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Impaired ß-cell regeneration in perinatally malnourished rats: a study with STZ

INSERM U 457, Hôpital Robert Debré, Paris, France

¹Correspondence: INSERM U 457, Hôpital Robert Debré, 48 boulevard Sérurier, 75019 Paris, France. E-mail: bbreant{at}infobiogen.fr

We investigated the mechanisms implicated in ß-cell mass reduction observed during late fetal and early postnatal malnutrition in the rat. Beta-cell regeneration, including proliferation and neogenesis, was studied after neonatal ß-cell destruction by streptozotocin (STZ). STZ was injected at birth and maternal food restriction was continued until weaning. Beta-cell mass, proliferation, and islet number were quantified by morphometrical measurements on pancreatic sections in STZ-injected normal (C-STZ) and malnourished (R-STZ) rats, with noninjected C and R rats as controls. At day 4, only 20% of the ß cell-mass remained in C-STZ rats. It regenerated to 50% that of noninjected controls, mainly through active neogenesis, as shown by the entire recovery of islet number/cm², and also through moderately increased ß-cell proliferation. In contrast, ß-cell mass from R-STZ animals poorly regenerated, despite a dramatic increase of ß-cell proliferation, because islet number/cm² recovered insufficiently. In conclusion, perinatal malnutrition impairs neogenesis and the capacity of ß-cell regeneration by neogenesis but preserves ß-cell proliferation, which remains the elective choice to increase ß-cell mass. These results provide an explanation for the impaired capacity of malnourished animals to adapt their ß-cell mass during aging or pregnancy, which aggravate glucose tolerance.—Garofano, A., Czernichow, P., and Bréant, B. Impaired ß-cell regeneration in perinatally malnourished rats: a study with STZ.

Key Words: malnutrition • ß-cell mass • proliferation • morphometry

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