Details

Autor(en) / Beteiligte

• BOUJENDAR, S
• REUSENS, B
• MEREZAK, S
• AHN, M.-T
• ARANY, E
• HILL, D
• REMACLE, C

Titel

Taurine supplementation to a low protein diet during foetal and early postnatal life restores a normal proliferation and apoptosis of rat pancreatic islets

Ist Teil von

• Diabetologia, 2002-06, Vol.45 (6), p.856-866

Ort / Verlag

Berlin: Springer

Erscheinungsjahr

2002

Link zum Volltext

Quelle

SpringerLINK Contemporary (Konsortium Baden-Württemberg)

Beschreibungen/Notizen

• In our previous studies a low protein diet (8% vs 20%) given during foetal and early postnatal life induced abnormal development of the endocrine pancreas; beta-cell mass and islet-cell proliferation were reduced while apoptosis was increased. Taurine, an important amino acid for development was also reduced in maternal and foetal plasma of protein deficient animals. In this study we aim to evaluate the role of taurine in the alterations observed in rats after a low protein diet. Four groups of rats were given either a control, a low protein, or control and low protein diets with 2.5% taurine in the drinking water. Diets were given to gestating and lactating mothers and to their pups until day 30. Beta and endocrine cell masses were analysed as well as DNA synthesis and apoptosis after taurine supplementation in foetuses and pups. We also investigated insulin like growth factor-II (IGF-II), inducible nitric oxide synthase (iNOS), and Fas by immunohistochemistry. In foetuses and neonates nourished with a low protein diet, taurine supplementation restored normal DNA synthesis and apoptosis. This led to adequate beta and endocrine cell mass in pups. In islet cells, immunoreactivity was increased for IGF-II, reduced for Fas and unchanged for iNOS after taurine supplementation. Taurine supplementation to a low protein diet in foetal and early postnatal life prevents the abnormal development of the endocrine pancreas. The mechanisms by which taurine acts on DNA synthesis and apoptosis rate of endocrine cells involve IGF-II, Fas regulation but not iNOS.