山奈霉素在短期高脂高糖饮食干预后调节小鼠肝脏AMPK磷酸化和PEPCK表达。

IF 1.4 Q3 NUTRITION & DIETETICS
Ingrid Candido Garofolo, Paloma Freire Santos, Milena Ferreira Silva, Viviane de Mello Veneza, Thiago André Moura Veiga, Vera Lucia Flor Silveira, Maria Isabel Cardoso Alonso-Vale, Luciana Chagas Caperuto
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引用次数: 0

摘要

背景:2型糖尿病是一种以高血糖和高胰岛素血症为特征的代谢性疾病,与肥胖密切相关。根据国际糖尿病联合会的数据,2021年,近670万20-79岁的成年人死于糖尿病并发症。鉴于这一令人担忧的统计数据,新的替代品,包括生物活性化合物如类黄酮,正在进行临床和科学评估,以阻止代谢紊乱的进展或可能避免其发作。目的:我们假设山奈霉素可能对高脂高糖饮食(HFHS)小鼠24小时的血糖稳态起作用。方法:以100 mg/kg剂量的山奈霉素喂给2月龄雄性C57BL/6小鼠,分别饲喂HFHS饮食3、6、24 h。通过口服葡萄糖耐量试验(oGTT)评估葡萄糖耐受不良。在肝脏中,采用western blotting检测amp活化蛋白激酶(AMPK),采用定量PCR (qPCR)检测磷酸烯醇丙酮酸羧激酶(PEPCK)酶的基因表达。结果:在6 h时,山奈素与仅接受HFHS饮食的组相比,降低了PEPCK基因的表达。对于HFHS饮食的24小时挑战,山奈霉素没有预防葡萄糖耐受不良(oGTT)。与HFHS组相比,山奈霉素降低了pAMPK/AMPK比值和PEPCK基因表达量。结论:山奈霉素与高热量和高脂血症患者同时服用时,即使是短时间服用,也不能预防葡萄糖耐受不良。然而,它确实导致AMPK磷酸化和PEPCK基因表达的显著调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Kaempferitrin modulates AMPK phosphorylation and PEPCK expression in the liver after a short-term high-fat, high-sucrose diet intervention in mice.

Background: Type 2 Diabetes Mellitus is a metabolic disease characterized by hyperglycemia and hyperinsulinemia, closely linked to obesity. According to the International Diabetes Federation, in 2021, almost 6.7 million adults aged 20-79 died due to complications from diabetes. In light of this concerning statistic, novel alternatives, including bioactive compounds such as flavonoids, are undergoing clinical and scientific evaluation to hinder the advancement of metabolic disorders or maybe avert their onset. Aim: We postulate that kaempferitrin may act on glycemic homeostasis in mice challenged with high-fat, high-sucrose diet (HFHS) for 24 h. Methods: Kaempferitrin at a 100 mg/kg dose was administered to two-month-old male C57BL/6 mice challenged with a HFHS diet for 3, 6, or 24 h. Glucose intolerance was assessed by an oral glucose tolerance test (oGTT). In the liver, AMP-activated protein kinase (AMPK) was measured via western blotting, and gene expression of the phosphoenolpyruvate carboxykinase (PEPCK) enzyme was assessed by quantitative PCR (qPCR). Results: At 6 h, kaempferitrin reduced the PEPCK gene expression compared to the group receiving only the HFHS diet. For the 24 h challenge with the HFHS diet, kaempferitrin did not prevent glucose intolerance (oGTT). However, kaempferitrin reduced the pAMPK/AMPK ratio and the PEPCK gene expression compared to the HFHS group. Conclusions: Kaempferitrin, when administered alongside a hypercaloric and hyperlipidic diet, even for short periods, did not prevent glucose intolerance. Nevertheless, it did lead to significant modulations in AMPK phosphorylation and PEPCK gene expression.

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来源期刊
Nutrition and health
Nutrition and health Medicine-Medicine (miscellaneous)
CiteScore
3.50
自引率
0.00%
发文量
160
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