To inhibit the AGEs development is supposed to show part in the inhibition of diabetic problems. Study of dietary bioactive combinations with antiglycation properties delivers future views for inhibition or mediation associated to AGEs complications. Many study show the possibility of dietary constituents to stop AGE development. Therefore, search for natural compounds able to prevent glycation and have the potential therapeutic ability to inhibit diabetes and age associated diseases. The purpose of this review is to critically evaluate the existing literature on different phenolics on AGEs inhibition.
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Advanced Glycation End Products: Building on the Concept of the "Common Soil" in Metabolic Disease.
Ruiz, HH, Ramasamy, R, Schmidt, AM
Endocrinology. 2020;(1)
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Abstract
The role of advanced glycation end products (AGEs) in promoting and/or exacerbating metabolic dysregulation is being increasingly recognized. AGEs are formed when reducing sugars nonenzymatically bind to proteins or lipids, a process that is enhanced by hyperglycemic and hyperlipidemic environments characteristic of numerous metabolic disorders including obesity, diabetes, and its complications. In this mini-review, we put forth the notion that AGEs span the spectrum from cause to consequence of insulin resistance and diabetes, and represent a "common soil" underlying the pathophysiology of these metabolic disorders. Collectively, the surveyed literature suggests that AGEs, both those that form endogenously as well as exogenous AGEs derived from environmental factors such as pollution, smoking, and "Western"-style diets, contribute to the pathogenesis of obesity and diabetes. Specifically, AGE accumulation in key metabolically relevant organs induces insulin resistance, inflammation, and oxidative stress, which in turn provide substrates for excess AGE formation, thus creating a feed-forward-fueled pathological loop mediating metabolic dysfunction.
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Dietary Advanced Glycation Endproducts and the Gastrointestinal Tract.
van der Lugt, T, Opperhuizen, A, Bast, A, Vrolijk, MF
Nutrients. 2020;(9)
Abstract
The prevalence of inflammatory bowel diseases (IBD) is increasing in the world. The introduction of the Western diet has been suggested as a potential explanation of increased prevalence. The Western diet includes highly processed food products, and often include thermal treatment. During thermal treatment, the Maillard reaction can occur, leading to the formation of dietary advanced glycation endproducts (dAGEs). In this review, different biological effects of dAGEs are discussed, including their digestion, absorption, formation, and degradation in the gastrointestinal tract, with an emphasis on their pro-inflammatory effects. In addition, potential mechanisms in the inflammatory effects of dAGEs are discussed. This review also specifically elaborates on the involvement of the effects of dAGEs in IBD and focuses on evidence regarding the involvement of dAGEs in the symptoms of IBD. Finally, knowledge gaps that still need to be filled are identified.
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The Relevance of Toxic AGEs (TAGE) Cytotoxicity to NASH Pathogenesis: A Mini-Review.
Sakasai-Sakai, A, Takata, T, Takino, JI, Takeuchi, M
Nutrients. 2019;(2)
Abstract
Non-alcoholic fatty liver disease (NAFLD) is currently the most common feature of chronic liver disease. Non-alcoholic steatohepatitis (NASH) is a severe form of NAFLD, and one of its risk factors is hyperglycemia. The chronic ingestion of excessive amounts of high-fructose corn syrup is associated with an increased prevalence of fatty liver. Under hyperglycemic conditions, advanced glycation end-products (AGEs) are generated through a non-enzymatic glycation reaction between the ketone or aldehyde groups of sugars and amino groups of proteins. Glyceraldehyde (GA) is a metabolic intermediate of sugars, and GA-derived AGEs (known as toxic AGEs (TAGE)) have been implicated in the development of NASH. TAGE accumulates more in serum or liver tissue in NASH patients than in healthy controls or patients with simple steatosis. Furthermore, the TAGE precursor, GA, causes cell damage through protein dysfunctions by TAGE modifications and induces necrotic-type hepatocyte death. Intracellular TAGE may leak outside of necrotic-type cells. Extracellular TAGE then induce inflammatory or fibrotic responses related to the pathology of NASH in surrounding cells, including hepatocytes and hepatic stellate cells. This review focuses on the contribution of TAGE to the pathology of NASH, particularly hepatic cell death related to NASH.
