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An insight on the additive impact of type 2 diabetes mellitus and nonalcoholic fatty liver disease on cardiovascular consequences.
Mol Biol Rep
January 2025
Department of Pharmaceutical Sciences & Technology, BIT Mesra, Ranchi, 835215, India.
Background: Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM) are associated with a multifactorial complicated aetiology that is often coexisting and has a strong and distinct connection with cardiovascular diseases (CVDs). In order to accomplish effective and appropriate therapeutic strategies, a deeper understanding of the bidirectional interaction between NAFLD patients, NAFLD patients with T2DM, and NAFLD patients with CVDs is required to control the concomitant rise in prevalence of these conditions worldwide. This article also aims to shed light on the epidemiology and mechanisms behind the relationship between T2DM, NAFLD and the related cardiovascular consequences.
View Article and Find Full Text PDFResearch on the function of epigenetic regulation in the inflammation of non-alcoholic fatty liver disease.
Life Med
August 2024
Department of Hepatobiliary Surgery, Xi-Jing Hospital, Fourth Military Medical University, Changle West Road, Xincheng District, Xi'an, Shaanxi 710032, China.
Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver condition, characterized by a spectrum that progresses from simple hepatic steatosis to nonalcoholic steatohepatitis, which may eventually lead to cirrhosis and hepatocellular carcinoma. The precise pathogenic mechanisms underlying NAFLD and its related metabolic disturbances remain elusive. Epigenetic modifications, which entail stable transcriptional changes without altering the DNA sequence, are increasingly recognized as pivotal.
View Article and Find Full Text PDFGolgi protein 73: charting new territories in diagnosing significant fibrosis in MASLD: a prospective cross-sectional study.
Front Endocrinol (Lausanne)
January 2025
Department of Gastroenterology, Beijing Ditan Hospital, Capital Medical University, Beijing, China.
Objectives: To explore the correlation between serum Golgi protein 73 (GP73) levels and the degree of fibrosis in Metabolic dysfunction associated steatotic liver disease (MASLD); to establish a non-invasive diagnostic algorithm based on serum GP73 and liver elasticity.
Methods: This is a prospective cross-sectional study, including 228 patients diagnosed with MASLD from May 2018 to January 2024 at two tertiary hospitals. Clinical data and hepatic pathological features and the correlation between serum GP73 and liver fibrosis were assessed.
Liver Organoids From Hepatocytes of Healthy Humans and Non-alcoholic Fatty Liver Disease (NAFLD) Patients Display Multilineage Architecture and can be Used to Develop an Model of Steatohepatitis.
J Clin Exp Hepatol
December 2024
BRIC-Translational Health Science and Technology Institute, Faridabad, Haryana, India.
Background/aim: Non-alcoholic fatty liver disease (NAFLD) is a global health concern with limited treatment options. The paucity of predictive models in preclinical settings seems to be one of the limitations of identifying effective medicines. We therefore aimed to develop an model that can display the key hallmarks of NAFLD, such as steatosis, inflammation, and fibrosis.
View Article and Find Full Text PDFFatty acid oxidation-induced HIF-1α activation facilitates hepatic urate synthesis through upregulating NT5C2 and XDH.
Life Metab
October 2024
CAS Key Laboratory of Nutrition, Metabolism, and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences (CAS), Shanghai 200031, China.
Dyslipidemia affects approximately half of all people with gout, and prior Mendelian randomization analysis suggested a causal role for elevated triglycerides in hyperuricemia (HU), but the underlying mechanisms remain elusive. We hypothesize that dyslipidemia promotes hepatic urate biosynthesis in HU and gout and fatty acid (FA) oxidation (FAO) drives this process. Here we developed a targeted metabolomics to quantify major metabolites in purine metabolic pathway in the sera of a human cohort with HU, gout, and normaluricemic controls.
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