Serum leptin levels in post-hepatitis liver cirrhosis

Greco, Aldo V.; Mingrone, Geltrude; Favuzzi, Angela Maria Rita; Capristo, Esmeralda; Gniuli, Donatella; Addolorato, Giovanni; Brunani, Amelia; Cavagnin, Francesco; Gasbarrini, Giovanni

doi:10.1016/s0168-8278(00)80157-9

Cited by 45 publications

(31 citation statements)

References 24 publications

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“…Previous studies have demonstrated that TNFα levels are elevated in the ascitic fluid of cirrhotic patients with spontaneous bacterial peritonitis [32] . Nevertheless Giannini et al [13] found that serum and ascitic TNFα levels are significantly elevated but serum and ascites TNFα levels were not correlated and the ascitic fluid leptin levels were either twice as high as serum levels or positively correlated in cirrhotic patients with sterile ascites.…”

Section: Discussionmentioning

confidence: 97%

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: 97%

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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“…Recent studies have focused on serum leptin levels in cirrhotic patients, showing that serum leptin levels may vary with the etiology of the liver disease. Greco et al (2000) reported a significant reduction in leptin levels in patients with post-hepatitis cirrhosis while Testa Leptin regulates adipose tissue mass through hypothalamic effects on satiety and energy expenditure and may be considered as a signal of energy deficiency and an integrator of neuroendocrine function (Soliman et al, 2000). Serum leptin levels are low in many forms of malnutrition, including intrauterine growth retardation, untreated anorexia nervosa and malnourishment in chronically ill elderly patients (Jaquet et al, 1998;Boguszewski et al, 1997;Eckert et al, 1998;Cederholm et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…During prolonged nutritional deprivation, the decreased energy intake, diminished subcutaneous fat mass and declining insulin concentration suppress leptin production showing that leptin appears to be an important signal in the process of metabolism=endocrine adaptation (Soliman et al, 2000). Because malnutrition has a high prevalence in patients with liver cirrhosis, recent studies have analyzed serum leptin levels in the course of liver disease (McCullough et al, 1998;Shimizu et al, 1997;Greco et al, 2000;Testa et al, 2000). These studies have reported different results according to gender, the cause of liver cirrhosis and the degree of liver failure.…”

Section: Introductionmentioning

confidence: 99%

Serum leptin levels in alcoholic liver cirrhosis: relationship with gender, nutritional status, liver function and energy metabolism

Campillo¹,

Sherman²,

Richardet³

et al. 2024

Eur J Clin Nutr

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Objective: To determine serum leptin levels in alcoholic liver cirrhosis and the relationship with gender, nutritional status, liver function, energy metabolism, inflammatory state and refeeding. Subjects: Thirty-seven hospitalized alcoholic cirrhotic patients (M=F: 24=13), 27 hospitalized patients at risk of malnutrition but with normal liver function (M=F: 15=12) as control patients, and 31 healthy control subjects (M=F: 17=14) participated. Design: Liver function was assessed from Child -Pugh classification; anthropometric parameters and resting energy expenditure (REE) were measured; caloric intake was evaluated over 5 days; and serum leptin and insulin were assayed. The same protocol was performed after 1 month refeeding in 22 patients. Healthy subjects were studied as controls for anthropometric parameters and serum leptin levels. Results: Serum leptin levels were higher in male cirrhotic patients than in the other two male groups (P ¼ 0.0079) and in the same range in the female groups. They were higher in female than in male subjects in the three groups. In female cirrhotic patients, logarithmically transformed serum leptin levels correlated significantly with fat mass (P ¼ 0.0043), insulin levels (P ¼ 0.0072), REE (P ¼ 0.0133), bilirubin levels (P < 0.0001), prothrombin time (P ¼ 0.0003) and Pugh score (P ¼ 0.0266) in simple regression analysis and with insulin levels (P ¼ 0.0137), but not with fat mass (P ¼ 0.0761), Pugh score (P ¼ 0.4472) and REE (P ¼ 0.4576) in multiple regression analysis. In the male cirrhotic and control patients, log (leptin) levels correlated with CRP (C reactive protein) (r ¼ 0.365, P ¼ 0.0223). Log (leptin) levels did not correlate with caloric intake in any of the groups. Leptin levels (P < 0.05) and fat mass (P < 0.02) increased with refeeding while liver function improved (P < 0.01). Conclusion: There is a gender difference in regulation of serum leptin level in alcoholic liver cirrhosis. Insulin level is the best determinant of leptin level in female patients while inflammatory state related to alcoholic hepatitis seems to have a greater influence in male patients. Although leptin levels positively correlated with REE in female patients, there is no evidence that leptin reduces caloric intake and fat stores in these patients. Descriptors: leptin; liver cirrhosis; nutritional status; liver failure; energy metabolism European Journal of Clinical Nutrition (2001) 55, 980-988

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Serum leptin levels in post-hepatitis liver cirrhosis

Cited by 45 publications

References 24 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

Serum leptin levels in alcoholic liver cirrhosis: relationship with gender, nutritional status, liver function and energy metabolism

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