Increased leptin messenger RNA and serum leptin levels in children with Prader-Willi syndrome and nonsyndromal obesity

被引:22
作者
Lindgren, AC
Marcus, C
Skwirut, C
Elimam, A
Hagenas, L
Schalling, M
Anvret, M
Lonnqvist, F
机构
[1] KAROLINSKA HOSP,DEPT MOL MED & NEUROL,S-17176 STOCKHOLM,SWEDEN
[2] HUDDINGE HOSP,DEPT MED,S-14186 HUDDINGE,STOCKHOLM,SWEDEN
[3] HUDDINGE HOSP,DEPT PEDIAT,S-14186 HUDDINGE,STOCKHOLM,SWEDEN
关键词
D O I
10.1203/00006450-199711000-00007
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
To study the potential role of the ob gene pathway in childhood obesity, we have investigated leptin mRNA levels in s.c. adipose tissue obtained from nonobese prepubertal children (n = 20), obese nonsyndromal children (n = 6), and children with Prader-Willi syndrome (n = 6) by in situ hybridization histochemistry. We have also investigated the fasting serum leptin levels in such children. Compared with nonobese children, leptin mRNA expression was higher both in children with Prader-Willi syndrome and in children with nonsyndromal obesity (p < 0.01). Furthermore, the serum leptin levels were also significantly higher in both children with Prader-Willi syndrome and nonsyndromal obesity compared with the nonobese children (p < 0.001). However, no significant differences in adipose tissue leptin mRNA or serum leptin levels were observed between children with Prader-Willi syndrome and nonsyndromal obese children. As expected both fasting serum leptin levels and leptin mRNA expression levels correlated to body mass index (r(s) = 0.80 and 0.73, respectively, p < 0.005). No difference in leptin expression between Prader-Willi syndrome and nonsyndromal childhood obesity could be revealed in the present study. However, differences in the hypothalamic response to leptin between the two forms of obesity cannot be excluded.
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收藏
页码:593 / 596
页数:4
相关论文
共 20 条
  • [1] Decreased cerebrospinal-fluid/serum leptin ratio in obesity: A possible mechanism for leptin resistance
    Caro, JF
    Kolaczynski, JW
    Nyce, MR
    Ohannesian, JP
    Opentanova, I
    Goldman, WH
    Lynn, RB
    Zhang, PL
    Sinha, MK
    Considine, RV
    [J]. LANCET, 1996, 348 (9021) : 159 - 161
  • [2] Cassidy S B, 1984, Curr Probl Pediatr, V14, P1
  • [3] Serum immunoreactive leptin concentrations in normal-weight and obese humans
    Considine, RV
    Sinha, MK
    Heiman, ML
    Kriauciunas, A
    Stephens, TW
    Nyce, MR
    Ohannesian, JP
    Marco, CC
    McKee, LJ
    Bauer, TL
    Caro, JF
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1996, 334 (05) : 292 - 295
  • [4] EVIDENCE AGAINST EITHER A PREMATURE STOP CODON OR THE ABSENCE OF OBESE GENE MESSENGER-RNA IN HUMAN OBESITY
    CONSIDINE, RV
    CONSIDINE, EL
    WILLIAMS, CJ
    NYCE, MR
    MAGOSIN, SA
    BAUER, TL
    ROSATO, EL
    COLBERG, J
    CARO, JF
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (06) : 2986 - 2988
  • [5] GWOHWA L, 1996, NATURE, V379, P632
  • [6] INCREASED OBESE MESSENGER-RNA EXPRESSION IN OMENTAL FAT-CELLS FROM MASSIVELY OBESE HUMANS
    HAMILTON, BS
    PAGLIA, D
    KWAN, AYM
    DEITEL, M
    [J]. NATURE MEDICINE, 1995, 1 (09) : 953 - 956
  • [7] Hassink SG, 1996, PEDIATRICS, V98, P201
  • [8] Hill James O, 1990, Dysmorphol Clin Genet, V4, P27
  • [9] HOLM VA, 1993, PEDIATRICS, V91, P398
  • [10] ANGELMAN AND PRADER-WILLI SYNDROMES SHARE A COMMON CHROMOSOME-15 DELETION BUT DIFFER IN PARENTAL ORIGIN OF THE DELETION
    KNOLL, JHM
    NICHOLLS, RD
    MAGENIS, RE
    GRAHAM, JM
    LALANDE, M
    LATT, SA
    [J]. AMERICAN JOURNAL OF MEDICAL GENETICS, 1989, 32 (02): : 285 - 290