Ontogeny of serum leptin concentrations in the human

被引:32
作者
Geary, M
Herschkovitz, R
Pringle, PJ
Rodeck, CH
Hindmarsh, PC
机构
[1] UCL, London Ctr Paediat Endocrinol, London, England
[2] UCL, Dept Obstet & Gynaecol, London, England
关键词
D O I
10.1046/j.1365-2265.1999.00758.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVE Serum leptin concentrations reflect the fat mass of an individual. Fetal growth is rapid and it might be expected that major changes in circulating leptin concentrations in the fetus and neonate take place. We have studied the ontogeny of serum leptin concentrations in cord blood samples obtained by cordocentesis between 14 end 32 weeks of gestation and in samples obtained at term. PATIENTS Cordocentesis samples from 10 appropriately grown for gestational age (AGA) and 10 intrauterine growth restricted (IUGR) fetuses. The results were compared with cord serum leptin concentrations obtained in 39 term healthy pregnancies. RESULTS In the AGA and term pregnancies serum leptin concentrations changed little up until 38 weeks of gestation when there was an increase in concentration (Pre 38 weeks 3.5 mu g/l (SEM 0.3); Post 38 weeks 5.6 mu g/l (SEM 0.7): Mann Whitney P = 0.03). Serum leptin concentrations were similar in the AGA and IUGR fetuses (AGA 5.9 mu g/l (SEM 3.0); IUGR 4.2 mu g/l (SEM 1.5): Mann-Whitney P = ns). Serum leptin was strongly related to birth weight (r = 0.58; P< 0.001) and birth length (r = 0.32; P = 0.05) in the term babies but not in the AGA or IUGR groups. CONCLUSION Serum leptin concentrations in the fetus appear to be independent of gestational age and only rise towards the end of gestation. This late change probably reflects the changes in the accretion of body fat. There appears to be little difference in serum leptin concentrations between AGA and IUGR fetuses.
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页码:189 / 192
页数:4
相关论文
共 17 条
[1]   FETAL NUTRITION AND CARDIOVASCULAR-DISEASE IN ADULT LIFE [J].
BARKER, DJP ;
GLUCKMAN, PD ;
GODFREY, KM ;
HARDING, JE ;
OWENS, JA ;
ROBINSON, JS .
LANCET, 1993, 341 (8850) :938-941
[2]  
Blum WF, 1997, J CLIN ENDOCR METAB, V82, P2904, DOI 10.1210/jc.82.9.2904
[3]  
BURDI AR, 1985, INT J OBESITY, V9, P247
[4]   The OB protein (leptin) pathway - A link between adipose tissue mass and central neural networks [J].
Campfield, LA ;
Smith, FJ ;
Burn, P .
HORMONE AND METABOLIC RESEARCH, 1996, 28 (12) :619-632
[5]  
FREEMANTLE M, 1995, CHEM ENG NEWS, V73, P25, DOI 10.1021/cen-v073n005.p025
[6]   Leptin and leptin receptor mRNA and protein expression in the murine fetus and placenta [J].
Hoggard, N ;
Hunter, L ;
Duncan, JS ;
Williams, LM ;
Trayhurn, P ;
Mercer, JG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (20) :11073-11078
[7]   Ontogeny of leptin in human fetuses and newborns: Effect of intrauterine growth retardation on serum leptin concentrations [J].
Jaquet, D ;
Leger, J ;
Levy-Marchal, C ;
Oury, JF ;
Czernichow, P .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (04) :1243-1246
[8]   The placenta is not the main source of leptin production in pregnant rat: Gestational profile of leptin in plasma and adipose tissues [J].
Kawai, M ;
Yamaguchi, M ;
Murakami, T ;
Shima, K ;
Murata, Y ;
Kishi, K .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 240 (03) :798-802
[9]   Nonadipose tissue production of leptin: Leptin as a novel placenta-derived hormone in humans [J].
Masuzaki, H ;
Ogawa, Y ;
Sagawa, N ;
Hosoda, K ;
Matsumoto, T ;
Mise, H ;
Nishimura, H ;
Yoshimasa, Y ;
Tanaka, I ;
Mori, T ;
Nakao, K .
NATURE MEDICINE, 1997, 3 (09) :1029-1033
[10]   MODULATION OF OBESE GENE-EXPRESSION IN RAT BROWN AND WHITE ADIPOSE TISSUES [J].
MOINAT, M ;
DENG, CJ ;
MUZZIN, P ;
ASSIMACOPOULOSJEANNET, F ;
SEYDOUX, J ;
DULLOO, AG ;
GIACOBINO, JP .
FEBS LETTERS, 1995, 373 (02) :131-134