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• W2768056799 abstract "Fructose is a reducing and highly lipogenic sugar that has unique metabolic effects in the liver. Non-enzymatic fructosylation of proteins generates advanced glycation end products (AGEs). Human serum albumin (HSA) may undergo fructosylation vis-à-vis AGEs formation. High fructose consumption may lead to structurally altered and functionally compromised fructosylated-HSA-AGEs, which can cause damage to hepatocytes resulting in hepatic macro- and microvesicular steatosis. In this study, HSA was incubated with varying concentrations of fructose for 10days and the induced changes were studied. Fructosylated-HSA exhibited hyperchromicity, increased AGE-specific fluorescence, quenching of tryptophan fluorescence and increased melting temperature. Nε-[carboxymethyl]-lysine (CML), was detected by liquid chromatography mass spectrometry (LC-MS). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) results showed decreased mobility in fructosylated-HSA. Perturbations in secondary and tertiary structure were revealed by fourier transform-infrared spectroscopy (FT-IR), supported by far- and near-UV circular dichroism (CD). Dynamic light scattering (DLS) and Matrix-Assisted Laser Desorption Ionization-Time of Flight (MALDI-TOF) mass spectrometry studies suggested increase in molecular mass of fructosylated-HSA. Amyloidogenic aggregates were confirmed from Congo red, Thioflavin T assay and Scanning electron microscope (SEM). These investigations confirmed the structural alterations in fructosylated-HSA and warrants further study to probe the role of fructosylated-HSA-AGEs in hepatopathy vis-à-vis fatty liver diseases." @default.
• W2768056799 created "2017-11-17" @default.
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• W2768056799 date "2018-04-01" @default.
• W2768056799 modified "2023-10-16" @default.
• W2768056799 title "Fructose-human serum albumin interaction undergoes numerous biophysical and biochemical changes before forming AGEs and aggregates" @default.
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• W2768056799 doi "https://doi.org/10.1016/j.ijbiomac.2017.11.069" @default.
• W2768056799 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29133088" @default.
• W2768056799 hasPublicationYear "2018" @default.
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