赛马鲁肽
安普克
内科学
脂肪生成
内分泌学
医学
mTORC1型
PI3K/AKT/mTOR通路
脂质代谢
兴奋剂
胰高血糖素样肽1受体
2型糖尿病
受体
信号转导
利拉鲁肽
蛋白激酶A
生物
糖尿病
激酶
生物化学
作者
Pedro Henrique Reis-Barbosa,Ilitch Aquino Marcondes-de-Castro,Thatiany de Souza Marinho,Márcia Barbosa Águila,Carlos Alberto Mandarim‐de‐Lacerda
标识
DOI:10.1016/j.clinre.2022.101922
摘要
The liver regulates lipid metabolism. Decreasing mTOR (mechanistic target of rapamycin complex 1) and enhancing AMPK (AMP-activated protein kinase) help degrade hepatic diet-induced accumulated lipids. Therefore, the glucagon-like peptide type 1 receptor agonist (GLP-1) is indicated to treat obesity-related liver metabolic alterations. Then, we investigated the effects of semaglutide (recent GLP-1) by analyzing the liver mTORC1/AMPK pathway genes in obese mice.C57BL/6 male mice were separated into two groups and submitted for 16 weeks of obesity induction. Then they were treated for an additional four weeks with semaglutide (subcutaneous, 40 μg/kg once every three days). The groups formed were: C, control group; CS, control group plus semaglutide; HF, high-fat group; HFS, high-fat group plus semaglutide. Next, the livers were dissected, and rapidly fragments of all lobes were kept and frozen at -80° C for analysis (RT-qPCR).Liver markers for the mTOR pathway associated with anabolism and lipogenesis de novo were increased in the HF group compared to the C group but comparatively attenuated by semaglutide. Also, liver markers for the AMPK pathway, which regulates chemical pathways involving the cell's primary energy source, were impaired in the HF group than in the C group but partly restored by semaglutide.the mTOR pathway was attenuated, and the insulin signaling and the AMPK pathway were enhanced by semaglutide, ameliorating the liver gene expressions related to the metabolism of obese mice. These findings are promising in delaying the progression of nonalcoholic fatty liver disease.
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