Serum Leptin Levels in Patients With Nonalcoholic Steatohepatitis

Uygun, Ahmet; Kadayıfçı, Abdurrahman; Yeşilova, Zeki; Erdil, Ahmet; Yaman, Halıl; Saka, Mendane; Deveci, Mehmet Salih; Bağcı, Sait; Gülşen, Mustafa; Karaeren, Necmettin; Dağalp, Kemal

doi:10.1111/j.1572-0241.2000.03297.x

Cited by 219 publications

(63 citation statements)

References 21 publications

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“…Subjects with HS (particularly grades II-III) have higher leptin concentrations (Figure 2). This result is similar to other reports [28] , however it is not observed in all series. Hui et al [24] , found this pattern only in men, but other reports do not agree with this finding [29] .…”

Section: Discussionsupporting

confidence: 82%

Adiponectin as a protective factor in hepatic steatosis

Méndez-Sánchez

Chávez-Tapia²,

Villa³

et al. 2005

WJG

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AIM: Obesity and insulin resistance (IR) are closely related to hepatic steatosis (HS), and adiponectin is a hepatic insulin sensitizer that has important effects in liver function. This study aims at investigating the relationship between serum adiponectin concentration and the presence of HS. METHODS:We carried out a cross-sectional study in a check-up unit of a University Hospital in Mexico City. We enrolled 196 subjects, comprising 98 subjects with HS (27 women, 71 men) and 98 controls (37 women and 61 men). Anthropometric, metabolic and biochemical variables were measured in the two groups. Serum adiponectin and leptin concentrations were determined, their association with grade of HS tested, and concentrations, according to quartiles, compared between cases and controls.  2 analysis for linear trends was used to test for a dose-response relationship and logistic regression analysis was conducted to test for a protective effect of adiponectin. RESULTS:The HS subjects were older and more obese than controls, with a central obesity pattern. In the fourth quartile of adiponectin concentrations, HS was less common and severe. In a multivariate model of the fourth quartile of the adiponectin concentrations, we observed a protective effect (OR = 0.17, 95%CI: 0.04-0.67, P = 0.01).In subjects with more severe HS, we observed higher leptin concentrations, and caloric intakes, total fat and iron consumption were higher than in controls. CONCLUSION:The results of the present study suggest that a high serum concentration of adiponectin is associated with a protective effect against HS.

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Section: Discussionsupporting

confidence: 82%

Adiponectin as a protective factor in hepatic steatosis

Méndez-Sánchez

Chávez-Tapia²,

Villa³

et al. 2005

WJG

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“…Also, low amounts of leptin has been shown to be secreted by other tissues, such as placenta, skeletal muscles, stomach fundus and culture-activated hepatic stellate cells[108]. Leptin plays the role of a peptide hormone, regulating food uptake and energy consumption of the body through central feedback mechanisms and relating eating to hypothalamus and adipose tissue mass ( i.e ., it controls food uptake and increases energy consumption)[102,108,109]. The importance of this regulatory role is such that recombinant leptin has been studied for treatment of all prevalent types of obesity in different clinical trials[110-113].…”

Section: Inflammatory Markersmentioning

confidence: 99%

“…It has been shown that increased serum leptin level in patients with steatohepatitis has no relation with BMI of these patients, and this increase could not be easily justified by the patient’s sex, obesity or type 2 diabetes[109,114]. In contrast, another study indicated a correlation between human serum level of leptin and body fat percent and BMI[115].…”

Section: Inflammatory Markersmentioning

confidence: 99%

“…Some studies have shown that serum leptin level is directly associated with severity of hepatic steatosis and that increased levels of serum leptin may lead to increase of hepatic steatosis and steatohepatitis, but no association with emergence of inflammation and fibrosis was found[109,114]. Some other studies, however, have failed to show a significant association between serum level of leptin and steatosis[120] or steatohepatitis[46].…”

Section: Inflammatory Markersmentioning

confidence: 99%

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Nonalcoholic fatty liver disease: Diagnostic biomarkers

Hadizadeh

Faghihimani

Adibi

2017

WJGP

138

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Nonalcoholic fatty liver disease is a common medical condition worldwide and its prevalence has increased notably in the past few years due to the increases in prevalence of obesity and metabolic syndrome. However, diagnosis of this disease is still a matter of debate because of disease variations and pathophysiologic alterations. Specific single markers have gained considerable attention recently, among them markers related to hepatic pathophysiology, inflammation, adipocytokines and so forth. But, it seems that no single marker is sufficient for diagnosis and staging of the disease, and applying a panel including different types of tests may be more useful.

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“…Among all of these cytokines, IL-6 is both proinflammatory and a useful marker for obesity-associated inflammation. In the liver, IL-6 is mainly secreted by KC and hepatic stellate cells (HSC) and to a lesser extent by stimulated hepatocytes [86, 87]. Earlier studies have also revealed that both IL-6 and TNF increase hepatic production of C-reactive protein (CRP), a major acute phase protein, which is a nonspecific but sensitive marker of infection and tissue inflammation that is increased in obesity [88–90].…”

Section: The Common Causes Of Genetic Alterations and Genomic Instmentioning

confidence: 99%

Involvement of DNA Damage Response Pathways in Hepatocellular Carcinoma

Yang

Chang

Wei

et al. 2014

BioMed Research International

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Hepatocellular carcinoma (HCC) has been known as one of the most lethal human malignancies, due to the difficulty of early detection, chemoresistance, and radioresistance, and is characterized by active angiogenesis and metastasis, which account for rapid recurrence and poor survival. Its development has been closely associated with multiple risk factors, including hepatitis B and C virus infection, alcohol consumption, obesity, and diet contamination. Genetic alterations and genomic instability, probably resulted from unrepaired DNA lesions, are increasingly recognized as a common feature of human HCC. Dysregulation of DNA damage repair and signaling to cell cycle checkpoints, known as the DNA damage response (DDR), is associated with a predisposition to cancer and affects responses to DNA-damaging anticancer therapy. It has been demonstrated that various HCC-associated risk factors are able to promote DNA damages, formation of DNA adducts, and chromosomal aberrations. Hence, alterations in the DDR pathways may accumulate these lesions to trigger hepatocarcinogenesis and also to facilitate advanced HCC progression. This review collects some of the most known information about the link between HCC-associated risk factors and DDR pathways in HCC. Hopefully, the review will remind the researchers and clinicians of further characterizing and validating the roles of these DDR pathways in HCC.

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Serum Leptin Levels in Patients With Nonalcoholic Steatohepatitis

Cited by 219 publications

References 21 publications

Adiponectin as a protective factor in hepatic steatosis

Adiponectin as a protective factor in hepatic steatosis

Nonalcoholic fatty liver disease: Diagnostic biomarkers

Involvement of DNA Damage Response Pathways in Hepatocellular Carcinoma

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