title: [Insulin resistance and protein catabolism in critically ill patients].
abstract: Hyperglycemia is a frequently observed phenomenon in critically ill patients, affecting numerous patients without a history of impaired glucose tolerance or diabetes. During critical illness, hyperglycemia may result from decreased peripheral glucose uptake and/or utilisation in presence of normal or elevated plasma insulin levels (peripheral insulin resistance) as well as an increase in hepatic glucose production due to augmented glycogenolysis and gluconeogenesis resulting from stress and/or central (hepatic) insulin resistance. As there are a number of factors that cause or aggravate hyperglycemia / insulin resistance during the intensive care unit (ICU) stay, a multifactorial etiology is likely. Furthermore, animal models of sepsis suggest a decrease in anabolic insulin signalling within skeletal muscle.
authors.affiliation: Klinik für Anästhesiologie mit Schwerpunkt operative Intensivmedizin, Campus Charité Mitte, der Charité-Universitätsmedizin Berlin, Germany. Jeff rey.Bierbrauer@charite.de
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Bierbrauer
authors.forename: Steffen
authors.initials: S
authors.lastname: Weber-Carstens
mesh_terms: D000758:Anesthesia; D001284:Atrophy; D001786:Blood Glucose / Q000378:metabolism; D003422:Critical Care; D016638:Critical Illness; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000150:complications / Q000209:etiology; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D007333:Insulin Resistance / Q000235:genetics / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000473:pathology; D011506:Proteins / Q000378:metabolism*; D013312:Stress, Physiological
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D011506:Proteins; D007334:Insulin-Like Growth Factor I