Adipokines and cytokines in non‐alcoholic fatty liver disease

Jarrar, Mohammed; Baranova, Ancha; Collantes, Rochelle; Ranard, Benjamin L.; Stepanova, Maria; Bennett, C.; Fang, Yun; Elariny, Hazem; Goodman, Zachary; Chandhoke, Vikas; Younossi, Zobair M.

doi:10.1111/j.1365-2036.2007.03586.x

Cited by 393 publications

(370 citation statements)

References 29 publications

(44 reference statements)

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“…24 whereas others have shown lower resistin levels in NASH versus simple fatty liver. 25 In our study, resistin levels increased significantly in the subjects receiving orlistat. Additionally, a significant correlation was found between resistin levels and weight loss.…”

Section: Discussionmentioning

confidence: 61%

Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial

Fecht²,

et al. 2008

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The aim of this study was to determine if orlistat, an inhibitor of fat absorption, combined with caloric restriction in overweight subjects with nonalcoholic steatohepatitis results in weight loss and improved liver histology. Fifty overweight subjects (body mass index ‫؍‬ >27) with biopsy proven nonalcoholic steatohepatitis were randomized to receive a 1,400 Kcal/day diet plus vitamin E (800 IU) daily with or without orlistat (120 mg three times a day) for 36 weeks. Liver biopsies were repeated at week 36. Twenty-three subjects in the orlistat/diet/vitamin E group and 18 in the diet/vitamin E group completed the study. The mean age was 47 ؎ 9.0 (standard deviation) years and mean body mass index was 36.4 ؎ 6.3 kg/m 2 . Four subjects were diabetic. The orlistat group lost a mean of 8.3% body weight compared to 6.0% in the diet plus vitamin E group (not significant). Both groups also had similarly improved serum aminotransferases, hepatic steatosis, necroinflammation, ballooning, and nonalcoholic fatty liver disease activity scores. Stratified according to weight loss instead of treatment group, a loss of >5% body weight (n ‫؍‬ 24) compared to <5% body weight (n ‫؍‬ 17) correlated with improvement in insulin sensitivity (P ‫؍‬ 0.001) and steatosis (P ‫؍‬ 0.015). Comparing subjects who lost >9% of body weight (n ‫؍‬ 16), to those that did not (n ‫؍‬ 25), improved insulin sensitivity (P < 0.001), adiponectin (P ‫؍‬ 0.03), steatosis (P ‫؍‬ 0.005), ballooning (P ‫؍‬ 0.04), inflammation (P ‫؍‬ 0.045), and nonalcoholic fatty liver disease activity score (P ‫؍‬ 0.009) were seen. Increases in adiponectin strongly correlated with improved ballooning and nonalcoholic fatty liver disease activity score (P ‫؍‬ 0.03). Orlistat did not enhance weight loss or improve liver enzymes, measures of insulin resistance, and histopathology. However, subjects who lost >5% of body weight over 9 months improved insulin resistance and steatosis, and those subjects who lost >9% also achieved improved hepatic histologic changes. (HEPATOLOGY 2009;49:80-86.)

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Section: Discussionmentioning

confidence: 61%

Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial

Fecht²,

et al. 2008

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“…17 The complex role of visceral adipocytes as an important source of cytokines, adipokines and para-endocrine substances may be involved. 44,45 Routine biochemical and histological parameters of inflammation, however, showed no significant differences or correlations in this study cohort.…”

Section: Discussionmentioning

confidence: 69%

Visceral adiposity and insulin resistance are independent predictors of the presence of non-cirrhotic NAFLD-related portal hypertension

et al. 2010

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Introduction: We previously demonstrated in an animal model that steatosis, in the absence of fibrosis, induces a significant rise in portal pressure, indicating substantial changes in liver hemodynamics. As assessment of portal pressure is an invasive procedure, non-invasive parameters are needed to identify patients at risk. Aims: To study the portal pressure in nonalcoholic fatty liver disease patients and to identify factors that are possibly related to steatosis-induced changes in liver hemodynamics. Materials and methods: Patients presenting with a problem of overweight or obesity, and in whom non-invasive investigations showed signs of liver involvement, were proposed for transjugular hepatic vein catheterization and liver biopsy. The biopsy was scored according to the Nonalcoholic Steatohepatitis Clinical Research Network Scoring System. Results: A total of 50 consecutive patients were studied. Their mean age was 47.9 ± 1.8 years; 31 (62%) were female. Hepatic venous pressure gradient was normal in 36 (72%) and elevated in 14 (28%) patients. The degree of steatosis was the only histological parameter that differed significantly between the two groups (P ¼ 0.016), and was a predictor of the presence of portal hypertension (PHT) in regression analysis (P ¼ 0.010). Comparing normal versus portal hypertensive patients, waist circumference (117 ± 2 versus 128 ± 4 cm, P ¼ 0.005), waist-hip ratio (0.96 ± 0.06 versus 1.04 ± 0.03, P ¼ 0.003), visceral fat (229 ± 15 versus 292 ± 35 cm 2 , P ¼ 0.022), fasting insulin (15.4 ± 1.7 versus 21.8 ± 2.4 mU ml À1 , P ¼ 0.032), fasting c-peptide (1.22 ± 0.06 versus 1.49 ± 0.09 nmol l À1 , P ¼ 0.035) and homeostasis model assessment-insulin resistance (HOMA IR) (3.28 ± 0.29 versus 4.81 ± 0.57, P ¼ 0.019) were significantly higher. Age, gender, liver enzymes, ferritin and high-sensitive C-reactive protein were not significantly different. In regression analysis, waist circumference (P ¼ 0.008) and HOMA IR (P ¼ 0.043) were independent predictors of PHT. Conclusions: Estimates of both visceral adiposity and IR are predictors for the presence of PHT, related to the degree of steatosis, and may help in identifying patients who are at risk of developing steatosis-related complications.

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“…A few studies have reported that serum resistin levels did not differ between patients with NAFLD and without the disease [92,93]. However, one study has shown that excessive ectopic accumulation of fat in the liver and skeletal muscle of insulin-resistant subjects is associated with lower concentrations of resistin in the serum, while another reports increased levels of resistin, but only in patients with severe liver disease [94,95].…”

Section: Resistin and Non-alcoholic Fatty Liver Diseasementioning

confidence: 99%

The role of resistin as a regulator of inflammation: Implications for various human pathologies

Filková

Haluzı́k

Šenolt

2009

Clinical Immunology

372

297

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Adipokines and cytokines in non‐alcoholic fatty liver disease

Abstract: SUMMARY BackgroundSeveral adipocytokines have been implicated in the pathogenesis nonalcoholic fatty liver disease (NAFLD).

Cited by 393 publications

References 29 publications

Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial

Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial

Visceral adiposity and insulin resistance are independent predictors of the presence of non-cirrhotic NAFLD-related portal hypertension

The role of resistin as a regulator of inflammation: Implications for various human pathologies

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