Immune phenotype and serum leptin in children with obesity-related liver disease

被引:15
作者
Iorio, R
Sepe, A
Giannattasio, A
Cirillo, F
Spagnuolo, MI
Franzese, A
Fontana, S
Aufiero, D
Perna, F
Vegnente, A
Matarese, G
机构
[1] Univ Naples Federico II, Dept Pediat, I-80131 Naples, Italy
[2] CNR, Ist Endocrinol & Oncol Sperimentale, I-80125 Naples, Italy
[3] Lab Immunol AO Monaldi, I-80131 Naples, Italy
关键词
D O I
10.1210/jc.2005-1054
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Context: Little is known about pathogenesis of obesity-related liver disease in childhood. Data on the relationship among leptin, immunological parameters, and liver disease in obese children are lacking. Objective: Thus, the objective of this study was to evaluate immune phenotype and leptin serum levels in obese children with and without obesity-related liver disease. Design: The study was performed in two groups of consecutive obese children: the first formed by children with obesity-related liver disease, diagnosed in the presence of chronic hypertransaminasemia, liver steatosis at ultrasound, and absence of known etiologies; the second composed of children with isolated obesity. In all patients serum leptin, immunoglobulins, peripheral T, B, and natural killer (NK) cells were evaluated. Results: Twenty-three children in the first group and 16 children in the second were considered eligible. Serum leptin was increased in both groups but without any significant difference. No significant correlation was found between leptin and aminotransferases, lipid serum levels, and all tested lymphocyte subpopulations. Patients with obesity-related liver disease showed significantly higher peripheral NK and B cell counts and IgA levels than children with isolated obesity. Furthermore, no correlation was found between severity of liver disease and lymphocyte subpopulations. Conclusion: In our study, leptin did not correlate with hepatic steatosis, aminotransferases, and serum lipids. Children with obesity-related liver disease showed significantly higher peripheral NK and B cells and IgA levels. Additional studies are required to define the pathogenetic role of these immunological findings.
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收藏
页码:341 / 344
页数:4
相关论文
共 20 条
[1]   Role of NK and NKT cells in the immunopathogenesis of HCV-induced hepatitis [J].
Ahmad, A ;
Alvarez, F .
JOURNAL OF LEUKOCYTE BIOLOGY, 2004, 76 (04) :743-759
[2]   Serum leptin in NASH correlates with hepatic steatosis but not fibrosis: A manifestation of lipotoxicity? [J].
Chitturi, S ;
Farrell, G ;
Frost, L ;
Kriketos, A ;
Lin, R ;
Liddle, C ;
Samarasinghe, D ;
George, J .
HEPATOLOGY, 2002, 36 (02) :403-409
[3]   Leptin and the regulation of body weight in mammals [J].
Friedman, JM ;
Halaas, JL .
NATURE, 1998, 395 (6704) :763-770
[4]  
Grummer-Strawn, 2000, ADV DATA, V8, P1
[5]   Essential roles of the Fas ligand in the development of hepatitis [J].
Kondo, T ;
Suda, T ;
Fukuyama, H ;
Adachi, M ;
Nagata, S .
NATURE MEDICINE, 1997, 3 (04) :409-413
[6]   Interferon gamma plays a critical role in T cell-dependent liver injury in mice initiated by concanavalin A [J].
Kusters, S ;
Gantner, F ;
Kunstle, G ;
Tiegs, G .
GASTROENTEROLOGY, 1996, 111 (02) :462-471
[7]  
Matarese G., 2002, Current Drug Targets - Inflammation and Allergy, V1, P13, DOI 10.2174/1568010023344931
[8]   Increased leptin levels in serum and peritoneal fluid of patients with pelvic endometriosis [J].
Matarese, G ;
Alviggi, C ;
Sanna, V ;
Howard, JK ;
Lord, GM ;
Carravetta, C ;
Fontana, S ;
Lechler, RI ;
Bloom, SR ;
De Placido, G .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2000, 85 (07) :2483-2487
[9]   HOMEOSTASIS MODEL ASSESSMENT - INSULIN RESISTANCE AND BETA-CELL FUNCTION FROM FASTING PLASMA-GLUCOSE AND INSULIN CONCENTRATIONS IN MAN [J].
MATTHEWS, DR ;
HOSKER, JP ;
RUDENSKI, AS ;
NAYLOR, BA ;
TREACHER, DF ;
TURNER, RC .
DIABETOLOGIA, 1985, 28 (07) :412-419
[10]   Activated natural killer T cells induce liver injury by Fas and tumor necrosis factor-α during alcohol consumption [J].
Minagawa, M ;
Deng, QG ;
Liu, ZX ;
Tsukamoto, H ;
Dennert, G .
GASTROENTEROLOGY, 2004, 126 (05) :1387-1399