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1 Laboratoire Biologie Cellulaire, Universite catholique de Louvain, Louvain-la-Neuve, Belgium
2 Metabolex, Hayward, CA, USA
* To whom correspondence should be addressed. E-mail: reusens{at}bani.ucl.ac.be.
We investigated the effect of an isocaloric maternal low protein diet during pregnancy in rats on the proliferative capacity of cultured foetal hepatocytes. The potential roles of these changes on the IGFs-IGFBPs axis, and the role of insulin and glucocorticoids in liver growth retardation, were also evaluated. Pregnant Wistar rats were fed a control (C) diet (20% protein) or a low protein (LP) diet (8%) throughout gestation. In primary culture, the DNA synthesis of hepatocytes derived from LP foetuses was decreased by about 30% when compared to control hepatocytes (p<0.05). Parallely, in vivo, moderate protein restriction in the dam reduced the foetal liver weight, IGF-I level in foetal plasma (p<0.01) and augmented the abundance of 29-32 KDa IGFBPs in foetal plasma (p<0.01) and foetal liver (p<0.01). By contrast, the abundance of IGF-II mRNA in liver of LP foetuses was unaffected by the low protein diet. In vitro, the LP-derived hepatocytes produced less IGF-I (p<0.01) and more 29-32 KDa IGFBPs (p<0.01) than hepatocytes derived from control foetuses. These alterations still appeared after 3 to 4 days of culture indicating some persistence in programming. Dexamethasone treatment of control-derived hepatocytes decreased cell proliferation (54% ± 2.3, p<0.01) and stimulated 29-32 kDa IGFBPs while insulin promoted fetal hepatocytes growth (127% ± 5.5, p<0.01) and inhibited 29-32 kDa IGFBPs. These results show that liver growth and cell proliferation in association with IGF-I and IGFBPs levels are affected in utero by foetal undernutrition. It also suggests that glucocorticoids and insulin may modulate these effects.
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