Sarcopenia in the setting of nonalcoholic fatty liver (original) (raw)
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Obesity Reviews, 2018
Sarcopenia, described as the loss of muscle mass and/or strength, is gaining importance as it can be increasingly related to many chronic diseases. It is also associated with chronic liver disease, and recently it has been more frequently linked to nonalcoholic fatty liver disease (NAFLD) in particular. Both sarcopenia and NAFLD are subject to complex and intermingled pathophysiological processes, of which some are in common. Furthermore, it is presently unclear if sarcopenia directly contributes to NAFLD or vice versa. The mechanisms that are involved may include obesity, insulin resistance, vitamin D deficiency, aging, physical inactivity and certain cytokines. Current clinical evidence is subject to an important heterogeneity in methods and definitions, with additionally also a relative overrepresentation of evidence in Asian ethnicities. Nonetheless, all studies so far point towards the same association between sarcopenia and NAFLD, including an association with NAFLD-severity and NAFLD-related fibrosis. Since the field is in its infancy, clear definitions and further research are needed to aid to improve understanding of the association between NAFLD and sarcopenia. This can eventually lead to additional potential therapeutic interventions. This review attempts to give an overview of the current published literature that links sarcopenia to NAFLD, followed by a discussion of the presumably involved pathophysiological factors, and ends by discussing current unmet needs.
Sarcopenic Obesity in Non-Alcoholic Fatty Liver Disease – The Union of Two Culprits
2020
Non-alcoholic fatty liver disease (NAFLD) continues to rise and has become the most common cause of chronic liver disease among all ages and ethnicities. Metabolic disorders such as obesity and insulin resistance are closely associated with sarcopenia and NAFLD. Sarcopenic obesity is a clinical disorder characterized by the simultaneous loss of skeletal muscle and gain of adipose tissue. It is associated with worse outcomes in individuals with NAFLD. It is projected that NAFLD and sarcopenia will rise as the prevalence of obesity continues to increase at an unparallel rate. Recently, sarcopenia and sarcopenic obesity have gained considerable interest, but we still lack a well-defined definition and a management approach. Therefore, it is imperative to continue shining the light on this topic and better understand the underlying mechanism as well as treatment options. In this review article, we aimed to address the pathophysiology, impact, and outcomes of sarcopenic obesity on NAFLD.
Nonalcoholic Fatty Liver Disease and Sarcopenia: Where Do We Stand?
Canadian Journal of Gastroenterology and Hepatology
The link between metabolic syndrome (MetS) and sarcopenia has not been extensively studied, but it is evident that they share several common features. Crucial mechanisms involved in sarcopenia-nonalcoholic fatty liver disease (NAFLD) interplay are based on effects of insulin resistance, chronic inflammation, oxidative stress, and crosstalk between organs by secretion of cytokines (hepatokines, adipokines, and myokines). Currently, published studies confirm the association of sarcopenia with the degree of NAFLD defined by liver histology. However, prospective studies that will give us information regarding the causal effect of NAFLD and sarcopenia are still needed. Furthermore, there is a need for a patient-friendly, noninvasive, low-cost method for detection of loss of skeletal muscle mass, strength, and physical performance in the context of NAFLD. Moreover, potential treatment strategies such as physical exercise and nutritional supplementation, that are usually a part of manageme...
Sarcopenic obesity in fatty liver
Current Opinion in Clinical Nutrition and Metabolic Care, 2019
Purpose of review Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steato hepatitis have an increasing prevalence among liver diseases. Overweight and obesity are frequently associated conditions in patients with fatty liver. Skeletal muscle mass depletion may also coexist with chronic liver disease even in obese patients. This review will focus on the relationship between sarcopenic obesity and fatty liver. Recent findings Obesity and sarcopenia are frequently encountered in patients with NAFLD. Adipose tissue is able to release molecules (adipokines) that regulate lipid metabolism, interact with insulin sensitivity and may contribute to induce fibrogenesis in the liver. Skeletal muscle tissue is able to secrete myokines regulating muscle metabolism and insulin sensitivity. Myokines perturbation has been reported to influence adipose tissue mass and fat deposition in the liver. Sarcopenia has been reported as independent risk factor for the development of NAFLD, and for a more severe liver fibrosis in patients with NAFLD.
