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首页> 外文期刊>Annals of Surgery >Exercise Improves Outcomes of Surgery on Fatty Liver in Mice A Novel Effect Mediated by the AMPK Pathway
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Exercise Improves Outcomes of Surgery on Fatty Liver in Mice A Novel Effect Mediated by the AMPK Pathway

机译：练习改善了在AMPK途径介导的小鼠小鼠脂肪肝脏上的手术结果

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Objective: To investigate whether exercise improves outcomes of surgery on fatty liver, and whether pharmacological approaches can substitute exercising programs. Summary of Background Data: Steatosis is the hepatic manifestation of the metabolic syndrome, and decreases the liver's ability to handle inflammatory stress or to regenerate after tissue loss. Exercise activates adenosine monophosphate-activated kinase (AMPK) and mitigates steatosis; however, its impact on ischemia-reperfusion injury and regeneration is unknown. Methods: We used a mouse model of simple, diet-induced steatosis and assessed the impact of exercise on metabolic parameters, ischemia-reperfusion injury and regeneration after hepatectomy. The same parameters were evaluated after treatment of mice with the AMPK activator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR). Mice on a control diet served as age-matched controls. Results: A 4-week-exercising program reversed steatosis, lowered insulin levels, and improved glucose tolerance. Exercise markedly enhanced the ischemic tolerance and the regenerative capacity of fatty liver. Replacing exercise with AICAR was sufficient to replicate the above benefits. Both exercise and AICAR improved survival after extended hepatectomy in mice challenged with a Western diet, indicating protection from resection-induced liver failure. Conclusions: Exercise efficiently counteracts the metabolic, ischemic, and regenerative deficits of fatty liver. AICAR acts as an exercise mimetic in settings of fatty liver disease, an important finding given the compliance issues associated with exercise. Exercising, or its substitution through AICAR, may provide a feasible strategy to negate the hepatic consequences of energy-rich diet, and has the potential to extend the application of liver surgery if confirmed in humans.
机译：目的：探讨运动是否改善脂肪肝脏手术的结果，以及药理方法是否可以替代行使计划。背景数据摘要：脂肪变性是代谢综合征的肝脏表现，并降低肝脏处理炎症应激或在组织损失后再生再生的能力。锻炼激活腺苷一磷酸活性激酶（AMPK）并减轻脂肪变性;然而，它对缺血再灌注损伤和再生的影响是未知的。方法：采用简单，饮食诱导的脂肪变性的小鼠模型，并评估运动对代谢参数，缺血再灌注损伤和再生术后再生的影响。用AMPK活化剂5-氨基咪唑-4-甲酰胺核糖核苷酸（AICAR）处理小鼠后评价相同的参数。对照饮食的小鼠作为年龄匹配的对照。结果：4周锻炼计划逆转脂肪变性，降低胰岛素水平，改善葡萄糖耐受性。运动显着提高了脂肪肝的缺血性耐受性和再生能力。用AICAR取代锻炼足以复制上述益处。在用西方饮食挑战小鼠的小鼠延长肝切除术后，运动和AICAR都会提高生存，表明切除诱导的肝功能衰竭的保护。结论：运动有效地抵消脂肪肝的代谢，缺血性和再生缺陷。 AICAR作为脂肪肝病的环境中的运动模拟，这是鉴于与运动相关的合规问题的重要发现。通过AICAR锻炼或替代，可以提供可行的策略来否定富含能量饮食的肝后果，并且如果在人类中确认，有可能延长肝脏手术的应用。

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