ABSTRACT
The rapid increase in the prevalence of metabolic syndrome, which is associated with a state of elevated systemic oxidative stress and inflammation, is expected to cause future increases in the prevalence of diabetes and cardiovascular diseases. Oxidation of polyunsaturated fatty acids and sugars produces reactive carbonyl species, which, due to their electrophilic nature, react with the nucleophilic sites of certain amino acids. This leads to formation of protein adducts such as advanced glycoxidation/lipoxidation end products (AGEs/ALEs), resulting in cellular dysfunction. Therefore, an effective reactive carbonyl species and AGEs/ALEs sequestering agent may be able to prevent such cellular dysfunction. There is accumulating evidence that histidine containing dipeptides such as carnosine (beta-alanyl-L-histidine) and anserine (beta-alanyl-methyl-L-histidine) detoxify cytotoxic reactive carbonyls by forming unreactive adducts and are able to reverse glycated protein. In this review, 1) reaction mechanism of oxidative stress and certain chronic diseases, 2) interrelation between oxidative stress and inflammation, 3) effective reactive carbonyl species and AGEs/ALEs sequestering actions of histidine-dipeptides and their metabolism, 4) effects of carnosinase encoding gene on the effectiveness of histidine-dipeptides, and 5) protective effects of histidine-dipeptides against progression of metabolic syndrome are discussed. Overall, this review highlights the potential beneficial effects of histidine-dipeptides against metabolic syndrome. Randomized controlled human studies may provide essential information regarding whether histidine-dipeptides attenuate metabolic syndrome in humans.
Subject(s)
Humans , Amino Acids , Anserine , Carbohydrates , Cardiovascular Diseases , Carnosine , Chronic Disease , Dipeptides , Fatty Acids, Unsaturated , Histidine , Inflammation , Metabolism , Oxidative Stress , Prevalence , Sequestering AgentsABSTRACT
Introduction: Advanced glycoxidation end-products (AGEs) are involved in age-related conditions and diabetic complications. Diet intake contributes to their circulating concentrations. Aim: To measure serum and urinary AGEs in non-diabetic volunteers and relate their concentration to body composition, blood chemistry and dietary ingesti¢n. Methods: We studied 41 adult men (31 middle-aged adults and 10 elderly). A nutritional assessment including a dietary recall designed for detection of AGE ingesti¢n (specifically carboxymethyl-lysine(CML)), and anthropometric measurements were performed. Also serum lipoproteins, insulin, glucose, leptin and C reactive protein (CRP). AGEs were measured in serum and urine samples using size exclusion chromatography and flow injection assay (FIA); the technical procedures were first employed in 11 heterogeneous diabetics, as positive controls for this methodology. Results: Serum and urinary chromatograms indicated that areas under the curve were not different in younger compared with elderly adults. AGEs did not correlate with dietary intake, body composition, nor metabolic parameters, however they correlated significantly with renal function and CRP concentration. Discussion: In these non-diabetic volunteers, with low CML intake, serum and urinary concentration of AGEs were not related to dietary intake. AGEs were related to renal function and CRP, but not to body composition, lipoproteins, insulin and glucose.
Subject(s)
Adult , Aged , Humans , Male , Middle Aged , Diet , /blood , /urine , Body Composition , Case-Control Studies , Chromatography, High Pressure Liquid , Fluorescence , Glucose/analysis , /administration & dosage , Lipoproteins/blood , Lysine/administration & dosage , Lysine/analogs & derivatives , Spectrometry, FluorescenceABSTRACT
To investigate the inhibitory effects of silymarin on diabetic blood vessels chroniccomplication. Methods:Silymarin was given to streptozocin-induced diabetic rats. Rats were killed 9 weeksafter treatment. Plasma LPO, fructosamine and RBC-SOD were measured. LPO, fruct0samine, fluores-cence intensities of AGEs, pentosidine and liperperoxide adducts in aorta were also measured. Results:The early nonenzymatic glycation products-fructosamine were not inhibited, however, LPO and f1uores-cence intensities of AGEs, pentosidine,MDA and HNE adducts in aorta were more significantly reducedthan DM group. Conclusion: The results suggest that silymarin may inhibit nonenzymatic glycation andoxidation in aorta of streptozocin-induced diabetic rats and control the diabetic chronic complication.