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Quercetin and calorie restriction improve leptin/adiponectin balance through reducing high-fat diet-induced oxidative stress in male BALB/c mice.
Biochem Biophys Res Commun
January 2025
Department of Clinical Biochemistry, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.
Throughout the recent decades, obesity has become a serious health problem that raises the risk of several diseases, including cancer, diabetes, hypertension, heart disease, neurological musculoskeletal disorders, and Non-alcoholic fatty liver disease. Some strategies, such as dietary interventions, calorie restriction (CR), and the use of antioxidant compounds, have been proposed to improve quality of life in relation to obesity. The goal of this study was to characterize the effects of CR and quercetin (QUER) on obesity-induced oxidative stress (OS).
View Article and Find Full Text PDFLiver magnetic resonance imaging, non-alcoholic fatty liver disease and metabolic syndrome risk in pre-pubertal Mexican boys.
Sci Rep
October 2024
Department of Neuroimaging, King's College London, London, UK.
Rising global pediatric obesity rates, increase non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MetS) prevalence, with MetS being a NAFLD risk factor. NAFLD can be asymptomatic, with liver function tests insensitive to mild disease, and liver biopsy, risking complications. Thus, we investigated multiparametric MRI (mpMRI) metrics of liver fat (proton density fat fraction, PDFF) and disease activity (fibro-inflammation; iron-corrected T1, cT1), in a Hispanic pre-pubertal pediatric cohort, with increased risk of NAFLD.
View Article and Find Full Text PDFDelphinidin or α-amyrin attenuated liver steatosis and metabolic disarrangement in rats fed a high-fat diet.
Biofactors
December 2024
Department of Pharmacology and Toxicology, Faculty of Pharmacy, October 6 University, Giza, Egypt.
Non-alcoholic fatty liver disease (NAFLD) is a liver pathology concomitant with metabolic disarrangement. This study assessed the therapeutic impacts of delphinidin, an anthocyanin, or α-amyrin, a pentacyclic triterpenoid, on NAFLD in rats and the underlying mechanisms involved. NAFLD was established by feeding a high-fat diet (HFD) for 10 weeks, either alone or in combination with delphinidin (40 mg/kg, oral) or α-amyrin (20 mg/kg, oral).
View Article and Find Full Text PDFAdipokine/hepatokines profiling of fatty liver in adolescents and young adults: cross-sectional and prospective analyses of the BCAMS study.
Hepatol Int
October 2024
Department of Endocrinology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, People's Republic of China.
Article Synopsis
- The study investigates the connection between obesity and non-alcoholic fatty liver disease (NAFLD) in Chinese youth, focusing on how specific adipokines and hepatokines serve as potential links between the two conditions.
- Analysis was conducted on data from the Beijing Children and Adolescents Metabolic Syndrome (BCAMS) study, examining metabolic risks through ultrasound and plasma biomarker measurements to evaluate the obesity-NAFLD relationship.
- Results showed strong associations between elevated levels of RBP4, FGF21, and leptin, along with decreased adiponectin, as predictors of NAFLD, indicating that dysregulated adipokines/hepatokines play a significant role in the development of obesity-related NAFLD in young individuals
Glucotoxicity suppresses function of pancreatic beta and duct cells via miR-335-targeted Runx2 and insulin-mediated mechanism.
Protoplasma
October 2024
Molecular Biology Section, Biology Department, Faculty of Science, Istanbul University, Vezneciler, 34134, Istanbul, Türkiye.
Pancreatic cell dynamics have important contributions to the development of type 2 diabetes and related diseases such as nonalcoholic fatty pancreas disease. The aim of this study was to investigate the effects of prolonged excessive glucose exposure on the functions of pancreatic beta cells and duct cells in single and co-culture conditions. In this study, we focused on the effects of glucotoxicity on insulin secretion which is the main function of beta cells and on progenitor functions of duct cells.
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