Increased subcutaneous and epicardial adipose tissue production of proinflammatory cytokines in cardiac surgery patients: possible role in postoperative insulin resistance.
BACKGROUND
Hyperglycemia and insulin resistance frequently occur in critically ill patients even without a history of diabetes.


OBJECTIVE
Our objective was to study the role of adipose tissue hormonal production in the development of insulin resistance in cardiac surgery patients. PARTICIPANTS, INTERVENTIONS, AND SETTINGS: Fifteen patients with elective cardiac surgery underwent blood sampling before, at the end, and 6, 12, 24, 48, and 120 h after the end of their operation. Epicardial and sc adipose tissue sampling was done at the beginning and at the end of surgery in the Department of Cardiac Surgery.


METHODS
We measured serum concentrations and sc and epicardial adipose tissue mRNA expression of IL-6, monocyte chemoattractant protein-1 (MCP-1), TNF-alpha, leptin, resistin, and adiponectin and sc and epicardial adipose tissue mRNA expression of CD14, CD45, and CD68.


RESULTS
The rate of insulin infusion required to maintain euglycemia increased up to 7-fold 12 h after the operation, suggesting the development of insulin resistance. Serum IL-6 levels increased 43-fold 12 h after surgery. MCP-1 peaked 6-fold at the end of surgery. Smaller peaks of TNF-alpha and leptin appeared 6 and 12 h after surgery, respectively. Resistin levels peaked 4-fold 24 h after surgery, but adiponectin levels were not significantly affected. TNF-alpha and CD45 mRNA expression increased markedly during the operation in sc adipose tissue. IL-6, resistin, and MCP-1 mRNA expression increased in both sc and epicardial adipose tissue. Leptin, adiponectin, CD14, and CD68 mRNA expression did not change significantly.


CONCLUSIONS
Both sc and epicardial adipose tissue is a source of proinflammatory cytokines in cardiac surgery patients and may contribute to the development of postoperative insulin resistance.
Kremen
Jaromir
J
Third Department of Medicine, First Faculty of Medicine, Charles University, U Nemocnice 1, 128 08, Prague 2, Czech Republic.
Dolinkova
Marketa
M
Krajickova
Jana
J
Blaha
Jan
J
Anderlova
Katerina
K
Lacinova
Zdena
Z
Haluzikova
Denisa
D
Bosanska
Lenka
L
Vokurka
Martin
M
Svacina
Stepan
S
Haluzik
Martin
M
D052436:Adipose Tissue, White / Q000378:metabolism*; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000097:blood / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D016207:Cytokines / Q000096:biosynthesis* / Q000502:physiology; D005260:Female; D006728:Hormones / Q000097:blood / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000188:drug therapy / Q000209:etiology; D007121:Immunocompetence / Q000502:physiology; D018836:Inflammation Mediators / Q000378:metabolism* / Q000502:physiology; D007260:Infusion Pumps; D007328:Insulin / Q000008:administration & dosage / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D010496:Pericardium / Q000166:cytology*; D011184:Postoperative Period; D012333:RNA, Messenger / Q000378:metabolism; D050151:Subcutaneous Fat / Q000378:metabolism*; D013903:Thoracic Surgery
D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D001786:Blood Glucose; D016207:Cytokines; D006728:Hormones; D018836:Inflammation Mediators; D007328:Insulin; D012333:RNA, Messenger