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  • Title: Increased susceptibility to streptozotocin and impeded regeneration capacity of beta-cells in adult offspring of malnourished rats.
    Author: Goosse K, Bouckenooghe T, Sisino G, Aurientis S, Remacle C, Reusens B.
    Journal: Acta Physiol (Oxf); 2014 Jan; 210(1):99-109. PubMed ID: 23701924.
    Abstract:
    BACKGROUND: Epidemiological studies related poor maternal nutrition and subsequent growth retardation in the progeny to the development of diabetes later in life. Low-protein diet during gestation altered the beta-cell development of the rat progeny by decreasing beta-cell proliferation and increasing their sensitivity to nitric oxide and cytokines in the foetus. This disturbed maternal environment had long-lasting consequences because the higher beta-cell vulnerability was maintained at adulthood. AIM: The aim of this study was to determine whether early malnutrition influences the vulnerability and the regeneration capacity of beta-cells after streptozotocin (STZ) damage at adulthood. METHODS: Gestating rats were fed either a control or a low-protein diet until weaning. Adult female offspring received injections of Freund's adjuvant weekly for 5 weeks followed 24 h later by STZ. Half of the cohort was killed at d34, whereas the other half was maintained until d48 to analyse the regeneration capacity of the beta-cells. RESULTS: Although control and low-protein rats had equivalent pancreatic insulin content and beta-cell volume density at d34, hyperglycaemia appeared earlier and was more dramatic in low-protein rats than in control rats. STZ treatment increased beta-cell proliferation similarly in both groups. At d48, apoptotic rate was higher in the low-protein group. Regeneration appeared in control, but not in the low-protein rats, where beta-cell aggregates/surface area and Reg1-positive area were decreased compared to control. CONCLUSION: Maternal malnutrition programmes a more vulnerable endocrine pancreas in the progeny which is unable to regenerate after injury, therefore predisposing it to develop glucose intolerance and diabetes later in life.
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