Abstract
The aim of this study was to determine the release and
regulation of leptin, resistin and adiponectin from human
placenta and fetal membranes, and maternal subcutaneous
adipose tissue and skeletal muscle obtained from normal
and gestational diabetes mellitus (GDM)-complicated
pregnancies at the time of Cesarean section. Tissue
explants were incubated in the absence (basal control) or
presence of 10 g/ml lipopolysaccharide (LPS), 10, 20 or
40 ng/ml tumor necrosis factor- (TNF-), interleukin
(IL)-6 and IL-8, 1 M phorbol myristate acetate, 10, 20
and 40 mM glucose, 01, 1 and 10 M insulin and 01 1
and 10 M dexamethasone, progesterone and estrogen.
After an 18-h incubation, the medium was collected and
the release of leptin, resistin and adiponectin was quantified by ELISA. Human gestational tissues and maternal
tissues released immunoreactive leptin, resistin and adiponectin; however, there was no dierence in the release
of either resistin or adiponectin between normal pregnant
women and women with gestational diabetes. The release
of leptin was significantly higher in placenta, amnion and
choriodecidua obtained from normal pregnant women
Introduction
Recent investigations have focused on several new potential mediators of insulin resistance including leptin, resistin
and adiponectin. Leptin, resistin and adiponectin are
known to be produced within the intrauterine environment (Masuzaki et al. 1997, Lea et al. 2000, Lepercq et al.
2001, Akerman et al. 2002, Lindsay et al. 2003, Yura et al.
2003); however their expression and regulation in gestational tissues and in relation to gestational diabetes mellitus
(GDM) remains to be fully elucidated.
Leptin was originally discovered as a protein involved in
the development of obesity, and although it is now
recognized as a hormone that is produced by several
tissues, adipose tissue is the principal site of leptin production and the major determinant of the level of circulating
hormone (Wauters et al. 2000). The functions attributed
to leptin are extensive, including the regulation of food
intake and energy balance through central hypothalamic
pathways, acting as a major signal to the reproductive
system, inhibition of insulin secretion by pancreatic
-cells, and stimulation of glucose transport (reviewed in
Wauters et al. 2000). Leptin is produced in the human
placenta and is secreted into both the maternal and fetal
circulation (Masuzaki et al. 1997). Expression of leptin has
been identified in placenta, chorionic villi, chorion laeve
and amnion (Akerman et al. 2002). Human leptin mRNA
and protein are also localized to the villous vascular
DOI: 10.1677/joe.1.06227
Online version via http://www.endocrinology-journals.org
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Control patients
(n=9)
GDM patients*
(n=11)
31713
28526
38703
3287160
4/9
5/9
4502
6807
5804
15324
355108
3408
4705
35917
24815
38804
3402165
6/11
5/11
5002
9803
8601
25629
24655
2302
3204
P values
NS
NS
NS
NS
<005
<005
<005
<005
NS
NS
<005
*Eight diet controlled GDM and seven insulin-controlled GDM patients; Students t-test; based on first
antenatal vist at approximately 12 weeks. NS, not significant.
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Eect of high glucose on leptin, resistin and adiponectin release Placenta and adipose tissue obtained from
normal pregnant women (n=5) were incubated in the
presence of increasing concentrations of glucose (10, 20
and 40 mM). There was no eect of glucose on the release
of leptin, resistin and adiponectin from placenta or adipose
tissue (data no shown).
Eect of insulin on leptin, resistin and adiponectin
release Human placentas obtained form normal pregnant
women (n=5) were incubated in the presence of increasing concentrations of insulin (01, 1 and 10 M). There
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