ArticleCell biochemistry and biophysics2024
Investigation of Advanced Glycation End Products in Liver, Adipose, and Renal Tissue of Mice on a High-Fat Diet.
Article in Cell biochemistry and biophysics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- The Advanced Glycation End-Products (AGE)-Receptor for AGE System (RAGE): An Inflammatory Pathway Linking Obesity and Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- Role of metabolic conditions in cardiorenal diseases: initiating pathways and therapeutic targeting.Frontiers in nutrition · 2025Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is a complex condition associated with disruptions in carbohydrate, protein, and fat metabolism, linked to increased insulin resistance and glucose intolerance. High levels of Advanced Glycation End-products (AGEs) are associated with a range of chronic diseases, including kidney diseases, diabetic complications, cardiovascular diseases, and neurodegenerative diseases. Our study aims to investigate the accumulation of AGEs in the liver, renal and adipose tissues of mice fed a high-fat diet, contributing to a deeper understanding of obesity and its related metabolic disorders. Our study consists of three different groups fed with diets containing 60% and 10% fat. The Experiment 1 group was maintained on their diet for 12 weeks, while the obese 2 and control groups continued their diets for 24 weeks. AGEs in the liver and kidney tissues obtained were measured using the High-performance liquid chromatography grade (HPLC) method. Higher accumulation of AGEs has been observed in kidney tissue compared to adipose and liver tissues (p < 0.05). Moreover, the GO levels were notably higher in liver tissue than in adipose tissue of the D1 and D2 groups (p < 0.0001). Our results suggest that particularly in kidney tissue, increased filtration burden, functional impairment, and receptor interaction due to obesity may be effective. The lower levels of AGEs detected, especially in the obese groups compared to the control, can be attributed to the inability to metabolize AGEs due to tissue damage caused by obesity.
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