Methylglyoxal Independently Contributes to Liver Fibrosis in Obesity: Study
A new study has determined that increased concentrations of methylglyoxal (MGO), a potent reactive byproduct of glucose metabolism, can independently cause the onset of liver fibrosis among obese individuals. The finding is consistent with mounting evidence indicating that MGO and similar compounds not only initiate inflammation and produce deleterious advanced glycation end products (AGEs), but also are key players in liver injury involved with metabolic dysfunction-associated steatotic liver disease (MASLD).
The research, which quantified plasma concentrations of MGO, glyoxal (GO), and 3-deoxyglucosone (3-DG), had significant correlations with severity of liver fibrosis, even in non-type 2 diabetic subjects. The study was conducted by Oluwatomisono I. and colleagues published in the journal of Diabetes Obesity and Metabolism.
264 severely obese subjects undergoing bariatric surgery were studied as part of the BARIA cohort. Among the participants, 22% had type 2 diabetes, 77% were female, the median age was 47 years (IQR: 39–54 years), and the median BMI was 39 kg/m² (IQR: 36–41 kg/m²). Plasma concentrations of MGO, GO, and 3-DG were measured in a research setting using ultra-high-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS). Liver fibrosis was assessed by two different approaches: the non-invasive Fibrosis-4 (FIB-4) Index and direct liver histology score from biopsies.
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