Maternal malnutrition can alter developmental biology, programming health and disease in offspring. The increase in sugar consumption during the peripubertal period, a worldwide concern, also affects health through adulthood. Studies have shown that maternal exposure to a low protein diet (LPD) is associated with an increase in prostate disease with aging. However, the combined effects of maternal LPD and early postnatal sugar consumption on offspring prostate disorders were not investigated. The effects on aging were evaluated using a maternal gestational model with lactational LPD (6% protein) and sugar consumption (10%) from postnatal day (PND) 21–90, associating the consequences on ventral prostate (VP) rats morphophysiology on PND540. An increase was shown in mast cells and in the VP of the CTR + SUG and Gestational and Lactational Low Protein (GLLP) groups. In GLLP + SUG, a significant increase was shown in TGF-β1 expression in both the systemic and intra-prostatic forms, and SMAD2/3p had increased. The study identified maternal LPD and sugar consumption as risk factors for prostatic homeostasis in senility, activating the TGFβ1-SMAD2/3 pathway, a signaling pathway with potential markers for prostatic disorders.

中文翻译：

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与产后糖消耗相关的母亲营养不良会增加大鼠后代的炎症反应和前列腺疾病

母亲营养不良会改变发育生物学，影响后代的健康和疾病。青春期前后糖摄入量的增加是一个全世界关注的问题，也会影响成年后的健康。研究表明，母亲接触低蛋白饮食（LPD）与随着年龄增长前列腺疾病的增加有关。然而，尚未研究母体 LPD 和产后早期糖消耗对后代前列腺疾病的综合影响。使用母体妊娠模型评估对衰老的影响，该模型从出生后（PND）21-90天开始哺乳LPD（6％蛋白质）和糖消耗（10％），并将其对腹侧前列腺（VP）大鼠形态生理学的影响与PND540相关联。 CTR + SUG 以及妊娠和哺乳期低蛋白 (GLLP) 组的肥大细胞和 VP 有所增加。在 GLLP + SUG 中，全身和前列腺内形式的 TGF-β1 表达均显着增加，并且 SMAD2/3p 也增加。该研究确定母亲 LPD 和糖消耗是衰老时前列腺稳态的危险因素，激活 TGFβ1-SMAD2/3 通路，这是一种具有前列腺疾病潜在标志物的信号通路。