A: Pentosidine exposure significantly altered the levels of various metabolites in adipose tissue. For example, pyruvic acid and inositol levels increased, while petroselinic acid and D-glucuronic acid levels decreased. These changes were dose-dependent, indicating that pentosidine exposure can lead to significant disruptions in the metabolic balance of adipose tissue. The most notable changes were observed in fatty acids and amino acids, suggesting that pentosidine primarily affects energy and lipid metabolism.

A: The key metabolic pathways disrupted by pentosidine include ascorbate and aldarate metabolism, glycine, serine, and threonine metabolism, sulfur metabolism, pyruvate metabolism, aminoacyl-tRNA biosynthesis, alanine, aspartate, and glutamate metabolism, glyoxylate and dicarboxylate metabolism, the TCA cycle, glycolysis/gluconeogenesis, inositol phosphate metabolism, cysteine and methionine metabolism, and pentose and glucuronate interconversions. These pathways are crucial for energy metabolism, fatty acid metabolism, and amino acid metabolism, indicating that pentosidine exposure can lead to significant metabolic disturbances in adipose tissue.

A: Pentosidine exposure significantly inhibited body weight gain in rats in a dose-dependent manner. Histopathological analysis revealed that adipocytes in the high-dose group exhibited remarkable changes in size and shape, with some cells significantly larger than those in the normal diet group. Additionally, cell membranes appeared damaged, and inflammatory cell infiltration was observed. These results indicate that pentosidine exhibits toxicity in adipose tissue, leading to histological alterations and weight changes.

A: A study revealed that pentosidine exposure significantly altered the metabolic profiles of adipose tissue in rats. A total of 42 differential metabolites were identified, with 16 upregulated and 26 downregulated metabolites. The most impacted pathways included ascorbate and aldarate metabolism, glycine, serine, and threonine metabolism, sulfur metabolism, pyruvate metabolism, and the TCA cycle. Pyruvic acid was identified as a key upregulated metabolite involved in 34 pathways, while α-ketoglutaric acid was a key downregulated metabolite involved in 19 pathways. These findings suggest that pentosidine disrupts energy metabolism, fatty acid metabolism, and amino acid metabolism in adipose tissue, potentially leading to tissue dysfunction.