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Maternal Broccoli Powder Intake Ameliorates Insulin Resistance and Inflammation via AMPK/mTOR Pathway in the Livers of High‐Fructose‐Fed Male Rat Offspring Exposed to Maternal Protein Restriction
Molecular Nutrition & Food Research ( IF 4.5 ) Pub Date : 2024-10-18 , DOI: 10.1002/mnfr.202400472
Anishma Karmacharya, Shiho Kasai, Yuuka Mukai, Shin Sato

ScopeSub‐optimal prenatal conditions such as maternal undernutrition during pregnancy and lactation posit high risks of adult metabolic diseases. High fructose intake causes insulin resistance and liver inflammation contributing to metabolic diseases. However, food‐based preventive measure for these metabolic diseases in the offspring is under‐researched. This study aims to investigate the effect of maternal broccoli powder (BP) intake during lactation on insulin resistance and liver inflammation in high‐fructose‐diet‐fed adult male offspring exposed to maternal protein restriction.Methods and resultsPregnant Wistar rats are provided normal protein (NP) or low protein (LP) diets and 0% or 0.74% BP‐containing NP diets and 0% or 0.74% BP‐containing LP diet during lactation. At weaning, offspring receiving water (W) or 10% fructose solution (Fr) are assigned into six groups: NP/NP/W, NP/NP/Fr, NP/NPBP/Fr, LP/LP/W, LP/LP/Fr, and LP/LPBP/Fr. At week 13, plasma insulin, macrophage infiltration, activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) phosphorylation, and autophagy flux markers are examined. LP/LPBP/Fr shows lower insulin levels and Homeostatic model assessment for insulin resistance (HOMA‐IR) values than LP/LP/Fr. Liver macrophage infiltration are decreased in LP/LPBP/Fr. LP/LPBP/Fr exhibits upregulated AMPK phosphorylation, downregulated mTOR phosphorylation, and increased Microtubule‐associated protein1A/1B‐light chain 3B‐II (LC3B‐II) levels.ConclusionMaternal BP intake during lactation ameliorates insulin resistance and inflammation in the livers of adult offspring on a high‐fructose diet from LP mothers.

中文翻译:


母体西兰花粉摄入量通过暴露于母体蛋白质限制的高果糖喂养雄性大鼠后代肝脏中的 AMPK/mTOR 途径改善胰岛素抵抗和炎症



范围次优产前状况,例如孕产妇在怀孕和哺乳期间的营养不良,是成人代谢疾病的高风险。高果糖摄入量会导致胰岛素抵抗和肝脏炎症,从而导致代谢疾病。然而,针对后代这些代谢疾病的基于食物的预防措施研究不足。本研究旨在调查哺乳期母体西兰花粉 (BP) 摄入量对暴露于母体蛋白质限制的高果糖饮食喂养成年雄性后代胰岛素抵抗和肝脏炎症的影响。方法和结果在哺乳期为怀孕的 Wistar 大鼠提供正常蛋白 (NP) 或低蛋白 (LP) 饮食以及 0% 或 0.74% 含 BP 的 NP 饮食和 0% 或 0.74% 含 BP 的 LP 饮食。断奶时,将接受水 (W) 或 10% 果糖溶液 (Fr) 的后代分为六组:NP / NP / W,NP / NP / Fr,NP / NPBP / Fr,LP / LP / W,LP / LP / Fr和LP / LPBP / Fr。在第 13 周,检查血浆胰岛素、巨噬细胞浸润、活化蛋白激酶 (AMPK) 和雷帕霉素 (mTOR) 磷酸化的机制靶标,以及自噬通量标志物。LP/LPBP/Fr 显示胰岛素水平和胰岛素抵抗稳态模型评估 (HOMA-IR) 值低于 LP/LPBP/Fr. LP/LPBP/Fr 中肝脏巨噬细胞浸润减少 LP/LPBP/Fr 表现出 AMPK 磷酸化上调,mTOR 磷酸化下调,微管相关蛋白 1A/1B-轻链 3B-II (LC3B-II) 水平增加。结论哺乳期母体血压摄入可改善 LP 母亲高果糖饮食成年后代肝脏的胰岛素抵抗和炎症。
更新日期:2024-10-18
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