Sarcopenia in chronic liver diseases: a translational overview
Expert Review of Gastroenterology & Hepatology, 2020
Introduction: Sarcopenia refers to a progressive and generalized muscle mass and strength loss. In liver diseases, it has been related with worse outcomes and high risk of decompensations. Areas covered: Sarcopenia is caused by a set of cellular processes in the muscle such as denervation, mitochondrial dysfunction, endotoxemia and inflammation; which are manifested through the alteration of several proteolytic pathways such as lysosomal, proteasomal and A c c e p t e d M a n u s c r i p t caspase systems. In autophagy, myostatin and oxidative stress; such as hyperammonemia, contributes importantly to liver sarcopenia through loss of muscle mass already demonstrated in in vitro and in vivo models. In addition, hormones and the regulation of the intestinal microbiota, influence in a not less important magnitude. In the clinical setting, early identification of sarcopenia has been established as a mandatory item to prevent progression of muscle mass loss; however, diagnostic methods have extreme variation according to methodology, population, etiology and severity of liver disease. Reversing sarcopenia should be an integral therapeutic strategy. Expert opinion: Clinical and nutritional interventions should be adapted to liver injury etiology and stage of disease, each of them share a similar sarcopenia development pathway. There are specific biomarkers that condition or exacerbate loss of skeletal muscle.
Sarcopenia in hiding: The risk and consequence of underestimating muscle dysfunction in NASH
Hepatology
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 interrelationships between sarcopenia and NASH. We will discuss the impact of sarcopenia in patients with NASH and therapeutic options for the management of sarcopenia.
Digestive Diseases and Sciences, 2016
Background Decreased muscle mass or sarcopenia has been associated with nonalcoholic fatty liver disease (NAFLD). However, the functional consequences of this association and its pathogenesis remain ill-defined. Aims To evaluate muscle mass and function in a diet-induced NAFLD mouse model and explore its association with changes in serum insulin-like growth factor-1 (IGF-1). Methods Weight gain, visceral fat, serum biochemical parameters, liver histology, and hepatic triglyceride content (HTC) were assessed in C57/Bl6 mice fed a westernized diet during 16 weeks. In addition, we determined muscle fiber size and strength of limb skeletal muscle, myosin heavy chain (MHC) protein levels, and IGF-1 serum levels. Results Westernized diet feeding was associated with weight gain, increased visceral fat mass (epididymal pad weight: 0.76 g ± 0.13 vs. 0.33 ± 0.27 g; p = 0.0023), hepatic steatosis (HTC: 118.2 ± 6.88 mg/g liver vs. 43.26 ± 5.63 mg/g\, p \ 0.05), and necroinflammation (histological scores: 1.29 ± 0.42 vs. 4.00 ± 0.53\, p \ 0.05). Also, mice fed the experimental diet had an increased proportion of low-diameter muscle fibers (0-30 lm) and a decreased proportion of high-diameter muscle fibers (60-90 lm), which correlated with decreased MHC protein levels, consistent with significant muscle atrophy. Functional studies showed that mice fed a westernized diet had reduced muscle strength and lower serum levels of IGF-1 (284.2 ± 20.04 pg/ml) compared with chow-fed mice (366.0 ± 12.42 pg/ml, p \ 0.05). Conclusion Experimental NAFLD is associated with sarcopenia, decreased muscle strength, and reduced IGF-1 serum levels. IGF-1 reduction may be involved in pathogenesis of NAFLD-associated sarcopenia.
Sarcopenic Obesity in Liver Cirrhosis: Possible Mechanism and Clinical Impact
International Journal of Molecular Sciences
The picture of chronic liver diseases (CLDs) has changed considerably in recent years. One of them is the increase of non-alcoholic fatty liver disease. More and more CLD patients, even those with liver cirrhosis (LC), tend to be presenting with obesity these days. The annual rate of muscle loss increases with worsening liver reserve, and thus LC patients are more likely to complicate with sarcopenia. LC is also characterized by protein-energy malnutrition (PEM). Since the PEM in LC can be invariable, the patients probably present with sarcopenic obesity (Sa-O), which involves both sarcopenia and obesity. Currently, there is no mention of Sa-O in the guidelines; however, the rapidly increasing prevalence and poorer clinical consequences of Sa-O are recognized as an important public health problem, and the diagnostic value of Sa-O is expected to increase in the future. Sa-O involves a complex interplay of physiological mechanisms, including increased inflammatory cytokines, oxidative...