Dijk, G. van,

Heinsbroek, A.C.M.,

English

University of Groningen Digital Archive

beta-cell development of their weanling offspring. In
contrast, offspring from dams fed a HFD throughout
gestation showed no significant changes in islet cell
development. Switching the maternal diet during gestation
appears to programme weanling progeny inducing diabeto-
genic effects characterized by compromised beta-cell
development and reduced GK expression.
0140
Effects of maternal obesity on metabolic syndrome in
the offspring
A. C. M. Heinsbroek, G. van Dijk;
Animal Physiology, Unit Neuroendocrinology, University
of Groningen, Haren, The Netherlands.
Background and Aims: Epidemiological studies have
shown that offspring born to women that have been starved
during pregnancy in the Second World War in the Nether-
lands, often had a low birth-weight and higher risk of
developing metabolic syndrome (diabetes, obesity, high
blood-pressure). This suggests that there are prenatal
environmental factors involved in development of the
metabolic syndrome.
Not only starvation, but also maternal obesity may be
important for the predisposition to the metabolic syndrome
in the offspring. In ethnic groups with a high incidence of
diabetes and obesity, like the Pima indians, children from
diabetic mothers have a higher risk of becoming diabetic
compared with children from non-diabetic mothers. This
effect is much stronger with maternal diabetes compared
with paternal diabetes, suggesting a non-genetic mode of
transfer to the offspring.In this project, the effects of
maternal obesity on the development of the metabolic
syndrome in the offspring were investigated in rats.
Materials and Methods: Maternal obesity was induced by
i3vt infusion of the melanocortin 34 antagonist SHU9119
during the last two weeks of pregnancy and the first two
weeks of lactation. Male offspring rats from these preg-
nancies were used at the age of 3–4 months to assess the
risk of metabolic syndrome.
Results: Body weight was increased in offspring from SHU
mothers, starting from 68 days of age. Food intake was not
changed, but water intake was increased in SHU offspring.
Respirometric measurements showed increased RQ and a
trend to decreased energy expenditure in the dark phase.
This was associated to decreased locomotor activity in the
dark phase. Oral glucose tolerance tests showed an increase
in basal glucose, with no difference in insulin levels,
suggesting glucose intolerance in SHU offspring.
Conclusion: We conclude that maternal obesity increases
the risk of the metabolic syndrome in the offspring in a
non-genetic way. This is mainly due to changes in fat and
glucose metabolism, and decreased physical activity,
resulting in high body weight and glucose intolerance.
Supported by a career development grant from the dutch
Diabetes Fonds to Dr. G. van Dijk on aetiology of the
insulin resistance syndrome.
0141
Intrauterine growth retardation leads to the functional
change of insulin secretion in the newborn rat
Q. X. Yuan
1, C. Liu
1, W. De
2;
1Department of Endocrinology, The First Affiliated
Hospital of Nanjing Medical University,
2Department of
Biochemistry and Molecular Biology, Nanjing Medical
University, China.
Background and Aims: Embryonic pancreatic develop-
ment had a close relation to adult diseases. Intrauterine
growth retardation (IUGR) is a common complication of
pregnancy and a risk factor for both perinatal disease and
disorders of later life, especially impaired glucose tolerance
and diabetes. The aim of this study is to investigate the
functional change of insulin secretion in IUGR newborn rat
and explore the mechanism of reduced blood insulin level.
Materials and Methods: SDpregnantratsweredividedinto
two groups: control group and intrauterine energy restriction
group. The animal model of IUGR in rats was made by 50%
calorie restriction in pregnant rats from gestational day 15
until term. Pancreata of control and IUGR newborn rats were
dissected respectively. After abstraction of totle RNA, RT-
PCR was used to study the expression of genes related to
insulin synthesis and exocytosis. Intraperitoneal glucose
tolerance tests(IPGTT) and ELISA were done to detect the
function of pancreatic islet.
Results: Birth weight and pancreas mass of IUGR newborn
rats were significantly lower than those of controls. Although
no significant differences were observed in genes expression
of insulin and PDX-1, the expressions of genes related to
insulin exocytosis such as munc13-1, vamp-2, syntaxin1a,
rab3a were reduced markedly in IUGR newborn rats. The
blood insulin level and insulin secretion response to glucose
challenge were also reduced simultaneously in IUGR new-
born rats compared with normal newborn rats.
90 Diabetologia (2006) 49:[Suppl1]1–755

Effects of maternal obesity on metabolic syndrome in the offspring

http://cbn.eldoc.ub.rug.nl/FILES/root/2006/DiabetolHeinsbroek/2006DiabetolHeinsbroek.pdf

Effects of maternal obesity on metabolic syndrome in the offspring

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