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Sarcopenia in hiding: The risk and consequence of underestimating muscle dysfunction in nonalcoholic steatohepatitis
Hepatology ( IF 12.9 ) Pub Date : 2017-10-30 , DOI: 10.1002/hep.29420
Rahima A. Bhanji 1 , Praveena Narayanan 2 , Alina M. Allen 1 , Harmeet Malhi 1 , Kymberly D. Watt 1
Affiliation  

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide. Up to one third of individuals with NAFLD will develop nonalcoholic steatohepatitis (NASH), which is associated with progression to cirrhosis and is rapidly becoming the leading indication for liver transplantation. Sarcopenia is defined as a progressive and generalized loss of skeletal muscle mass, strength, and function. It is observed in up to 60% of patients with end-stage liver disease and portends a poor prognosis. Recent studies have shown that sarcopenia is a novel risk factor for developing NAFLD. Pathophysiological mechanisms relating sarcopenia and NASH may include insulin resistance (IR) and increased inflammation. IR leads to accumulation of triglycerides in both muscle tissue and the liver. It also exacerbates proteolysis and leads to muscle depletion. Chronic inflammation leads to liver injury and progression of fibrosis. The inflammatory milieu also stimulates protein catabolism. Viewing skeletal muscle as an endocrine organ that secretes various salutary myokines may help us understand its role in the development of steatosis. A better understanding of the pathophysiology will aid in developing physical and pharmacological therapeutic interventions. In this review, we will explore the complex inter-relationships between sarcopenia and NASH. We will discuss the impact of sarcopenia in patients with NASH and therapeutic options for the management of sarcopenia. (Hepatology 2017;66:2055–2065)

中文翻译:

藏匿性少肌症:低估非酒精性脂肪性肝炎肌肉功能障碍的风险和后果

非酒精性脂肪肝疾病(NAFLD)是全世界慢性肝病的最常见原因。多达三分之一的NAFLD患者会发展为非酒精性脂肪性肝炎(NASH),与肝硬化的发展有关,并迅速成为肝移植的主要指征。肌肉减少症定义为骨骼肌质量,强度和功能的进行性和普遍性丧失。在多达60%的终末期肝病患者中观察到这种情况,预后不良。最近的研究表明,少肌症是发展NAFLD的新危险因素。与肌肉减少症和NASH相关的病理生理机制可能包括胰岛素抵抗(IR)和炎症增加。IR导致甘油三酸酯在肌肉组织和肝脏中积累。它还会加剧蛋白水解并导致肌肉衰竭。慢性炎症导致肝损伤和纤维化进展。炎性环境还刺激蛋白质分解代谢。将骨骼肌视为分泌各种有益肌动蛋白的内分泌器官可能有助于我们了解其在脂肪变性发展中的作用。对病理生理学的更好理解将有助于发展物理和药理学治疗干预措施。在这篇综述中,我们将探讨肌肉减少症与NASH之间的复杂相互关系。我们将讨论肌肉减少症对NASH患者的影响以及治疗肌肉减少症的治疗选择。(H 将骨骼肌视为分泌各种有益肌动蛋白的内分泌器官可能有助于我们了解其在脂肪变性发展中的作用。对病理生理学的更好理解将有助于发展物理和药理学治疗干预措施。在这篇综述中,我们将探讨肌肉减少症与NASH之间的复杂相互关系。我们将讨论肌肉减少症对NASH患者的影响以及治疗肌肉减少症的治疗选择。(H 将骨骼肌视为分泌各种有益肌动蛋白的内分泌器官可能有助于我们了解其在脂肪变性发展中的作用。对病理生理学的更好理解将有助于发展物理和药理学治疗干预措施。在这篇综述中,我们将探讨肌肉减少症与NASH之间的复杂相互关系。我们将讨论肌肉减少症对NASH患者的影响以及治疗肌肉减少症的治疗选择。(H 我们将讨论肌肉减少症对NASH患者的影响以及治疗肌肉减少症的治疗选择。(H 我们将讨论肌肉减少症对NASH患者的影响以及治疗肌肉减少症的治疗选择。(H流行病学; 2017年; 66:2055–2065)
更新日期:2017-11-21
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