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Development and Progression of Non-Alcoholic Fatty Liver Disease: The Role of Advanced Glycation End Products.
Fernando, DH, Forbes, JM, Angus, PW, Herath, CB
International journal of molecular sciences. 2019;(20)
Abstract
Non-alcoholic fatty liver disease (NAFLD) affects up to 30% of the adult population and is now a major cause of liver disease-related premature illness and deaths in the world. Treatment is largely based on lifestyle modification, which is difficult to achieve in most patients. Progression of simple fatty liver or steatosis to its severe form non-alcoholic steatohepatitis (NASH) and liver fibrosis has been explained by a 'two-hit hypothesis'. Whilst simple steatosis is considered the first hit, its transformation to NASH may be driven by a second hit. Of several factors that constitute the second hit, advanced glycation end products (AGEs), which are formed when reducing-sugars react with proteins or lipids, have been implicated as major candidates that drive steatosis to NASH via the receptor for AGEs (RAGE). Both endogenous and processed food-derived (exogenous) AGEs can activate RAGE, mainly present on Kupffer cells and hepatic stellate cells, thus propagating NAFLD progression. This review focuses on the pathophysiology of NAFLD with special emphasis on the role of food-derived AGEs in NAFLD progression to NASH and liver fibrosis. Moreover, the effect of dietary manipulation to reduce AGE content in food or the therapies targeting AGE/RAGE pathway on disease progression is also discussed.
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Influence of the Maillard Reaction on the Allergenicity of Food Proteins and the Development of Allergic Inflammation.
Toda, M, Hellwig, M, Henle, T, Vieths, S
Current allergy and asthma reports. 2019;(1):4
Abstract
PURPOSE OF REVIEW The Maillard reaction (MR) is a non-enzymatic reaction between reducing sugars and compounds with free amino groups such as proteins and takes place during thermal processing and storage of foods. This review aims to discuss potential effects of dietary MR products on the pathological mechanisms of allergic diseases. RECENT FINDINGS Since the MR leads to modification of proteins with various types of glycation structures, the impact of the MR on the immunogenicity and potential allergenicity of food proteins in many allergenic foods has been assessed. In addition, recent studies have suggested that the MR products, in particular "advanced glycation end products (AGEs)," contained in the diet may be involved in the development of chronic inflammation by acting as inflammatory components and affecting the gut microbiome. This review found that the biological, immunological, and allergic properties of dietary MR products are diverse due to the complexity of the MR.
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10.
Too sweet: Problems of protein glycation in the eye.
Bejarano, E, Taylor, A
Experimental eye research. 2019;:255-262
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Abstract
Laboratory and epidemiological data indicate that high blood sugar levels and/or consuming high glycemia diets are linked to multiple age-related diseases, including age-related macular degeneration, cataract, Parkinson's disease, Alzheimer's disease, diabetic retinopathy, and, apparently glaucoma. High concentrations of blood sugar and perturbations of the systems that regulate blood sugar lead to the accumulation of advanced-glycation end products (AGEs). AGEs are toxic compounds that are formed from the combination of sugars and their metabolites with biomolecules in a non-enzymatic biochemical reaction called glycation. In vitro and in vivo data indicate that high sugar consumption is associated with accumulation of AGEs in a variety of human tissues. Hyperglycemia, along with an oxidative environment and limited cell proliferation in many ocular tissues, encourages formation and precludes dilution of AGEs and associated damage by cell division. These circumstances make many eye tissues vulnerable to glycation-derived damage. Here, we summarize research regarding glycation-induced ocular tissue dysfunction and its contribution to the onset and development of eye disorders. We also discuss how management of carbohydrate nutrition may provide a low-cost way to ameliorate the progression of AGEs-related diseases, including age related macular degeneration and some cataracts, as they do for cardiovascular disease and diabetes.