Serum leptin levels in patients with viral chronic hepatitis or liver cirrhosis

Testa, Roberto; Franceschini, R.; Giannini, Edoardo G.; Cataldi, A.; Botta, Federica; Fasoli, Alberto; Tenerelli, Pasquale; Rolandi, E; Barreca, T

doi:10.1016/s0168-8278(00)80156-7

Cited by 97 publications

(81 citation statements)

References 25 publications

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“…Anorexia and increased energy expenditure usually accompanies cirrhosis [30] . In previous studies, association between the severity of posthepatitis cirrhosis and serum leptin levels is controversial [12,30,31] . In cirrhotic patients, a significant negative correlation was found between serum levels of leptin and Child-Pugh score [31] .…”

Section: Discussionmentioning

confidence: 99%

“…In previous studies, association between the severity of posthepatitis cirrhosis and serum leptin levels is controversial [12,30,31] . In cirrhotic patients, a significant negative correlation was found between serum levels of leptin and Child-Pugh score [31] . On the contrary, a significant elevation in leptin levels was observed as the Child-Pugh score worsened independently of gender and BMI in cirrhotic patients.…”

Section: Discussionmentioning

confidence: 99%

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Leptin levels in the differential diagnosis between benign and malignant ascites

Büyükberber

Koruk²,

Savaş³

et al. 2007

WJG

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AIM:To evaluate the role of leptin levels in the differential diagnosis of ascites. METHODS:Ascitic leptin, TNFα and serum leptin levels were measured in 77 patients with ascites (35 with malignancies, 30 cirrhosis and 12 tuberculosis). Control serum samples were obtained from 20 healthy subjects. Leptin and TNFα levels were measured by ELISA. Body mass index (BMI) and percentage of body fat (BFM) by skin fold measurement were calculated for all patients and control groups. Peritoneal biopsy, ascites cytology and cultures or biochemical values were used for the diagnosis of patients. RESULTS:In patients with malignancies, the mean serum and ascites leptin levels and their ratios were significantly decreased compared to the other patient groups and controls. In tuberculosis peritonitis, ascitic fluid TNFα levels were significantly higher than malignant ascites and cirrhotic sterile ascites. BMI and BFM values did not distinguish between patients and controls. CONCLUSION:In patients with malignant ascites, levels of leptin and TNFα were significantly lower than in patients with tuberculous ascites.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Leptin levels in the differential diagnosis between benign and malignant ascites

Büyükberber

Koruk²,

Savaş³

et al. 2007

WJG

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“…Epidemiological observations revealed that obesity was a risk factor of HCC complicated with cryptogenic cirrhosis and alcoholic liver disease [14,15] , and in addition, clinical investigations identified that the leptin level of serum had increased significantly in alcoholic and post-hepatitis liver cirrhosis patients with or without HCC as compared to control subjects w/o the complication [20][21][22][23][24] . Still, there were few studies on the involvement of leptin in HCC.…”

Section: Dissusionmentioning

confidence: 99%

Primary study of leptin and human hepatocellular carcinoma in vitro

Zhou¹,

Wei²,

Shen³

et al. 2008

WJG

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AIM:To investigate the expression level and effects of leptin in human hepatocellular carcinoma cells in vitro and to explore the correlation between them. METHODS: Human hepatocellular carcinoma cell lineHepG2 was cultured in vitro , and (the expression level) mRNA of leptin and leptin receptors in HepG2 were assessed using reverse transcription polymerase chain reaction (RT-PCR). Effects of different concentrations of leptin (50 ng/mL, 100 ng/mL, 200 ng/mL) on HepG2 were detected with colorimetric assay by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) after incubation periods of 24 h, 48 h, and 72 h. Flow cytometry was performed to assess cell cycle progression of different concentrations of leptin as stated above after each 24 h incubation period.RESULTS: mRNA of leptin and leptin receptors (including short and long isoforms) were expressed in HepG2. The 72 h incubation of leptin at different concentrations ( 5 0 n g / m L , 1 0 0 n g / m L , 2 0 0 n g / m L ) p r o m o t e d proliferation of HepG2 in a concentration-and timedependent manner. The experimental group shows significant statistical differences when compared to the controlled group which contained 0 ng/mL of leptin. As the concentration of leptin increases, significant fewer cells were detected in G0-G1 phase and more cells in S and G2-M phases. C O N C L U S I O N :L e p t i n a n d l e p t i n r e c e p t o r a r e simultaneously expressed in human hepatocellular carcinoma cell line HepG2. Addition of leptin (0 ng/mL-200 ng/mL) in 72 h periods indicated there is a concentration-and time-dependent correlation in the stimulation of HepG2 cell proliferation. The effect of proliferation by leptin is due to promotion of DNA synthesis and enhancement of mitotic activity. The relationship between leptin and human hepatocellular carcinoma cells might indicate that adipokine could be associated with the progression of human hepatocellular carcinoma.

