Background And Objectives: Non-alcoholic fatty liver disease (NAFLD) is a progressive liver disorder and is usually accompanied by obesity, metabolic syndrome, and diabetes mellitus. NAFLD progression can lead to impaired functions of hepatocytes such as alternations in expression and function of hepatic transporters. The present study aimed to summarize and discuss the results of clinical and preclinical human studies that investigate the effect of NAFLD on hepatic transporters.
Methods: The databases of PubMed, Scopus, Embase, and Web of Science were searched systematically up to 1 March 2022. The risk of bias was assessed for cross-sectional studies through the Newcastle-Ottawa Scale score.
Results: Our review included ten cross-sectional studies consisting of 485 participants. Substantial alternations in hepatic transporters were seen during NAFLD progression to non-alcoholic steatohepatitis (NASH) in comparison with control groups. A significant reduction in expression and function of several hepatic uptake transporters, upregulation of many efflux transporters, downregulation of cholesterol efflux transporters, and mislocalization of canalicular transporter ABCC2 are associated with NAFLD progression.
Conclusion: Since extensive changes in hepatic transporters could alter the pharmacokinetics of the drugs and potentially affect the safety and efficacy of drugs, close monitoring of drug administration is highly suggested in patients with NASH.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s13318-022-00802-8 | DOI Listing |
J Nutr
January 2025
Department of Nutritional Science and Food Management, Ewha Womans University, Seoul, 03760, Republic of Korea; Graduate Program in System Health Science and Engineering, Ewha Womans University, Seoul, 03760, Republic of Korea. Electronic address:
Background: Pine (Pinus koraiensis) nut oil (PNO) has been reported to have various beneficial effects on hepatic triglyceride accumulation and atherosclerosis in animal models. MicroRNAs (miRs) are involved in various diseases by modulating physiological processes. However, the mechanism underlying PNO's effects on the regulation of miRs involved in hepatic cholesterol homeostasis and inflammation remains unclear.
View Article and Find Full Text PDFToxicol Mech Methods
January 2025
Department of Pharmacology, Shri Vishnu College of Pharmacy, Vishnupur, Bhimavaram, Andhra Pradesh, India-534202.
The harmful by-product of paracetamol is known as N-Acetyl-p-benzoquinoneimine, (NAPQI). When paracetamol is given at therapeutic dosages or in excess, it undergoes Phase I metabolism in the liver via Cytochrome P-450 2E1 (CYP2E1), and then it produces NAPQI. Previous studies reported that a non-ionic surfactant known as Brij 35 (Polyoxyethylene lauryl ether) has been shown to be an effective inhibitor of CYP2E1 and P-glycoprotein (P-gp).
View Article and Find Full Text PDFCureus
December 2024
Diabetes Research Group, Swansea University Medical School, Swansea, GBR.
Introduction Type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD) have shared pathophysiology. We aim to explore associations between these diseases and the impact of T2D therapies on MASLD-related outcomes in a real-world population. Methods A retrospective cohort study included 153 patients with biopsy-proven MASLD.
View Article and Find Full Text PDFAm J Chin Med
January 2025
Department of Pharmacology, Shaanxi University of Chinese Medicine, No. 1, Middle Section of Century Avenue, Xianyang 712046, P. R. China.
This study aimed to clarify the protective effect of Glycyrrhizic acid (GL) against Diosbulbin B (DB) - induced liver injury in mice and investigate its mechanisms of action. A liver injury DB was established in mice through the oral administration of DB for 15 days. At the same time, GL was administered to the mice for treatment.
View Article and Find Full Text PDFArthritis Rheumatol
January 2025
Assistant Professor of Pathology and of Microbiology and Microbiology and Immunology, Stanford University, Stanford, CA, 94305.
Humans develop hyperuricemia via decreased urate elimination and excess urate production, consequently promoting monosodium urate crystal deposition and incident gout. Normally, approximately two thirds of urate elimination is renal. However, chronic kidney disease (CKD) and other causes of decreased renal urate elimination drive hyperuricemia in most with gout.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!