Beijing Key Laboratory of the Innovative Development of Functional Staple and the Nutritional Intervention for Chronic Disease, Department of Clinical Nutrition, Department of Health Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Center for Biomarker Discovery and Validation, Institute of Clinical Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Nutrients. 2024 Oct 17;16(20):3518. doi: 10.3390/nu16203518.
Highland barley (HB) consumption offers numerous health benefits; however, its impact on glycolipid metabolism abnormalities induced by a high-fat diet remains unclear. Consequently, this study aimed to investigate the therapeutic effects and underlying molecular mechanisms of HB in the context of obesity; Rats were fed either a high-fat diet (HFD) to induce obesity or a standard diet (SD) for six weeks. The rats in the HFD group were randomly assigned into five groups: HFD+HFD, HFD+SD, and low (30%), medium (45%), and high (60%) doses of the HB diet for an additional ten weeks. Analyses of serum lipid profiles, liver histology, transcriptomes, and untargeted metabolomes were conducted; HB intake resulted in decreased weight gain, reduced feed intake, lower serum triglyceride and cholesterol levels, and diminished hepatic lipid accumulation. It also improved insulin and fasting blood glucose levels, and antioxidant capacity in the HFD-fed rats. Transcriptome analysis revealed that HB supplementation significantly suppressed the HFD-induced increase in the expression of Angptl8, Apof, CYP7A1, GDF15, Marveld1, and Nr0b2. Furthermore, HB supplementation reversed the HFD-induced decrease in Pex11a expression. Untargeted metabolome analysis indicated that HB primarily influenced the pentose phosphate pathway, the Warburg effect, and tryptophan metabolism. Additionally, integrated transcriptome and metabolome analyses demonstrated that the treatments affected the expression of genes associated with glycolipid metabolism, specifically ABCG8, CYP2C12, CYP2C24, CYP7A1, and IRS2. Western blotting confirmed that HB supplementation impacted the IRS2/PI3K/AKT signaling pathway; HB alleviates HFD-induced obesity and liver injury in an obese rat model possibly through the IRS2/PI3K/Akt signaling pathway.
青稞（HB）的消费有许多健康益处；然而，它对高脂肪饮食引起的糖脂代谢异常的影响尚不清楚。因此，本研究旨在探讨 HB 在肥胖背景下的治疗效果及其潜在的分子机制；将大鼠分为正常饮食（SD）组和高脂饮食（HFD）组，HFD 组大鼠给予高脂饮食喂养 6 周，诱导肥胖；将 HFD 组大鼠随机分为 5 组：HFD+HFD、HFD+SD、HB 低（30%）、中（45%）、高（60%）剂量组，继续喂养 10 周；分析血清脂质谱、肝组织学、转录组和非靶向代谢组；HB 摄入可减少体重增加，降低饲料摄入量，降低血清甘油三酯和胆固醇水平，减少肝脂质堆积；还可改善 HFD 喂养大鼠的胰岛素和空腹血糖水平以及抗氧化能力；转录组分析表明，HB 补充可显著抑制 HFD 诱导的 Angptl8、Apof、CYP7A1、GDF15、Marveld1 和 Nr0b2 表达增加；此外，HB 补充可逆转 HFD 诱导的 Pex11a 表达降低；非靶向代谢组分析表明，HB 主要影响戊糖磷酸途径、沃伯格效应和色氨酸代谢；此外，整合转录组和代谢组分析表明，这些治疗方法影响与糖脂代谢相关的基因的表达，特别是 ABCG8、CYP2C12、CYP2C24、CYP7A1 和 IRS2；Western blot 验证了 HB 补充影响 IRS2/PI3K/AKT 信号通路；HB 通过 IRS2/PI3K/Akt 信号通路缓解 HFD 诱导的肥胖和肝损伤。
