Biosciences Department, Institute of Health and Society, Federal University of São Paulo, Campus Baixada Santista - UNIFESP, Santos, São Paulo, Brazil.
Institute of Metabolic Science, Metabolic Research Laboratories, Department of Clinical Biochemistry, University of Cambridge, Cambridge, CB2 OQQ, UK.
Eur J Nutr. 2024 Dec;63(8):3013-3024. doi: 10.1007/s00394-024-03485-w. Epub 2024 Sep 4.
Environmental factors in the early life stages can lead the descendant to adaptations in gene expression, permanently impacting several structures and organs. The amount and quality of fatty acids in the maternal diet in pregnancy and lactation were found to impact offspring metabolism. So, maternal diet and insulin resistance can affect the male and female descendants through distinct pathways and at different time points. We hypothesized that maternal high-fat diet (HFD) intake before conception and an adequate amount of different fatty acids intake during pregnancy and lactation could influence the energy homeostasis system of 21-day-old offspring. Female rats received control diet (C) or HFD (HF) for 8 weeks before pregnancy. During pregnancy and lactation C group remained with same diet (C-C), HF group were distributed into 4 groups and received C diet (HF-C), normolipidic diet based on saturated fatty acids (HF-S) or based on polyunsaturated fatty acids n-3 (HF-P) or remained in same diet (HF-HF). Maternal HFD in preconception, pregnancy, and lactation (HF-HF) led to lower glucagon-like peptide-1 levels in male (HF-HF21) compared to other groups (C-C21, HF-C21, and HF-P21) and compared to HF-HF21 females. Neuropeptide YY levels were higher in the HF-HF21, HF-C21, and HF-S21 male offspring compared to HF-P21. HF-P21 was similar to C-C21. Positive correlations were found among the energy homeostasis markers genes expressed in the offspring hypothalamus. Maternal diet changes to adequate quantities of fatty acids during pregnancy and lactation showed less impaired results but was not entirely avoided. A maternal diet based on PUFA n-3 during pregnancy and lactation seems to reverse the damage of an HFD in preconception. These results of homeostasis energy system disturbance in the offspring at weaning give us clues about changes that precede the onset of the disease in adult life - adding notes to the knowledge for future investigations of prevention and treatment of chronic diseases.
环境因素在生命早期阶段可以导致后代基因表达的适应性改变，永久影响多个结构和器官。在怀孕和哺乳期，母体饮食中的脂肪酸数量和质量被发现会影响后代的新陈代谢。因此，母体饮食和胰岛素抵抗可以通过不同的途径并在不同的时间点影响雄性和雌性后代。我们假设，在受孕前母体高脂肪饮食（HFD）的摄入以及在怀孕和哺乳期摄入足够数量的不同脂肪酸，可以影响 21 天大的后代的能量平衡系统。雌性大鼠在受孕前接受对照饮食（C）或高脂肪饮食（HF）8 周。在怀孕和哺乳期，C 组仍保持相同的饮食（C-C），HF 组分为 4 组，分别接受 C 饮食（HF-C）、基于饱和脂肪酸的正常脂质饮食（HF-S）或基于多不饱和脂肪酸 n-3 的饮食（HF-P）或仍保持相同饮食（HF-HF）。在受孕前、怀孕和哺乳期的母体 HFD（HF-HF）导致雄性（HF-HF21）的胰高血糖素样肽-1 水平低于其他组（C-C21、HF-C21 和 HF-P21），也低于 HF-HF21 雌性。雄性 HF-HF21、HF-C21 和 HF-S21 后代的神经肽 Y 水平高于 HF-P21。HF-P21 与 C-C21 相似。在后代下丘脑表达的能量平衡标志物基因之间发现了正相关。在怀孕和哺乳期，母体饮食向适当数量的脂肪酸的改变显示出较小的受损结果，但并未完全避免。在受孕前，基于 PUFA n-3 的母体饮食在怀孕和哺乳期似乎可以逆转 HFD 的损害。这些在断奶后代能量平衡系统紊乱的结果为我们提供了关于成年后疾病发生前变化的线索-为未来对慢性病的预防和治疗的研究增加了注释。
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