Plasma insulin, leptin, adiponectin, resistin, ghrelin, and melatonin in nonalcoholic steatohepatitis patients treated with melatonin

Gonciarz, Maciej; Bielański, Władysław; Partyka, Robert; Brzozowski, Tomasz; Konturek, P C; Eszyk, Jerzy; Celiński, Krzysztof; Reíter, Russel J.; Konturek, Stanisław J.

doi:10.1111/j.1600-079x.2012.01023.x

Cited by 49 publications

(49 citation statements)

References 61 publications

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“…when the study compared leptin levels between SS and NASH patients), since a comparison between NAFLD patients and controls could not be performed. Nine studies included all groups (controls, SS, NASH patients) [18, 28, 30-32, 34, 40, 43, 48]; 11 studies compared leptin levels between NASH patients and controls, without recruiting an SS group [21,23,24,26,27,37,38,44,46,47,49]; four studies compared leptin levels between NAFLD patients and controls, without providing separate data for SS and NASH [17,29,36,45] and nine studies compared leptin levels between SS and NASH patients, without recruiting a control group [19,20,22,25,33,35,39,41,42] (ESM Table 2). Subsequently, comparative data was provided as follows: 24 studies, NAFLD patients (n=1,231) vs controls (n=775); nine studies, SS patients (n=283) vs controls (n=313); 20 studies, NASH patients (n=699) vs controls (n=627) and 18 studies, SS (n=618) vs NASH patients (n=702).…”

Section: Resultsmentioning

confidence: 99%

Circulating leptin in non-alcoholic fatty liver disease: a systematic review and meta-analysis

et al. 2015

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Aims/hypothesis Clinical data regarding circulating leptin levels in patients with non-alcoholic fatty liver disease (NAFLD) are conflicting. The purpose of this meta-analysis was to compare leptin levels between the following groups: patients with biopsy-proven NAFLD vs controls; simple steatosis (SS) patients vs controls; non-alcoholic steatohepatitis (NASH) patients vs controls and NASH patients vs SS patients. Methods We performed a systematic search in PubMed, Scopus and the Cochrane Library. We analysed 33 studies, published between 1999 and 2014, including 2,612 individuals (775 controls and 1,837 NAFLD patients). Results Higher circulating leptin levels were observed in NAFLD patients vs controls (standardised mean difference [SMD] 0.640; 95% CI 0.422, 0.858), SS patients vs controls (SMD 0.358; 95% CI 0.043, 0.673), NASH patients vs controls (SMD 0.617; 95% CI 0.403, 0.832) and NASH patients vs SS patients (SMD 0.209; 95% CI 0.023, 0.395). These results remained essentially unchanged after excluding studies involving paediatric or adolescent populations and/or individuals undergoing bariatric surgery. There was moderate-tosevere heterogeneity among studies in all comparisons, but no significant publication bias was detected. Meta-regression analysis demonstrated that BMI was inversely associated with leptin SMD and accounted for 26.5% (p=0.014) and 32.7% (p=0.021) of the between-study variance in the comparison between NASH patients and controls and NAFLD patients and controls, respectively. However, when bariatric studies were excluded, BMI did not significantly explain the between-study variance. Conclusions/interpretation Circulating leptin levels were higher in patients with NAFLD than in controls. Higher levels of circulating leptin were associated with increased severity of NAFLD, and the association remained significant after the exclusion of studies involving paediatric or adolescent populations and morbidly obese individuals subjected to bariatric surgery.

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Section: Resultsmentioning

confidence: 99%

Circulating leptin in non-alcoholic fatty liver disease: a systematic review and meta-analysis

et al. 2015

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“…A relevant role in the pathogenesis of NASH is played by adipose tissue-derived mediators, such as adiponectin and leptin [6] , and other molecules such as ghrelin, visfatin and resistin [36,37] . Adiponectin and leptin are produced mainly by the adipose tissue.…”

Section: Foxp3mentioning

confidence: 99%

“…The former acts as an insulin sensitizing and an anti-inflammatory mediator. Hypoadiponectinemia has been found to be associated with the metabolic levels [37] . Visfatin is an insulin mimicking adipokine.…”

Section: Foxp3mentioning

confidence: 99%

“…The latter, under physiological conditions, has anorexigenic effects decreasing appetite and increasing energy expenditure, while in obese patients hyperleptinemia associated to leptin resistance has been described [17] . Moreover leptin has pro-inflammatory and pro-fibrogenic properties that play a role in liver disease, including NASH [37,39,40] . Adiponectin exerts its anti-inflammatory function inhibiting the pro-inflammatory cytokines (TNFα) and stimulating the anti-inflammatory cytokines (IL10 secreted by KC) [41] and via direct suppression of the macrophage function [42] .…”

