https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.28431

Global epidemiology of nonalcoholic fatty liver disease—Meta‐analytic assessment of prevalence, incidence, and outcomes

Hepatocellular Carcinoma: Epidemiology and Molecular Carcinogenesis

Nonalcoholic fatty liver disease (NAFLD) is present in up to one third of the general population and in the majority of patients with metabolic risk factors such as obesity and diabetes. Insulin resistance is a key pathogenic factor resulting in hepatic fat accumulation. Recent evidence demonstrates NAFLD in turn, exacerbates hepatic insulin resistance and often precedes glucose intolerance. Once hepatic steatosis is established, other factors including oxidative stress, mitochondrial dysfunction, gut-derived lipopolysaccharide and adipocytokines, may promote hepatocellular damage, inflammation and progressive liver disease. Confirmation of the diagnosis of NAFLD can usually be achieved by imaging studies, however staging the disease requires a liver biopsy. NAFLD is associated with an increased risk of all-cause death, probably because of complications of insulin resistance such as vascular disease, as well as due to cirrhosis and hepatocellular carcinoma, which occurs in a minority of patients. NAFLD is also now recognized to account for a substantial proportion of patients previously diagnosed with 'cryptogenic cirrhosis'. Diabetes, obesity and the necroinflammatory form of NAFLD known as non-alcoholic steatohepatitis, are risk factors for progressive liver disease. Current treatment relies on weight loss and exercise, although various insulin-sensitizing medications appear promising. Further research is needed to identify which patients will achieve the most benefit from therapy.

Nonalcoholic fatty liver disease.

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.29367

The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases.

Lipid homeostasis in vertebrate cells is regulated by a family of membrane-bound transcription factors designated sterol regulatory element–binding proteins (SREBPs). SREBPs directly activate the expression of more than 30 genes dedicated to the synthesis and uptake of cholesterol, fatty acids, triglycerides, and phospholipids, as well as the NADPH cofactor required to synthesize these molecules (1–4). In the liver, three SREBPs regulate the production of lipids for export into the plasma as lipoproteins and into the bile as micelles. The complex, interdigitated roles of these three SREBPs have been dissected through the study of ten different lines of gene-manipulated mice. These studies form the subject of this review.

/pdf/srebps-activators-of-the-complete-program-of-cholesterol-and-1sop601qwq.pdf

SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver

Jérôme Guéchot, Jérôme Boursier, Victor de Ledinghen, Thierry Poynard, Fabrice Carrat, Vincent Leroy, Grace Lai-Hung Wong, Mireen Friedrich-Rust, Mirella Fraquelli, Mario Plebani, Giada Sebastiani, Robert Myers, Paul Angulo, Sandrine Bertrais, Dominique Wendum, Ivan Bricault and Paul Calès, from the ARDENT group and/or AFEFa Liver-FibroSTARD checklist and glossary: tools for standardized design and reporting of diagnostic accuracy studies of liver fibrosis tests

/pdf/liver-fibrostard-checklist-and-glossary-tools-for-36dhm1jx2z.pdf

Paul Angulo

Papers

Liver-FibroSTARD checklist and glossary: tools for standardized design and reporting of diagnostic accuracy studies of liver fibrosis tests.

714 Prevalence of autoantibodies and autoimmune hepatitis in nonalcoholic fatty liver disease

Mo1814 Fulminant Liver Failure Secondary to “Saba Appetite Control and Energy” Weight Loss Supplement

Mycophenolate mofetil for patients with primary biliary cirrhosis with a suboptimal response to ursodeoxycholic acid

A Large Independent Validation Study of Nonivasive Scores to Predict Advanced Fibrosis in NAFLD