Abstract：Objective To explore the change in serum adiponectin levels and its significance in children with Kawasaki disease (KD). Methods Forty-five KD patients were enrolled in this study, including 18 with coronary artery lesions (CAL group) and 27 without coronary artery lesions (NCAL group). Twenty healthy children were recruited to the control group. Enzyme-linked immunosorbent assay was used to measure serum adiponectin levels, and an automatic biochemical analyzer was used to measure the levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C). Results The serum adiponectin levels in the CAL and NCAL groups were significantly lower than in the control group during the acute phase, subacute phase, and recovery phase (P<0.01), with lower levels observed during the acute phase and subacute phase (P<0.01). Compared with the NCAL group, the CAL group had significantly higher serum levels of adiponectin during the acute phase and recovery phase (P<0.05). The levels of TC, HDL, and LDL in the NCAL and CAL groups were significantly lower than in the control group (P<0.05). The levels of serum adiponectin in KD patients were positively correlated with the levels of TC, TG, and C-reactive protein and the occurrence of CAL (r=0.31, 0.30, 0.34, and 0.35, respectively; P<0.05). Conclusions Children with KD have metabolic disorders of blood lipids and reduced serum adiponectin levels. Reduced serum adiponectin levels may be the result of systemic inflammation, while increased adiponectin levels may be closely associated with the occurrence of CAL.
Takeshita S, Takabayashi H, Yoshida N. Circulating adiponectin levels in Kawasaki disease[J]. Acta Paediatr, 2006, 95(10): 1312-1314.
[2]
Ayusawa M, Sonobe T, Uemura S, et al. Revision of diagnostic guidelines for Kawasaki disease (the 5th revised edition)[J]. Pediatr Int, 2005, 47(2): 232-234.
Scherer PE, Williams S, Fogliano M, et al. A novel serum protein similar to C1q, produced exclusively in adipocytes[J]. J Biol Chem, 1995, 270(45): 26746-26749.
[5]
Furukawa S, Matsubara T, Ichiyama T. Regulation of proinflammatory cytokine cascade in Kawasaki disease[J]. Nihon Rinsho, 2008, 66(2): 258-264.
[6]
Simons PJ, van den Pangaart PS, Aerts JM, et al. Proinflammatory delipidizing cytokines reduce adiponectin secretion from human adipocytes without affecting adiponectin oligomerization[J]. J Endocrinol, 2007, 192: 289-299.
[7]
Iwaki M, Matsuda M, Maeda N, et al. Induction of adiponectin, a fat-derived antidiabetic and antiatherogenic factor, by nuclear receptors[J]. Diabetes, 2003, 52(7): 1655-1663.
[8]
Ruan Y, Ye B, Zhao X. Clinical characteristics of Kawasaki syndrome and the risk factors for coronary artery lesions in China[J]. Pediatr Infect Dis J, 2013, 32(10): e397-e402.
[9]
Akbiyik F, Ray DM, Gettings KF, et al. Human bone marrow megakaryocytes and platelets express PPARgamma, and PPARgamma agonists blunt platelet release of CD40 ligand and thromboxanes[J]. Blood, 2004, 104(5): 1361-1368.
[10]
Cabana VG, Gidding SS, Getz GS, et al. Serum amyloid A and high density lipoprotein participate in the acute phase response of Kawasaki disease[J]. Pediatr Res, 1997, 42(5): 651-655.
[11]
Naderali EK, Estadella D, Rocha M, et al. A fat-enriched, glucose-enriched diet markedly attenuates adiponectin mRNA levels in rat epididymal adipose tissue[J]. Clin Sci(Lond), 2003, 105(4): 403-408.
[12]
Suriyaprom K, Phonrat B, Namjuntra P, et a1. The-11377> G adiponectin gene polymorphism alters the adiponectin concentration and the susceptibility to type 2 diabetes in Thais[J]. Int J Vitam Nutr R, 2010, 80(3): 216-224.
[13]
Takaoka M, Suzuki H, Shioda S, et al. Endovascular injury induces rapid phenotypic changes in perivascular adipose tissue[J]. Arterioscler Thromb Vasc Biol, 2010, 30(8): 1576-1582.
[14]
Aghamohammadzadeh R, Withers S, Lynch F, et al. Perivascular adipose tissue from human systemic and coronary vessels: the emergence of a new pharmacotherapeutic target[J]. Br J Pharmacol, 2012, 165(3): 670-682.
[15]
Yu X, Hirono KI, Ichida F, et al. Enhanced iNOS expression in leukocytes and circulating endothelial cells is associated with the progression of coronary artery lesions in acute Kawasaki disease[J]. Pediatr Res, 2004, 55(4): 688-694.
[16]
Fukazawa R, Ikegam E, Watanabe M, et al. Coronary artery aneurysm induced by Kawasaki disease in children show features typical senescence[J]. Circ J, 2007, 71(5): 709-715.
[17]
Addabbo F, Nacci C, De Benedictis L, et al. Globular adiponectin counteracts VCAM-1-mediated monocyte adhesion via AdipoR1/NF-kappaB/COX-2 signaling in human aortic endothelial cells[J]. Am J Physiol Endocrinol Metab, 2011, 301(6): E1143-E1154.
[18]
Mantzoros CS, Li T, Manson JE, et al. Circulating adiponectin levels are associated with better glycemic control, more favorable lipid profile, and reduced inflammation in women with type 2 diabetes[J]. Clin Endocrinol Metab, 2005, 90(8): 4542-4528.
[19]
Yamauchi T, Kamon J, Minokoshi, et al. Adiponection stimulates glucose atilizationandfatty-acidoxidation by activating AMPactivated protein kinase[J]. Nature Med, 2002, 8(11): 1288-1295.
Ashouri N, Takahashi M, Dorey F, et al. Risk factors for nonresponse to therapy in Kawasaki disease[J]. J Pediatr, 2008, 153(3): 365-368.
[23]
Ou CY, Tseng YF, Lee CL, et al. Significant relationship between serum high-sensitivity C-reactive protein, high-density lipoprotein cholesterol levels and children with Kawasaki disease and coronary artery lesions[J]. Formos Med Assoc, 2009, 108(9): 719-724.
[24]
Ouchi N, Kihara S, Funahashi T, et al. Obesity, adiponectin and vascular inflammatory disease[J]. Curr Opin Lipidol, 2003, 14(6): 561-566.
[25]
Honkanen VE, Mccrindle BW, Laxer RM, et al. Clinical relevance of the risk factors for coronary artery inflammation in Kawasaki disease[J]. Pediatr Cardiol, 2003, 24(2): 122-126.
[26]
Kemmotsu Y, Saji T, Kusunoki N, et al. Serum adipokine profiles in Kawasaki disease[J]. Mod Rheumatol, 2012, 22(1): 66-72.
