Cord plasma adiponectin: A 20-fold rise between 24 weeks gestation and term

被引:113
作者
Kajantie, E
Hytinantti, T
Hovi, P
Andersson, S
机构
[1] Natl Publ Hlth Inst, SF-00300 Helsinki, Finland
[2] Univ Helsinki, Cent Hosp, Hosp Children & Adolescents, Helsinki 00029, Finland
[3] Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, Helsinki 00029, Finland
关键词
D O I
10.1210/jc.2004-0018
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Adiponectin is an adipocyte-derived hormone with profound insulin-sensitizing, antiinflammatory, and antiatherogenic effects. Apart from its obvious potential as a mediator of adult metabolic syndrome, adiponectin could have a significant role in regulating fetal growth. We measured plasma adiponectin concentrations by ELISA in cord vein of 197 infants. Of them, 122 were born preterm ( gestational age, 22 - 32 wk), and 75 at term ( 49 from a healthy and 26 from a diabetic pregnancy, with similar findings, and thus all data from term infants pooled). Mean adiponectin concentrations increased from less than 1 mug/ml at 24 wk gestation to approximately 20 mug/ml at term. One week increase in gestational age corresponded in preterm infants to 43% increase (95% confidence interval 34 - 53%; P < 0.0001) in adiponectin and term infants to 21% increase (12-31%; P < 0.0001). In preterm infants, one unit increase in birth weight SD score corresponded to 42% increase ( 22 - 66%; P = 0.0001) in adiponectin, and females had 57% higher adiponectin concentrations ( 0 - 146%; P = 0.05) than males. These differences were not seen in term infants. Adiponectin levels were lower in preterm infants with recent (< 12 h) exposure to maternal betamethasone but were unrelated to mode of delivery, preeclampsia, or impaired umbilical artery flow. In conclusion, adiponectin concentrations in fetal circulation show a 20-fold rise between 24 wk gestation and term and, in preterm infants are associated with birth weight SD score, sex, and glucocorticoid exposure. Adiponectin may play an important role in regulating fetal growth and explaining its links to the metabolic syndrome and its consequences during adult life.
引用
收藏
页码:4031 / 4036
页数:6
相关论文
共 41 条
[21]   CDNA cloning and expression of a novel adipose specific collagen-like factor, apM1 (Adipose most abundant gene transcript 1) [J].
Maeda, K ;
Okubo, K ;
Shimomura, I ;
Funahashi, T ;
Matsuzawa, Y ;
Matsubara, K .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1996, 221 (02) :286-289
[22]  
MCINTYRE J, 1996, PEDIAT PERINATOLOGY, P579
[23]   Reduced placental 11β-hydroxysteroid dehydrogenase type 2 mRNA levels in human pregnancies complicated by intrauterine growth restriction:: An analysis of possible mechanisms [J].
McTernan, CL ;
Draper, N ;
Nicholson, H ;
Chalder, SM ;
Driver, P ;
Hewison, M ;
Kilby, MD ;
Stewart, PM .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (10) :4979-4983
[24]   Adipocytokines, body composition, and fitness in children [J].
Dan Nemet ;
Ping Wang ;
Tohru Funahashi ;
Yuji Matsuzawa ;
Sachiyo Tanaka ;
Laszlo Engelman ;
Dan M Cooper .
Pediatric Research, 2003, 53 (1) :148-152
[25]   Is birth weight related to later glucose and insulin metabolism? a systematic review [J].
Newsome, CA ;
Shiell, AW ;
Fall, CHD ;
Phillips, DIW ;
Shier, R ;
Law, CM .
DIABETIC MEDICINE, 2003, 20 (05) :339-348
[26]   The postprandial response of adiponectin to a high-fat meal in normal and insulin-resistant subjects [J].
Peake, PW ;
Kriketos, AD ;
Denyer, GS ;
Campbell, LV ;
Charlesworth, JA .
INTERNATIONAL JOURNAL OF OBESITY, 2003, 27 (06) :657-662
[27]  
Pihkala J, 1989, Duodecim, V105, P1540
[28]   GROWTH AND DEVELOPMENT OF ADIPOSE-TISSUE [J].
POISSONNET, CM ;
LAVELLE, M ;
BURDI, AR .
JOURNAL OF PEDIATRICS, 1988, 113 (01) :1-9
[29]   THE CHRONOLOGY OF ADIPOSE-TISSUE APPEARANCE AND DISTRIBUTION IN THE HUMAN-FETUS [J].
POISSONNET, CM ;
BURDI, AR ;
GARN, SM .
EARLY HUMAN DEVELOPMENT, 1984, 10 (1-2) :1-11
[30]   Paradoxical elevation in adiponectin concentrations in women with preeclampsia [J].
Ramsay, JE ;
Jamieson, N ;
Greer, IA ;
Sattar, N .
HYPERTENSION, 2003, 42 (05) :891-894