![]() Marcos A, Fisher RA, Ham JM, Olzinski AT, Shiffman ML, Sanyal AJ, Luketic VA, et al. Determinants of the association of overweight with elevated serum alanine aminotransferase activity in the United States. Liver, muscle, and adipose tissue insulin action is directly related to intrahepatic triglyceride content in obese subjects. Korenblat KM, Fabbrini E, Mohammed BS, Klein S. Increased prevalence of insulin resistance and nonalcoholic fatty liver disease in Asian-Indian men. Petersen KF, Dufour S, Feng J, Befroy D, Dziura J, Dalla Man C, Cobelli C, et al. ![]() Magnetic resonance spectroscopy to measure hepatic triglyceride content: prevalence of hepatic steatosis in the general population. Szczepaniak LS, Nurenberg P, Leonard D, Browning JD, Reingold JS, Grundy S, Hobbs HH, et al. Improved nonalcoholic steatohepatitis after 48 weeks of treatment with the PPAR-gamma ligand rosiglitazone. Neuschwander-Tetri BA, Brunt EM, Wehmeier KR, Oliver D, Bacon BR. Design and validation of a histological scoring system for nonalcoholic fatty liver disease. Kleiner DE, Brunt EM, Van Natta M, Behling C, Contos MJ, Cummings OW, Ferrell LD, et al. Fatty liver: biochemical and clinical considerations. Hoyumpa Jr AM, Greene HL, Dunn GD, Schenker S. The natural history of nonalcoholic fatty liver disease: a population-based cohort study. Sauver J, Sanderson SO, Lindor KD, Feldstein A, Angulo P. Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Marchesini G, Bugianesi E, Forlani G, Cerrelli F, Lenzi M, Manini R, Natale S, et al. ![]() This process is experimental and the keywords may be updated as the learning algorithm improves. These keywords were added by machine and not by the authors. Microsomal Triglyceride Transfer Protein.Understanding the factors involved in the pathogenesis and pathophysiology of NAFLD will lead to a better understanding of the mechanisms responsible for the metabolic complications of obesity. However, whether NAFLD is the cause of metabolic dysfunction or whether metabolic dysfunction is responsible for excessive intrahepatic triglyceride accumulation remains unclear at this time. These metabolic abnormalities are likely responsible for many cardiometabolic risk factors associated with NAFLD, such as insulin resistance and dyslipidemia. Hepatic steatosis is associated with an array of adverse changes in glucose, fatty acid and lipoprotein metabolism, not only locally (in the liver) but also at the whole body level. Therefore, an increase in intrahepatic triglyceride content (steatosis) results from an imbalance between interacting metabolic events. Obesity is associated with increased deposition of fat in the liver (nonalcoholic fatty liver disease NAFLD), which develops when hepatic fatty acid availability from plasma and de novo synthesis exceeds hepatic fatty acid disposal by oxidation and triglyceride export. A late night airport shuttle ride home descends into darkness.
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