Nonalcoholic Fatty Liver Disease and Sarcopenia: Where Do We Stand?

Mikolašević, Ivana; Pavić, Tajana; Kanižaj, Tajana Filipec; Bender, Darija Vranešić; Domislovic, V.; Krznarić, Željko

doi:10.1155/2020/8859719

Cited by 11 publications

(11 citation statements)

References 95 publications

(75 reference statements)

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“…Third, loss of skeletal muscle mass in sarcopenia leads to the reduction of insulin signaling, insulin resistance, increased adipose tissue lipolysis, and increased in hepatic steatosis [39]. In summary, the mechanism that is involved in the sarcopenia-NAFLD relationship is mainly from insulin resistance, chronic inflammation, oxidative stress, and interlink between organs by secretion of cytokines (hepatokines, myokines, and adipokines) [40].…”

Section: Discussionmentioning

confidence: 99%

Association between Sarcopenic Obesity and Nonalcoholic Fatty Liver Disease and Fibrosis detected by Fibroscan

Wijarnpreecha

Aby

Ahmed

et al. 2021

JGLD

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Background and Aims: Nonalcoholic fatty liver disease (NAFLD) and sarcopenic obesity share several pathophysiologic backgrounds. No prior studies have determined a plausible association between sarcopenic obesity and NAFLD and NAFLD-associated fibrosis. We aim to investigate the association between sarcopenic obesity and NAFLD, and NAFLD-associated fibrosis detected by transient elastography. Methods: In a cross-sectional study from the 2017-2018 National Health and Nutrition Examination Survey, 1,925 participants were identified. NAFLD was defined by controlled attenuation parameter (CAP) scores and significant fibrosis (≥F2)/cirrhosis by liver stiffness measurements on transient elastography. Sarcopenic obesity was defined by appendicular lean mass and body fat. Results: Individuals with sarcopenic obesity had a significantly higher odds of having NAFLD [CAP score ≥263 dB/m, odds ratio (OR): 2.88, 95% confidence interval (CI): 1.82-4.57, and CAP score ≥285, OR: 3.71, 95%CI: 2.24-6.14] after adjusting for age, gender, and race/ethnicity. The association remained statistically significant after adjustment for socioeconomic status, lifestyle and behavioral risk factors, and metabolic conditions (CAP score ≥263, OR: 2.61, 95%CI: 1.51-4.50, and CAP score ≥285, OR: 3.31, 95%CI: 1.85-5.96). Sarcopenic obesity was also associated with higher odds of having NAFLD-associated significant fibrosis (OR 2.22, 95% CI: 1.03-4.80) in the multivariate model. While those with sarcopenic obesity had a higher prevalence of NAFLD-associated cirrhosis, this association did not reach statistical significance. Conclusions: Sarcopenic obesity was independently associated with an increased risk of NAFLD and NAFLD- associated significant fibrosis independent of well-defined risk factors. Targeted interventions to improve sarcopenic obesity may reduce the risk of NAFLD and NAFLD-associated siginificant fibrosis.

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Section: Discussionmentioning

confidence: 99%

Association between Sarcopenic Obesity and Nonalcoholic Fatty Liver Disease and Fibrosis detected by Fibroscan

Wijarnpreecha

Aby

Ahmed

et al. 2021

JGLD

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“…It acts on insulin sensitivity, and its plasma reduction is related to insulin resistance and glucose intolerance, predisposing to advanced liver injury [ 44 ]. Plasma levels of adiponectin can be reduced with the increase in pro-inflammatory cytokines such as TNF-α and IL-6, present in obesity, in addition to the levels of myostatin, a myokine that can elevate the adipose tissue mass [ 45 ]. This adipokine contributes significantly to anti-inflammatory action, thermogenesis, lipolysis, and oxidation of fatty acids in skeletal muscle and liver.…”

Section: Discussionmentioning

confidence: 99%

“…Unlike most myokines, exercise seems to decrease myostatin expression. Possibly, myostatin inhibition may be a therapeutic target for muscle mass loss disorders, such as atrophy, sarcopenia, and cancer [ 45 ]. In contrast, there is follistatin, a myokine, and hepatokine, released in the context of physical activity, which is opposed to myostatin’s actions, directly inhibiting it through binding.…”

Section: Discussionmentioning

confidence: 99%

“…Its contribution to resistance to the action of insulin occurs due to the decrease in phosphorylation of insulin receptor, compromising the entire insulin signaling pathway necessary to trigger its cellular actions [ 11 ]. Thus, the uptake of glucose by insulin-dependent tissues, such as skeletal muscle and adipose tissue, becomes impaired, promoting the state of hyperglycemia and allowing tissues such as those of the liver to capture the excess of glucose that will later be accumulated in the form of fat, characterizing hepatic steatosis [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

“…This environment constitutes fertile soil for atherosclerosis’s chronic inflammatory process, a prelude to several cardiovascular conditions [ 8 ]. Therefore, it is worth noting that myostatin has a role as a therapeutic target for managing these aforementioned metabolic disorders [ 45 ]. Many studies point to a decrease in myostatin through physical exercise, with positive effects in combating insulin resistance and reducing fat accumulation and muscle hypertrophy [ 95 ].…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Adipokines, Myokines, and Hepatokines: Crosstalk and Metabolic Repercussions

Santos

Zanuso

Miola

et al. 2021

IJMS

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Adipose, skeletal, and hepatic muscle tissues are the main endocrine organs that produce adipokines, myokines, and hepatokines. These biomarkers can be harmful or beneficial to an organism and still perform crosstalk, acting through the endocrine, paracrine, and autocrine pathways. This study aims to review the crosstalk between adipokines, myokines, and hepatokines. Far beyond understanding the actions of each biomarker alone, it is important to underline that these cytokines act together in the body, resulting in a complex network of actions in different tissues, which may have beneficial or non-beneficial effects on the genesis of various physiological disorders and their respective outcomes, such as type 2 diabetes mellitus (DM2), obesity, metabolic syndrome, and cardiovascular diseases (CVD). Overweight individuals secrete more pro-inflammatory adipokines than those of a healthy weight, leading to an impaired immune response and greater susceptibility to inflammatory and infectious diseases. Myostatin is elevated in pro-inflammatory environments, sharing space with pro-inflammatory organokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), resistin, and chemerin. Fibroblast growth factor FGF21 acts as a beta-oxidation regulator and decreases lipogenesis in the liver. The crosstalk mentioned above can interfere with homeostatic disorders and can play a role as a potential therapeutic target that can assist in the methods of diagnosing metabolic syndrome and CVD.

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Nonalcoholic Fatty Liver Disease and Sarcopenia: Where Do We Stand?

Cited by 11 publications

References 95 publications

Association between Sarcopenic Obesity and Nonalcoholic Fatty Liver Disease and Fibrosis detected by Fibroscan

Association between Sarcopenic Obesity and Nonalcoholic Fatty Liver Disease and Fibrosis detected by Fibroscan

Adipokines, Myokines, and Hepatokines: Crosstalk and Metabolic Repercussions

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