Dietary fat quantity and quality modifies advanced glycation end products metabolism in patients with metabolic syndrome
Advanced glycation end products (AGEs) increase in dysmetabolic conditions. Lifestyle, including diet, has shown be effective in preventing the development of metabolic syndrome (MetS). We investigated whether AGE metabolism is affected by diets with different fat quantity and quality in MetS patients.Methods and results:
A randomized, controlled trial assigned 75 MetS patients to one of four diets: high SFA (HSFA), high MUFA (HMUFA), and two low-fat, high-complex carbohydrate diets (LFHCC) supplemented with long-chain n-3 PUFA or placebo for 12-weeks each. Dietary and serum AGE [methylglyoxal (MG: lysine-MG-H1) and N-carboxymethyllysine] levels and gene expression related to AGE metabolism in peripheral blood mononuclear cells (AGER1, RAGE, GloxI, and Sirt1 mRNA) were determined. HMUFA diet reduced serum AGE (sAGE) and RAGE mRNA, increased AGER1 and GloxI mRNA levels compared to the other diets. LFHCC n-3 diet reduced sAGE levels and increased AGER1 mRNA levels compared to LFHCC and HSFA diets. Multiple regression analyses showed that sMG and AGER1 mRNA appeared as significant predictors of oxidative stress/inflammation-related parameters.Conclusions:
Low AGE content in HMUFA diet reduces sAGEs and modulates the gene expression related to AGE metabolism in MetS patients, which may be used as a therapeutic approach to reduce the incidence of MetS and related chronic diseases.
Advanced glycation end products (AGEs) contribute in the development and progression of chronic diseases, such as metabolic syndrome (MetS). Endogenous AGE formation and exogenous AGE content, mainly through diet, represent the total body load of AGEs. High MUFA-rich diet reduced serum AGE levels and modulated gene expression related to AGEs metabolism, with the subsequent reduction of oxidative stress and inflammation in patients with MetS, as a therapeutic approach to reduce the incidence of MetS and related chronic diseases.