Serum adipokines might predict liver histology findings in non-alcoholic fatty liver disease

Jamali, Raika; Razavizade, Mohsen; Arj, Abbas; Aarabi, Mohammad Hossein

doi:10.3748/wjg.v22.i21.5096

Cited by 50 publications

(61 citation statements)

References 26 publications

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“…Among them, the strongest association was with the grade of steatosis and then with portal information [ 68 ] Finally, in a recent evaluation of plasma biomarkers in a large well characterized biopsy proven NAFLD population ( n =648) by the NASH Clinical Research Network, resistin levels were similar between patients with a definite diagnosis of NASH vs borderline cases and healthy subjects, but were higher in patients with fibrosis stages 2 to 4 versus 0 to 1 (odds ratio, 1.12) [ 69 ]. These findings confirm previous results from smaller observational studies, that reported higher resistin levels in patients with histology proven NAFLD and advanced fibrosis [ 70 ].…”

Section: Resistinsupporting

confidence: 92%

Association of Adipokines with Development and Progression of Nonalcoholic Fatty Liver Disease

2018

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Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease affecting 30% of the general population and 40% to 70% of obese individuals. Adipose tissue plays a crucial role in its pathogenesis, as it produces and secretes pro- and anti-inflammatory cytokines called adipokines. Adiponectin and leptin have well-determined actions in terms of NAFLD pathophysiology. Adiponectin deficiency is associated with a pro-inflammatory condition, as it is observed in obesity and other metabolic disorders. On the other hand, increased leptin levels, above the normal levels, act as a pro-inflammatory stimulus. Regarding other adipokines (resistin, visfatin, chemerin, retinol-binding protein 4, irisin), data about their contribution to NAFLD pathogenesis and progression are inconclusive. In addition, pharmacological agents like thiazolidinediones (pioglitazone and rosiglitazone), that are used in the management of NAFLD exert favourable effects on adipokine levels, which in turn may contribute to the improvement of liver function. This review summarizes the current knowledge and developments in the association between adipokines and NAFLD and discusses possible therapeutic implications targeting the modulation of adipokine levels as a potential tool for the treatment of NAFLD.

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Section: Resistinsupporting

confidence: 92%

Association of Adipokines with Development and Progression of Nonalcoholic Fatty Liver Disease

2018

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“…In this study, the authors studied biomarkers in 648 histologically evaluated NAFLD patients demonstrating that fibrosis was associated with increased serum levels of resistin, IL-8, monocyte chemoattractant protein 1, soluble IL-1 receptor type and TNFα. Similar increased levels and an association with fibrosis were observed in another recent study suggesting that resistin may probably reflect a pro-inflammatory profibrogenic adipokine in NAFLD [ 88 ]. In contrast to mice, monocytes/macrophages are considered as the major source for resistin which may point towards a different biology in rodents and humans.…”

Section: Other Adipokinessupporting

confidence: 82%

Adipokines and Non-Alcoholic Fatty Liver Disease: Multiple Interactions

Adolph

Grander

Grabherr

et al. 2017

IJMS

178

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Accumulating evidence links obesity with low-grade inflammation which may originate from adipose tissue that secretes a plethora of pro- and anti-inflammatory cytokines termed adipokines. Adiponectin and leptin have evolved as crucial signals in many obesity-related pathologies including non-alcoholic fatty liver disease (NAFLD). Whereas adiponectin deficiency might be critically involved in the pro-inflammatory state associated with obesity and related disorders, overproduction of leptin, a rather pro-inflammatory mediator, is considered of equal relevance. An imbalanced adipokine profile in obesity consecutively contributes to metabolic inflammation in NAFLD, which is associated with a substantial risk for developing hepatocellular carcinoma (HCC) also in the non-cirrhotic stage of disease. Both adiponectin and leptin have been related to liver tumorigenesis especially in preclinical models. This review covers recent advances in our understanding of some adipokines in NAFLD and associated HCC.

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“…Similar heterogenicity exists regarding the role of resistin in the pathogenesis of IR in PCOS (99,100). In patients with NAFLD, serum resistin levels correlate with the severity of steatosis, inflammation and fibrosis (95,101,102).…”

Section: Molecular Basis Including Endocrine Disruptorsmentioning

confidence: 98%

MANAGEMENT OF ENDOCRINE DISEASE: Polycystic ovary syndrome and nonalcoholic fatty liver disease

Macut

Božić-Antić

Bjekić-Macut

et al. 2017

European Journal of Endocrinology

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Polycystic ovary syndrome (PCOS) is a frequent endocrine disease in women, with a number of metabolic and reproductive consequences. Obesity, insulin resistance (IR) and type 2 diabetes are prominent metabolic characteristics of PCOS and common factors affecting liver function and generating nonalcoholic fatty liver disease (NAFLD). Multiple genes involved in the synthesis of androgens, cytokines and IR, as well as acquired factors, such as endocrine disruptors, could associate the etiopathogenesis of PCOS and NAFLD. Besides the high prevalence of PCOS in general population, NAFLD was shown to be a frequent condition in transition periods, such as adolescence and menopause. Although liver biopsy is considered to be the gold standard for diagnosing liver damage, its routine use in such a prevalent condition as PCOS can be related to a higher rate of complications. Therefore, it is necessary to be able to diagnose NAFLD using simple and reliable surrogate markers. Recently, fatty liver index and NAFLD fatty liver score analyzed in large cohorts of PCOS women have been shown as accurate markers of liver damage in this metabolically vulnerable population. Lifestyle changes are still the mainstay of the management of NAFLD in PCOS, although prospective randomized controlled clinical studies remain a priority in the field. With regard to medications, metformin may be the drug of choice for treating PCOS patients with NAFLD when pharmacologic therapy is considered. Liraglutide use in obese PCOS has shown favorable effects on the predictors of liver fibrosis. In this review, we aim to summarize the influence of the common risk factors and to discuss the diagnostic approaches and management options for NAFLD in patients with PCOS.

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Serum adipokines might predict liver histology findings in non-alcoholic fatty liver disease

Abstract: Certain adipokines may determine the severity of NAFLD histology accurately.

Cited by 50 publications

References 26 publications

Association of Adipokines with Development and Progression of Nonalcoholic Fatty Liver Disease

Association of Adipokines with Development and Progression of Nonalcoholic Fatty Liver Disease

Adipokines and Non-Alcoholic Fatty Liver Disease: Multiple Interactions

MANAGEMENT OF ENDOCRINE DISEASE: Polycystic ovary syndrome and nonalcoholic fatty liver disease

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