title: NAFLD and diabetes mellitus.
abstract: The liver constitutes a key organ in systemic metabolism, contributing substantially to the development of insulin resistance and type 2 diabetes mellitus (T2DM). The mechanisms underlying these processes are not entirely understood, but involve hepatic fat accumulation, alterations of energy metabolism and inflammatory signals derived from various cell types including immune cells. Lipotoxins, mitochondrial function, cytokines and adipocytokines have been proposed to play a major part in both NAFLD and T2DM. Patients with NAFLD are commonly insulin resistant. On the other hand, a large number of patients with T2DM develop NAFLD with its inflammatory complication, NASH. The high incidence of NASH in patients with T2DM leads to further complications, such as liver cirrhosis and hepatocellular carcinoma, which are increasingly recognized. Therapeutic concepts such as thiazolidinediones (glitazones) for treating T2DM also show some efficacy in the treatment of NASH. This Review will describe the multifaceted and complex interactions between the liver and T2DM.
authors.affiliation: Department of Internal Medicine I, Gastroenterology, Endocrinology &Metabolism, Medical University Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria.
authors.forename: Herbert
authors.initials: H
authors.lastname: Tilg
authors.affiliation: Department of Internal Medicine I, Gastroenterology, Endocrinology &Metabolism, Medical University Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria.
authors.forename: Alexander R
authors.initials: AR
authors.lastname: Moschen
authors.affiliation: Department of Endocrinology and Diabetology, Medical Faculty, Heinrich-Heine University, c/o Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.|Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine University, c/o Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.|German Center of Diabetes Research, Ingolstädter Landstraße 1, 85764, München-Neuherberg, Germany.
authors.forename: Michael
authors.initials: M
authors.lastname: Roden
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000209:etiology; D016207:Cytokines / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism*; D004734:Energy Metabolism; D005943:Gluconeogenesis / Q000502:physiology; D006801:Humans; D051550:I-kappa B Kinase / Q000378:metabolism; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008066:Lipolysis / Q000502:physiology; D008099:Liver / Q000378:metabolism; D008103:Liver Cirrhosis / Q000209:etiology; D008113:Liver Neoplasms / Q000209:etiology; D024821:Metabolic Syndrome / Q000150:complications / Q000378:metabolism; D008930:Mitochondria, Liver / Q000378:metabolism; D065626:Non-alcoholic Fatty Liver Disease / Q000150:complications / Q000378:metabolism* / Q000628:therapy
chemical_list: D016207:Cytokines; D051550:I-kappa B Kinase