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尼普利素缺乏会降低高脂肪食小鼠的肝脏葡萄糖生成

Nathalie Esser¹, Stephen M Mongovin², Thomas O Mundinger³

¹Veterans Affairs Puget Sound Health Care System, Seattle, WA, United States; Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington, Seattle, WA, United States; Laboratory of Immunometabolism and Nutrition, GIGA-I3, CHU Liège, University of Liège, Liège, Belgium.

|August 12, 2023

概括

在小鼠中, neprilysin 的遗传删除会降低肝脏葡萄糖的产生. 尼普利辛的抑制可能提供一种降低2型糖尿病和肥胖症葡萄糖的策略.

科学领域:

代谢研究的研究.
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

尼普利素 (NEP) 分裂葡萄糖调节,如GLP-1和CCK.
抑制NEP可能会改善血糖,胰岛素分泌和糖尿病/肥胖症的敏感性.
抑制NEP对肝脏葡萄糖代谢的影响在很大程度上尚未被探索.

研究的目的:

调查基因NEP删除是否抑制高脂肪饮食小鼠的肝葡萄糖 (HGP) 生产.
为了确定NEP缺乏是否影响肝脏葡萄糖生成和肝脏糖原储存.
评估肠选择性NEP抑制是否影响肝脏葡萄糖生成.

主要方法:

高脂肪饮食养Nep^+/+和Nep^-/-小鼠16周.
酸盐耐受性测试 (PTT) 用于评估肝脏葡萄糖生成.
在禁食和食状态下测量肝脏糖原含量.
测试肠道选择性NEP抑制对葡萄糖生成的影响.

主要成果:

与Nep^-/-小鼠相比,Nep^+/+小鼠在PTT期间显示葡萄糖外流减少.
在禁食的Nep-/-小鼠中,肝糖原水平显著更高.
肠选择性NEP抑制模仿了全身抑制肝脏葡萄糖生成的抑制.
在Nep^-/-小鼠中观察到血CCK生物活性增加.

结论:

尼普利辛缺乏抑制肝脏葡萄糖的产生,可能是通过增加GLP-1和CCK.
针对普里利辛活性的策略可能有利于在2型糖尿病和肥胖症中控制肝脏葡萄糖的产生.

关键词:

胆囊性托基尼尼的使用.类似于葡萄糖的-1 葡萄糖的产生和生成.糖原溶解 (glycogenolysis) 是一种肝脏肝脏肝脏肝脏尼普利利辛 (Neprilysin) 是一种药物.

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