Developmental changes in hepatic growth hormone binding sites were examined in the genetically obese male fa/fa rats and in the lean littermates. At 16 days, fa/fa pups are normoinsulinemic; the specific binding of 125I-hGH to liver membranes is comparable in the two genotypes. At 4 weeks and later on, plasma membranes and Golgi fractions of male obese Zucker rats have more GH binding sites than lean littermates. The GH pituitary content is comparable in the two genotypes from 2 to 8 weeks and in 14-week-old fa/fa rats it is half that in lean animals. In the two genotypes plasma IGFI dramatically increases during puberty. At 4 weeks, plasma IGFI level is significantly higher in fa/fa rats than in lean littermates. In this model of genetic obesity, an increased GH binding to liver membranes is observed after the third week of life, shortly after the onset of hyperinsulinemia in the fa/fa rat.

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Virtual poster abstracts subdiaphragmatic bronchopulmonary sequestration. Fetal abdominal mass continued to grow to 4.7 x 3.0 cm at 35weeks of gestation. When a woman came to delivery unit due to labour pain at 38 weeks' gestation, the size of mass increased to 5.1 X 3.5 cm with mixed echogenicity and hepatomegaly was accompanied. After a vaginal delivery, postnatal ultrasonography and MRI revealed a left suprarenal space neuroblastoma, multiple liver metastasis with marked hepatomegaly, and splenomegaly. Poorly differentiated neuroblastoma was diagnosed on excision biopsy. Although most of stage 4s neuroblastoma shows good prognosis, rapid growing mass and hepatomegaly, followed by abdominal expansion and dyspnea are considered as a main obstacle to full patient cure. We conclude that a prenatal rapid growing mass in suprarenal area, which is suggestive of neuroblastoma, requires close monitoring with disease staging. Planned delivery may be considered for prompt neonatal treatment, because disease progression can be overwhelmingly rapid. VP11.16 Multicystic dysplasic kidney: postnatal involution and compensatory hypertrophy

Insulin is an anabolic hormone that plays a central role in glucose homeostasis. Synthesis, secretion and appearance of insulin in portal and peripheral circulation are complex and tightly regulated. As many of the tissues involved are not directly accessible, mathematical models have been developed to describe insulin kinetics. This paper presents a mathematical synthesis of models for the study of insulin kinetics and is meant as a supplemental to our recent review of glucose kinetics models, some of which encompass insulin sub-models. Models are described in steady and non-steady state and are grouped into compartmental and non-compartmental schemes.