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Elevated methylglyoxal and related dicarbonyls (GO, 3-DG) are independently associated with increased liver fibrosis in obese adults, even in those without type 2 diabetes.
A novel study has uncovered a significant connection between methylglyoxal (MGO), a reactive compound in the body, and the progression of liver fibrosis in severely obese individuals. The research, conducted on participants from the BARIA cohort, sheds light on the role of dicarbonyl stress in metabolic dysfunction-associated steatotic liver disease (MASLD), paving the way for potential therapeutic interventions.
MGO is a highly reactive dicarbonyl known to modify proteins, forming advanced glycation end products and triggering inflammatory pathways. Elevated levels of MGO have been previously linked to ailments such as type 2 diabetes (T2D) and atherosclerosis. However, its role in liver fibrosis, especially in the context of obesity and metabolic dysfunction, had remained unclear until now.
Oluwatomisono Akinrimisi and other researchers analyzed 264 severely obese individuals (median age 47 years, 77% female, median body mass index [BMI] 39 kg/m²) preparing for bariatric surgery. Around 22% of participants had T2D. Plasma levels of MGO and related dicarbonyl compounds—glyoxal (GO) and 3-deoxyglucosone (3-DG)—were measured via advanced ultra-high-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS). Liver fibrosis was assessed through histological biopsy scoring and the fibrosis-4 (FIB-4) index.
Key findings
Thus, dicarbonyl stress, particularly MGO, is an independent contributor to liver damage in obesity. By identifying MGO as a potential therapeutic target, researchers suggest that interventions aimed at lowering MGO levels could slow or prevent liver fibrosis in high-risk individuals.
Diabetes, Obesity and Metabolism
Higher plasma dicarbonyl levels are associated with liver fibrosis in obese individuals
Oluwatomisono Akinrimisi et al.
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