Increased proinflammatory cytokine production in adipose tissue of obese patients with chronic kidney disease

. 2010 Aug ; 122 (15-16) : 466-73. [epub] 20100728

Jazyk angličtina Země Rakousko Médium print-electronic

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/pmid20658196

BACKGROUND: Obesity is a known high-risk factor for the development of vascular diseases and chronic kidney disease (CKD). In this study we aimed to elucidate the impact of adipose tissue on the inflammatory state in CDK patients with obesity. PATIENTS AND METHODS: A cohort of 40 patients with CKD (stages 3-4) with mild proteinuria (2.3-3.5 g/day) were analyzed in a prospective cross-sectional study: single blood samples and visceral and subcutaneous samples of adipose tissue were taken from 20 patients with obesity and 20 without obesity (control group) during elective abdominal surgery (laparoscopic cholecystectomy). Serum concentrations of asymmetric dimethylarginine (ADMA), adiponectin, C-reactive protein, interleukin-6, tumor necrosis factor-alpha, pentosidine and monocyte chemoattractant protein-1 were measured. Messenger RNA expression of tumor necrosis factor-alpha, monocyte chemoattractant protein-1, adiponectin receptors 1 and 2, and immunocompetent cell marker CD68 was measured in subcutaneous and visceral fat samples using real-time PCR. Adipose tissue was examined immunohistochemically for CD68-positive cells. Other biochemical parameters (insulin, glycated hemoglobin, cholesterol, LDL cholesterol, and triglycerides) were assessed in the two groups of patients at the same time. RESULTS: Serum concentrations of ADMA, C-reactive protein, pentosidine, interleukin-6, tumor necrosis factor-alpha and monocyte chemoattractant protein-1 were significantly higher in obese CKD patients than in the control group; adiponectin was lower in the obese group. Subcutaneous and visceral mRNA expressions of tumor necrosis factor-alpha, CD68, adiponectin receptor-1, and monocyte chemoattractant protein-1 were significantly increased in the obese patients, whereas expression of adiponectin, interleukin-6, and adiponectin receptor-2 did not significantly differ between the patient groups. In general, mRNA expressions were higher in visceral than in subcutaneous samples (P < 0.01 vs. P < 0.05). Increased infiltration of subcutaneous and visceral adipose tissue by CD68-positive immunocompetent cells was found in the obese CKD group. With respect to lipid metabolism parameters, a small but significant increase in levels was found in the obese patients (P < 0.02). Changes in triglycerides were more marked in this group (P < 0.01) and a similar increase was noted in insulin and HbA1c levels (P < 0.02). CONCLUSION: Increased expression of proinflammatory cytokines and increased infiltration by immunocompetent cells were found in adipose tissue of obese patients with CKD stages 3-4. This upregulated inflammation may contribute to the induction of a systemic proinflammatory state in patients with CKD and could accelerate the progression of renal dysfunction.

Zobrazit více v PubMed

J Clin Endocrinol Metab. 2006 Nov;91(11):4620-7 PubMed

Diabetes Care. 2003 Jun;26(6):1673-8 PubMed

J Clin Endocrinol Metab. 2002 May;87(5):2407 PubMed

Nephrol Dial Transplant. 2007 Jan;22(1):171-8 PubMed

Diabetes. 2005 Dec;54(12):3358-70 PubMed

J Clin Invest. 1995 May;95(5):2409-15 PubMed

J Biol Chem. 2002 Jul 19;277(29):25863-6 PubMed

J Clin Endocrinol Metab. 2005 Mar;90(3):1366-70 PubMed

J Clin Endocrinol Metab. 2001 Aug;86(8):3815-9 PubMed

Atheroscler Suppl. 2003 Dec;4(4):23-8 PubMed

Circulation. 2003 Nov 18;108(20):2460-6 PubMed

Circulation. 1999 Jun 22;99(24):3092-5 PubMed

J Clin Endocrinol Metab. 2006 May;91(5):1896-900 PubMed

Endocrinology. 2005 Sep;146(9):4024-35 PubMed

Minerva Urol Nefrol. 2004 Sep;56(3):237-48 PubMed

Biochem Biophys Res Commun. 1999 Apr 2;257(1):79-83 PubMed

Kidney Int. 2006 Aug;70(4):781-7 PubMed

Circulation. 1999 Mar 9;99(9):1141-6 PubMed

Scand J Urol Nephrol. 2004;38(5):405-16 PubMed

J Am Soc Nephrol. 2005 Apr;16(4):1091-8 PubMed

Clin Sci (Lond). 2005 Sep;109(3):243-56 PubMed

J Am Coll Cardiol. 2008 Jun 24;51(25):2375-84 PubMed

Neth J Med. 2004 May;62(5):143-50 PubMed

J Nephrol. 2007 Sep-Oct;20(5):554-9 PubMed

J Clin Invest. 2006 Jan;116(1):33-5 PubMed

J Clin Endocrinol Metab. 2004 Dec;89(12):6277-81 PubMed

J Clin Invest. 2003 Dec;112(12):1821-30 PubMed

Nutrition. 2009 Jul-Aug;25(7-8):762-8 PubMed

Curr Opin Nephrol Hypertens. 2006 May;15(3):314-20 PubMed

Science. 2001 Aug 31;293(5535):1673-7 PubMed

Arch Physiol Biochem. 2006 Apr;112(2):114-8 PubMed

Diabetologia. 2006 Apr;49(4):744-7 PubMed

J Clin Invest. 2002 May;109(10):1345-50 PubMed

N Engl J Med. 2002 Feb 21;346(8):570-8 PubMed

Physiol Res. 2008;57(6):911-917 PubMed

Mayo Clin Proc. 2008 Mar;83(3):333-42 PubMed

Metabolism. 2004 Aug;53(8):1072-5 PubMed

Atherosclerosis. 1991 Aug;89(2-3):109-16 PubMed

Blood Purif. 2001;19(1):53-61 PubMed

J Biol Chem. 2004 Mar 26;279(13):12152-62 PubMed

Hepatology. 2005 Apr;41(4):753-60 PubMed

Cardiovasc Diabetol. 2006 Jan 13;5:1 PubMed

Arterioscler Thromb Vasc Biol. 2000 Jun;20(6):1595-9 PubMed

Diabetes Care. 2006 May;29(5):1071-6 PubMed

J Clin Invest. 2005 May;115(5):1111-9 PubMed

J Clin Invest. 2003 Dec;112(12):1796-808 PubMed

Wien Klin Wochenschr. 2008;120(15-16):478-85 PubMed

Blood Purif. 2001;19(2):143-51 PubMed

Nature. 2001 Jan 18;409(6818):307-12 PubMed

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...