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Nonalcoholic fatty liver disease (Nepal) is a global pandemic that affects one-quarter of the world's population. Recently, it has been suggested that metabolic-related fatty liver disease, a more appropriate term to describe the disease than NAFLD, which has heightened emphasis on the crucial role of metabolic dysfunction in the disease's pathogenesis. Further we explore findings that mitochondrial function modulates NAFLD, as well as mitochondrial targeting mitochondrial function is a promising new avenue for drug delivery to treat NAFLD/NASH.
Source link: https://doi.org/10.3390/ijms23137280
Nonalcoholic fatty liver disease has a high incidence among obese people with obesity, ranging from simple steatosis to nonalcoholic steatohepatitis, without and with fibrosis. Since NAFLD is an independent risk factor for diabetes and cardiovascular disease, it's clinically relevant. In addition, NASH predisposes patients to cirrhosis and hepatocellular carcinoma, and NASH cirrhosis is the fastest growing indication for liver transplantation in the United States.
Source link: https://doi.org/10.1210/clinem/dgac088
Type 2 diabetes is characterized by insulin resistance, decreased pancreatic u03b-cell insulin secretion, and nonalcoholic fatty liver disease. Insulation absorption in adipose, skeletal muscle, and endothelium is hindered by a Tissue-specific SWELL1 ablation, which also affects u03b2-cell insulin secretion and glucose regulation, which also impairs glycemic control. In murine and human diabetes, ICl,SWELL, and SWELL1 protein are reduced in adipose and SWELL1 protein, according to here. These results reveal that SWELL1 channel modulators improve SWELL1-dependent systemic metabolism in Type 2 diabetes, which is a first-in-class therapeutic therapy for diabetes and nonalcoholic fatty liver disease.
Source link: https://doi.org/10.1038/s41467-022-28435-0
In the diagnosis of fatty liver disease, this paper discusses the complicated interactions between diet, the gut microbiome, and bile acids. Nonalcoholic fatty liver disease can affect a large population of the world's population, and a significant number of these individuals will suffer from nonalcoholic steatohepatitis. Currently, the only approved treatment for NAFLD and NASH is a change in diet and exercise. Hepatic bile acid transporters are impaired by inflammation, slowing their enterohepatic circulation and allowing conjugated bile acids to rise in the serum and liver of NASH patients. CBA in the liver is hypothesized to stimulate sphingosine-1-phosphate receptor 2, which is responsible for pro-inflammatory and fibrosis pathways in NASH progression. Emerging new molecular technologies may help in deciphering the intricate physiological pathways that contribute to fatty liver disease and enable more effective prevention and treatment.
Source link: https://doi.org/10.1002/cphy.c210024
Due to the global epidemic of obesity, the prevalence of nonalcoholic fatty liver disease has risen dramatically. Bile acids are not only effective physiological detergents for the absorption of lipid-soluble nutrients in the intestine but also metabolic regulators. NAFLD disease severity has been attributed to dysregulation of BA homeostasis. Different BAs' discovery of nuclear receptors and G-protein-coupled receptors not only increased the current knowledge of NAFLD/NASH disease progression but also provided the opportunity to develop potential drugs for NAFLD/NASH. In addition, the clinical benefits of focusing on BA-mediated signaling pathways for NAFLD will be addressed.
Source link: https://doi.org/10.3390/cells10112806
Global health inequalities, particularly in the United States, are a result of cultural eating habits and lifestyle, including non-alcoholic fatty liver disease. Pathological research into NAFLD has mainly concentrated on hepatocytes and other inflammatory cell types; however, the impact of other biliary epithelial cells in NAFLD promotion is increasing.
Source link: https://doi.org/10.3390/cells10082072
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