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“…This suggests that hyperleptinemia and leptin resistance may be involved in the first steps of the pathogenesis of LS, but not necessarily on its progression to steatohepatitis. Indeed, relative hypoleptinemia has been described in advanced forms of liver disease, probably as an index of poor nutritional status (34,36). Our data indicate that hyperleptinemia, an indirect index of resistance to the action of endogenous leptin, could mediate the accumulation of triglycerides in the liver observed in insulin-resistant states in the context of low-to-moderate alcohol intake, a model of LS that is likely to represent the vast majority of non-HCV fatty livers identified in our environment since regular alcohol consumption is widespread in the Parma area.…”

Section: Relationship Among Leptin Insulin and Lsmentioning

confidence: 99%

Relationship between leptin, insulin, body composition and liver steatosis in non-diabetic moderate drinkers with normal transaminase levels

Valtueña¹,

Numeroso²,

Ardigò³

et al. 2005

eur j endocrinol

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Objective: Obesity and insulin resistance play a major role in the development of liver steatosis (LS), but also relative leptin resistance has been reported to correlate with LS in humans. Our objective was to investigate the relationship between serum leptin, insulin, obesity and LS in non-diabetic males (n ¼ 74) and postmenopausal females (n ¼ 50) with normal transaminase levels and low-tomoderate alcohol intake. Methods: A medical history to retrieve information about health status, current medications, alcohol consumption and history of viral or toxic hepatitis; a physical examination including height, weight, waist circumference and blood pressure; a fasting blood draw for the determination of glucose, insulin, leptin, lipid profile, transaminases and uric acid; an oral glucose tolerance test to exclude type 2 diabetes; a dual-energy X-ray absorptiometry scan to assess fat mass (FM) and lean body mass (LBM), and an echography of the liver to assess LS. Results: Fasting leptin and insulin were highly correlated with FM in men (R ¼ 0.767 and R ¼ 0.495 respectively, P , 0.001) and women (R ¼ 0.713 and R ¼ 0.526 respectively, P , 0.001). After correction for FM, leptin showed a significant negative correlation with LBM in men (R ¼ 2 0.240, P ¼ 0.039), but not in women (R ¼ 2 0.214, P ¼ 0.132). The positive relationship observed between leptin, insulin and LS persisted after adjustment of leptin and insulin for body composition only in men (R ¼ 0.415, P , 0.001 and R ¼ 0.339, P ¼ 0.003 respectively for leptin and insulin vs LS). Adjusted means (95% confidence intervals) of leptin increased significantly across categories of LS in men even when insulin was considered in the model (absent ¼ 7.1 ng/ml (5.6-8.5), mild ¼ 8.2 ng/ml (7.2 -9.2), moderate/severe ¼ 12.1 ng/ml (10.3 -14.0); P , 0.001), whereas no significant relationship was observed between insulin and LS after leptin was accounted for. Conclusion: Serum concentrations of leptin and insulin are positively correlated in men independently of body composition, but not in postmenopausal women. In men, the steatogenic effect of hyperinsulinemia/insulin resistance in the context of low-to-moderate alcohol consumption appears to be mediated by high concentrations of serum leptin, whereas body fat alone could identify postmenopausal women at high risk for LS. European Journal of Endocrinology 153 283-290

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Serum leptin levels in patients with viral chronic hepatitis or liver cirrhosis

Cited by 97 publications

References 25 publications

Leptin levels in the differential diagnosis between benign and malignant ascites

Leptin levels in the differential diagnosis between benign and malignant ascites

Primary study of leptin and human hepatocellular carcinoma in vitro

Relationship between leptin, insulin, body composition and liver steatosis in non-diabetic moderate drinkers with normal transaminase levels

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