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 (β-alanyl-
L-histidine) and
anserine (β-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.