The gut plays a crucial role in metabolism by regulating the passage of nutrients, water and microbial-derived substances to the portal circulation. Additionally, it produces incretins, such as glucose-insulinotropic releasing peptide (GIP) and glucagon-like derived peptide 1 (GLP1, encoded by gene) in response to nutrient uptake. We aimed to investigate whether offspring from overweight rats develop anomalies in the barrier function and incretin transcription. We observed pro-inflammatory related changes along with a reduction in Claudin-3 levels resulting in increased gut-permeability in fetuses and offspring from overweight rats. Importantly, we found decreased mRNA levels in both fetuses and offspring from overweight rats. Differently, mRNA levels were upregulated in fetuses, downregulated in female offspring and unchanged in male offspring from overweight rats. When cultured with high glucose, intestinal explants showed an increase in and mRNA levels in control offspring. In contrast, offspring from overweight rats did not exhibit any response in mRNA levels. Additionally, while females showed no response, male offspring from overweight rats did exhibit an upregulation in mRNA levels. Furthermore, female and male offspring from overweight rats showed sex-dependent anomalies when orally challenged with a glucose overload, returning to baseline glucose levels after 120 min.

中文翻译：

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超重大鼠所生后代的肠道改变和轻度葡萄糖稳态损伤

肠道通过调节营养物质、水和微生物衍生物质进入门静脉循环，在新陈代谢中发挥着至关重要的作用。此外，它还会响应营养吸收而产生肠促胰岛素，例如葡萄糖促胰岛素释放肽 (GIP) 和胰高血糖素样衍生肽 1（GLP1，由基因编码）。我们的目的是研究超重大鼠的后代是否会出现屏障功能和肠促胰岛素转录异常。我们观察到促炎相关的变化以及 Claudin-3 水平的降低，导致超重大鼠的胎儿和后代的肠道通透性增加。重要的是，我们发现超重大鼠的胎儿和后代的 mRNA 水平均下降。不同的是，超重大鼠的胎儿中mRNA水平上调，雌性后代中下调，而雄性后代中mRNA水平没有变化。当用高葡萄糖培养时，对照后代的肠道外植体的 mRNA 水平增加。相比之下，超重大鼠的后代在 mRNA 水平上没有表现出任何反应。此外，虽然雌性大鼠没有表现出任何反应，但超重大鼠的雄性后代确实表现出 mRNA 水平的上调。此外，超重大鼠的雌性和雄性后代在口服葡萄糖超载挑战时表现出性别依赖性异常，120分钟后恢复到基线葡萄糖水平。