Differences
This shows you the differences between two versions of the page.
| Both sides previous revisionPrevious revision | |
| steatohepatitis [2025/09/29 04:59] – [non-alcoholic steatohepatitis (NASH)] gary1 | steatohepatitis [2025/09/29 04:59] (current) – [non-alcoholic steatohepatitis (NASH)] gary1 |
|---|
| * Obesity impairs hepatocyte ureagenic and oxidative gene expression. Hepatocyte Arg2 deletion impairs ureagenesis, TCA cycle, and mitochondrial function. **Hepatocyte Arg2 deficiency drives obesity, liver steatosis, and insulin resistance with aging**. The urea cycle defects lead to secondary impairment in the tricarboxylic acid (TCA) cycle, a key pathway for energy metabolism. This disruption results in inefficient calorie utilization and excessive fat storage in the liver, which can subsequently cause inflammation and fibrosis, contributing to the progression of the disease. (([[https://www.sciencedirect.com/science/article/pii/S155041312400278X|Cell Metab. 2024: Hierarchical tricarboxylic acid cycle regulation by hepatocyte arginase 2 links the urea cycle to oxidative metabolism]])) | * Obesity impairs hepatocyte ureagenic and oxidative gene expression. Hepatocyte Arg2 deletion impairs ureagenesis, TCA cycle, and mitochondrial function. **Hepatocyte Arg2 deficiency drives obesity, liver steatosis, and insulin resistance with aging**. The urea cycle defects lead to secondary impairment in the tricarboxylic acid (TCA) cycle, a key pathway for energy metabolism. This disruption results in inefficient calorie utilization and excessive fat storage in the liver, which can subsequently cause inflammation and fibrosis, contributing to the progression of the disease. (([[https://www.sciencedirect.com/science/article/pii/S155041312400278X|Cell Metab. 2024: Hierarchical tricarboxylic acid cycle regulation by hepatocyte arginase 2 links the urea cycle to oxidative metabolism]])) |
| * **role of miR-93 in MASLD** | * **role of miR-93 in MASLD** |
| * "miR-93 was significantly upregulated in the livers of patients with MASLD and diet-induced obese mice. miR-93 KO mice exhibited reduced hepatic steatosis. Specifically, miR-93 deficiency upregulated genes involved in fatty acid oxidation and downregulated genes associated with cholesterol biosynthesis. Sirtuin 1 (SIRT1) was identified as a direct target of miR-93, and miR-93 KO enhanced SIRT1 expression and activated the LKB1-AMPK signaling pathway. **Niacin treatment downregulated miR-93, ameliorating hepatic steatosis** by enhancing SIRT1 activity" (([[https://www.metabolismjournal.com/article/S0026-0495(25)00135-0/abstract|2025: Hepatic miR-93 promotes the pathogenesis of metabolic dysfunction-associated steatotic liver disease by suppressing SIRT1]]) | * "miR-93 was significantly upregulated in the livers of patients with MASLD and diet-induced obese mice. miR-93 KO mice exhibited reduced hepatic steatosis. Specifically, miR-93 deficiency upregulated genes involved in fatty acid oxidation and downregulated genes associated with cholesterol biosynthesis. Sirtuin 1 (SIRT1) was identified as a direct target of miR-93, and miR-93 KO enhanced SIRT1 expression and activated the LKB1-AMPK signaling pathway. **Niacin treatment downregulated miR-93, ameliorating hepatic steatosis** by enhancing SIRT1 activity" (([[https://www.metabolismjournal.com/article/S0026-0495(25)00135-0/abstract|2025: Hepatic miR-93 promotes the pathogenesis of metabolic dysfunction-associated steatotic liver disease by suppressing SIRT1]])) |
| |
| =====acute fatty liver of pregnancy (AFLP)===== | =====acute fatty liver of pregnancy (AFLP)===== |
