Chen Jie, Wang Shuting, Guo Fuchuan, Gong Yupeng, Chen Tianbao, Shaw Chris, Jiang Rencai, Huang Fang, Lin Dai
Department of Nutrition and Food Safety, School of Public Health Fujian Medical University Fuzhou Fujian China.
School of Pharmacy Queen's University Belfast UK.
Food Sci Nutr. 2024 Mar 5;12(6):4049-4062. doi: 10.1002/fsn3.4061. eCollection 2024 Jun.
The primary objective of this investigation was to explore the beneficial impacts of polysaccharide (EP) on dysglycemia in Zucker diabetic fatty (ZDF) rats, while also shedding light on its potential mechanism using H-NMR-based metabolomics. The results demonstrated a noteworthy reduction in fasting blood glucose (FBG, 46.3%), fasting insulin (50.17%), glycosylated hemoglobin A1c (HbA1c, 44.1%), and homeostatic model assessment of insulin resistance (HOMA-IR, 59.75%) following EP administration, while the insulin sensitivity index (ISI, 19.6%) and homeostatic model assessment of β-cell function (HOMA-β, 2.5-fold) were significantly increased. These findings indicate that EP enhances β-cell function, increases insulin sensitivity, and improves insulin resistance caused by diabetes. Moreover, EP significantly reduced serum lipid levels, suggesting improvement of dyslipidemia. Through the analysis of serum metabolomics, 17 metabolites were found to be altered in diabetic rats, 14 of which were upregulated and 3 of which were downregulated. Notably, the administration of EP successfully reversed the abnormal levels of 9 out of the 17 metabolites. Pathway analysis further revealed that EP treatment partially restored metabolic dysfunction, with notable effects observed in valine, leucine, and isoleucine metabolism; aminoacyl-transfer RNA (tRNA) biosynthesis; and ketone body metabolism. These findings collectively indicate the potential therapeutic efficacy of EP in preventing glycemic abnormalities and improving insulin resistance. Thus, EP holds promise as a valuable treatment option for individuals with diabetes.
本研究的主要目的是探讨多糖（EP）对Zucker糖尿病脂肪（ZDF）大鼠血糖异常的有益影响，同时利用基于氢核磁共振的代谢组学揭示其潜在机制。结果表明，给予EP后，空腹血糖（FBG，降低46.3%）、空腹胰岛素（降低50.17%）、糖化血红蛋白A1c（HbA1c，降低44.1%）和胰岛素抵抗稳态模型评估（HOMA-IR，降低59.75%）均显著降低，而胰岛素敏感指数（ISI，升高19.6%）和β细胞功能稳态模型评估（HOMA-β，升高2.5倍）显著升高。这些发现表明，EP可增强β细胞功能，提高胰岛素敏感性，并改善糖尿病引起的胰岛素抵抗。此外，EP显著降低了血脂水平，提示血脂异常得到改善。通过血清代谢组学分析，发现糖尿病大鼠中有17种代谢物发生了变化，其中14种上调，3种下调。值得注意的是，给予EP成功逆转了17种代谢物中9种的异常水平。通路分析进一步表明，EP治疗部分恢复了代谢功能障碍，在缬氨酸、亮氨酸和异亮氨酸代谢、氨酰基转移RNA（tRNA）生物合成以及酮体代谢方面观察到显著效果。这些发现共同表明EP在预防血糖异常和改善胰岛素抵抗方面具有潜在的治疗效果。因此，EP有望成为糖尿病患者的一种有价值的治疗选择。
