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Peter, A. ; Schleicher, E. ; Kliemank, E. ; Szendroedi, J. ; Königsrainer, A.* ; Häring, H.-U. ; Nawroth, P.P. ; Fleming, T.

Accumulation of non-pathological liver fat is associated with the loss of glyoxalase I activity in humans.

Metabolites 14:209 (2024)
Verlagsversion DOI PMC
Creative Commons Lizenzvertrag
The underlying molecular mechanisms for the development of non-alcoholic fatty liver (NAFL) and its progression to advanced liver diseases remain elusive. Glyoxalase 1 (Glo1) loss, leading to elevated methylglyoxal (MG) and dicarbonyl stress, has been implicated in various diseases, including obesity-related conditions. This study aimed to investigate changes in the glyoxalase system in individuals with non-pathological liver fat. Liver biopsies were obtained from 30 individuals with a narrow range of BMI (24.6-29.8 kg/m2). Whole-body insulin sensitivity was assessed using HOMA-IR. Liver biopsies were analyzed for total triglyceride content, Glo1 and Glo2 mRNA, protein expression, and activity. Liquid chromatography-tandem mass spectrometry determined liver dicarbonyl content and oxidation and glycation biomarkers. Liver Glo1 activity showed an inverse correlation with HOMA-IR and liver triglyceride content, but not BMI. Despite reduced Glo1 activity, no associations were found with elevated liver dicarbonyls or glycation markers. A sex dimorphism was observed in Glo1, with females exhibiting significantly lower liver Glo1 protein expression and activity, and higher liver MG-H1 content compared to males. This study demonstrates that increasing liver fat, even within a non-pathological range, is associated with reduced Glo1 activity.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Nafl ; Advanced Glycation Endproducts ; Dicarbonyls ; Glyoxalase 1 ; Insulin Resistance ; Liver Triglycerides; Cardiovascular-disease; Dicarbonyl Stress; Sex-differences; Phosphorylation; Methylglyoxal; Protein; Detoxification; Expression; Cells
ISSN (print) / ISBN 2218-1989
e-ISSN 2218-1989
Zeitschrift Metabolites
Quellenangaben Band: 14, Heft: 4, Seiten: , Artikelnummer: 209 Supplement: ,
Verlag MDPI
Verlagsort St Alban-anlage 66, Ch-4052 Basel, Switzerland
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Cancer (IDC)
Institute of Diabetes Research and Metabolic Diseases (IDM)
Förderungen Deutsche Forschungsgemeinschaft