Section: Treatment Perspectivesmentioning

confidence: 99%

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Cross talk of the immune system in the adipose tissue and the liver in non-alcoholic steatohepatitis: Pathology and beyond

Vonghia

Francque

2015

WJH

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Non-alcoholic steatohepatitis (NASH) is considered to be the hepatic manifestation of the metabolic syndrome, thus has a tight correlation with systemic metabolic impairment. The complex mechanisms underlying the pathogenesis of NASH involve different organs and systems that cross talk together contributing to the onset of NASH. A crucial role is played by inflammatory mediators, especially those deriving from the adipose tissue and the liver, which are involved in the cascade of inflammation, fibrosis and eventually tumorigenesis. In this setting cytokines and adipokines as well as immunity are emerging drivers of the key features of NASH. The immune system participates in this process with disturbances of the cells constituting both the innate and the adaptive immune systems that have been reported in different organs, such as in the liver and in the adipose tissue, in clinical and preclinical studies. The role of the immune system in NASH is increasingly studied, not only because of its contribution to the pathogenetic mechanisms of NASH but also because of the new potential therapeutic options it offers in this setting. Indeed, novel treatments acting on the immune system could offer new options in the management of NASH and the correlated clinical consequences.Key words: Non-alcoholic steatohepatitis; Immune system; Adipokines; Inflammation; Fibrosis Core tip: Non-alcoholic steatohepatitis (NASH) is considered to be the hepatic manifestation of the metabolic syndrome, thus has a tight correlation with systemic metabolic impairment. The complex mechanisms underlying the pathogenesis of NASH involve different organs, including liver, adipose tissue and immune system, which cross talk together contributing to the onset of NASH. Increasing interest has been aroused by the role of the immune system in NASH, not only because of its Cross talk of the immune system in the adipose tissue and the liver in non-alcoholic steatohepatitis: Pathology and beyond contribution to the pathogenetic mechanisms of NASH but also considering the new potential therapeutic options in this setting.Vonghia L, Francque S. Cross talk of the immune system in the adipose tissue and the liver in non-alcoholic steatohepatitis: Pathology and beyond.

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“…In animal models, MLT modifies circulating levels of insulin [105], leptin [106], ghrelin, and peptide YY [107]. In patients with chronic nonalcoholic liver disease, a significant increase in plasma levels of adiponectin, leptin, and ghrelin have been detected, in response to MLT treatment [108]. MLT can also exert its effects on metabolic processes throughout epigenetic modifications [109].…”

Section: Lan and Circadian Disruption Of Metabolic Responsesmentioning

confidence: 99%

Artificial light-at-night – a novel lifestyle risk factor for metabolic disorder and cancer morbidity

Zubidat

Haim

2017

Journal of Basic and Clinical Physiology and Pharmacology

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Both obesity and breast cancer are already recognized worldwide as the most common syndromes in our modern society. Currently, there is accumulating evidence from epidemiological and experimental studies suggesting that these syndromes are closely associated with circadian disruption. It has been suggested that melatonin (MLT) and the circadian clock genes both play an important role in the development of these syndromes. However, we still poorly understand the molecular mechanism underlying the association between circadian disruption and the modern health syndromes. One promising candidate is epigenetic modifications of various genes, including clock genes, circadian-related genes, oncogenes, and metabolic genes. DNA methylation is the most prominent epigenetic signaling tool for gene expression regulation induced by environmental exposures, such as artificial light-at-night (ALAN). In this review, we first provide an overview on the molecular feedback loops that generate the circadian regulation and how circadian disruption by ALAN can impose adverse impacts on public health, particularly metabolic disorders and breast cancer development. We then focus on the relation between ALAN-induced circadian disruption and both global DNA methylation and specific loci methylation in relation to obesity and breast cancer morbidities. DNA hypo-methylation and DNA hyper-methylation, are suggested as the most studied epigenetic tools for the activation and silencing of genes that regulate metabolic and monostatic responses. Finally, we discuss the potential clinical and therapeutic roles of MLT suppression and DNA methylation patterns as novel biomarkers for the early detection of metabolic disorders and breast cancer development.

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Plasma insulin, leptin, adiponectin, resistin, ghrelin, and melatonin in nonalcoholic steatohepatitis patients treated with melatonin

Cited by 49 publications

References 61 publications

Circulating leptin in non-alcoholic fatty liver disease: a systematic review and meta-analysis

Circulating leptin in non-alcoholic fatty liver disease: a systematic review and meta-analysis

Cross talk of the immune system in the adipose tissue and the liver in non-alcoholic steatohepatitis: Pathology and beyond

Artificial light-at-night – a novel lifestyle risk factor for metabolic disorder and cancer morbidity

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