title: Changes in adipose tissue gene expression and plasma levels of adipokines and acute-phase proteins in patients with critical illness.
abstract: Insulin resistance develops rapidly during critical illness. The release of adipokines from adipose tissue is thought to play a key role in the development of insulin resistance, as are elevated levels of acute-phase proteins. The aim of this study was to identify changes in adipose tissue gene expression and plasma levels of adipokines and acute-phase proteins during critical illness. From 8 patients with subarachnoidal hemorrhage, consecutive blood samples and adipose tissue biopsies were obtained at 3 time points, twice during intensive care (1-2 days [IC1] and 7-9 days after subarachnoidal hemorrhage) and once after 8 months (recovery). The patients received a continuous insulin infusion to maintain normal glucose levels reflecting insulin resistance. The DNA microarray analysis showed increased zink-alpha2 glycoprotein (ZAG) and phospholipase A2, group IIA messenger RNA levels during intensive care compared with recovery (P < .05). Real-time polymerase chain reaction confirmed the increased expression of ZAG and phospholipase A2, group IIA. Plasma levels of ZAG, serum amyloid A, and C-reactive protein were higher at 7 to 9 days after subarachnoidal hemorrhage compared with either IC1 or recovery (P = .0001); and plasma levels of retinol-binding protein 4 and adiponectin were lower at IC1 compared with recovery (P = .05). The described changes in adipose tissue gene expression and plasma levels of adipokines and acute-phase proteins may influence the development of insulin resistance during critical illness.
authors.affiliation: Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, SE 413 45 Gothenburg, Sweden. margareta.jernas@medic.gu.se
authors.forename: Margareta
authors.initials: M
authors.lastname: Jernås
authors.forename: Bob
authors.initials: B
authors.lastname: Olsson
authors.forename: Kajsa
authors.initials: K
authors.lastname: Sjöholm
authors.forename: Anders
authors.initials: A
authors.lastname: Sjögren
authors.forename: Mats
authors.initials: M
authors.lastname: Rudemo
authors.forename: Bengt
authors.initials: B
authors.lastname: Nellgård
authors.forename: Lena M S
authors.initials: LM
authors.lastname: Carlsson
authors.forename: C David
authors.initials: CD
authors.lastname: Sjöström
mesh_terms: D000209:Acute-Phase Proteins / Q000235:genetics / Q000378:metabolism*; D054392:Adipokines / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics; D000273:Adipose Tissue / Q000378:metabolism / Q000502:physiology*; D001706:Biopsy; D001786:Blood Glucose / Q000378:metabolism; D016638:Critical Illness; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007328:Insulin / Q000627:therapeutic use; D007333:Insulin Resistance / Q000235:genetics / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D020411:Oligonucleotide Array Sequence Analysis; D012313:RNA / Q000737:chemistry / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013345:Subarachnoid Hemorrhage / Q000097:blood / Q000235:genetics*
chemical_list: D000209:Acute-Phase Proteins; D054392:Adipokines; D001786:Blood Glucose; D007328:Insulin; D012313:RNA