Hepatic tumor necrosis factor-α, leptin and adiponectin expression in morbid obese patients: Clinicopathological correlations

Phui Ly Liew, Chi Long Chen, Yi Chih Lee, Ming Te Huang, Weu Wang, Wei Jei Lee

Research output: Contribution to journalArticle

Abstract

Background: Nonalcoholic fatty liver disease (NAFLD) is associated with obesity. We retrospectively studied the clinicopathology and different hepatic adipocytokine expressions between nonalcoholic steatohepatitis (NASH) and non-NASH in morbid obesity. Methods: We enrolled 40 patients undergoing liver biopsy during bariatric surgery. We analyzed hepatic mRNA and immunohistochemistry of TNF-α, leptin, adiponectin and adiponectin receptor. Results: Thirty patients (75%) presented with NASH, including 11 with mild fibrosis and 19 with advanced fibrosis. The HbA1c (P = 0.000), AST (P = 0.000), ALT (P = 0.000), GGT (P = 0.016) and liver fibrosis (P = 0.028) have statistically difference between NASH and non-NASH groups. Steatosis was the only significant factor (r = 0.348, P <0.05) associated with TNF-α mRNA level. Adiponectin mRNA was inversely associated with C-peptide (r = -0.416, P <0.05) and uric acid level (r = -0.426, P <0.05). The best predictors for TNF-α immunostain were hemoglobin (r = 0.432, P <0.01), AST (r = 0.371, P <0.05), lobular inflammation (r = 0.315, P <0.05), portal inflammation (r = 0.331, P <0.05), and NAS (r = 0.365, P <0.05). Leptin immunostain was correlated with C-peptide (r = 0.356, P <0.05) and portal inflammation (r = 0.334, P <0.05). The AdipoRII immunoexpression was negatively correlated with systolic blood pressure (r = -0.481, P <0.01). Multivariate linear regressions of adipocytokine profile related mostly to age, gender, systolic blood pressure, serum uric acid, steatosis, NAS and portal inflammation. Conclusion: Although different adipocytokines may be associated with NAFLD progression in morbid obesity, their major correlations in the pathogenesis of obesity-related NASH are not clear. Additional confirmatory studies are deserved.

Original languageEnglish
JournalObesity Research and Clinical Practice
Volume6
Issue number1
DOIs
Publication statusPublished - Jan 2012

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Adiponectin
Leptin
Tumor Necrosis Factor-alpha
Adipokines
Liver
Blood Pressure
Inflammation
Morbid Obesity
C-Peptide
Fatty Liver
Uric Acid
Messenger RNA
Fibrosis
Obesity
Adiponectin Receptors
Leptin Receptors
Bariatric Surgery
Tumor Necrosis Factor Receptors
Liver Cirrhosis
Disease Progression

Keywords

  • Clinicopathology
  • Hepatic adipocytokines
  • Morbid obesity

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

Cite this

@article{ca3fb6497e6f4319ac9a2f39c3185814,
title = "Hepatic tumor necrosis factor-α, leptin and adiponectin expression in morbid obese patients: Clinicopathological correlations",
abstract = "Background: Nonalcoholic fatty liver disease (NAFLD) is associated with obesity. We retrospectively studied the clinicopathology and different hepatic adipocytokine expressions between nonalcoholic steatohepatitis (NASH) and non-NASH in morbid obesity. Methods: We enrolled 40 patients undergoing liver biopsy during bariatric surgery. We analyzed hepatic mRNA and immunohistochemistry of TNF-α, leptin, adiponectin and adiponectin receptor. Results: Thirty patients (75{\%}) presented with NASH, including 11 with mild fibrosis and 19 with advanced fibrosis. The HbA1c (P = 0.000), AST (P = 0.000), ALT (P = 0.000), GGT (P = 0.016) and liver fibrosis (P = 0.028) have statistically difference between NASH and non-NASH groups. Steatosis was the only significant factor (r = 0.348, P <0.05) associated with TNF-α mRNA level. Adiponectin mRNA was inversely associated with C-peptide (r = -0.416, P <0.05) and uric acid level (r = -0.426, P <0.05). The best predictors for TNF-α immunostain were hemoglobin (r = 0.432, P <0.01), AST (r = 0.371, P <0.05), lobular inflammation (r = 0.315, P <0.05), portal inflammation (r = 0.331, P <0.05), and NAS (r = 0.365, P <0.05). Leptin immunostain was correlated with C-peptide (r = 0.356, P <0.05) and portal inflammation (r = 0.334, P <0.05). The AdipoRII immunoexpression was negatively correlated with systolic blood pressure (r = -0.481, P <0.01). Multivariate linear regressions of adipocytokine profile related mostly to age, gender, systolic blood pressure, serum uric acid, steatosis, NAS and portal inflammation. Conclusion: Although different adipocytokines may be associated with NAFLD progression in morbid obesity, their major correlations in the pathogenesis of obesity-related NASH are not clear. Additional confirmatory studies are deserved.",
keywords = "Clinicopathology, Hepatic adipocytokines, Morbid obesity",
author = "Liew, {Phui Ly} and Chen, {Chi Long} and Lee, {Yi Chih} and Huang, {Ming Te} and Weu Wang and Lee, {Wei Jei}",
year = "2012",
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language = "English",
volume = "6",
journal = "Obesity Research and Clinical Practice",
issn = "1871-403X",
publisher = "Elsevier BV",
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}

TY - JOUR

T1 - Hepatic tumor necrosis factor-α, leptin and adiponectin expression in morbid obese patients

T2 - Clinicopathological correlations

AU - Liew, Phui Ly

AU - Chen, Chi Long

AU - Lee, Yi Chih

AU - Huang, Ming Te

AU - Wang, Weu

AU - Lee, Wei Jei

PY - 2012/1

Y1 - 2012/1

N2 - Background: Nonalcoholic fatty liver disease (NAFLD) is associated with obesity. We retrospectively studied the clinicopathology and different hepatic adipocytokine expressions between nonalcoholic steatohepatitis (NASH) and non-NASH in morbid obesity. Methods: We enrolled 40 patients undergoing liver biopsy during bariatric surgery. We analyzed hepatic mRNA and immunohistochemistry of TNF-α, leptin, adiponectin and adiponectin receptor. Results: Thirty patients (75%) presented with NASH, including 11 with mild fibrosis and 19 with advanced fibrosis. The HbA1c (P = 0.000), AST (P = 0.000), ALT (P = 0.000), GGT (P = 0.016) and liver fibrosis (P = 0.028) have statistically difference between NASH and non-NASH groups. Steatosis was the only significant factor (r = 0.348, P <0.05) associated with TNF-α mRNA level. Adiponectin mRNA was inversely associated with C-peptide (r = -0.416, P <0.05) and uric acid level (r = -0.426, P <0.05). The best predictors for TNF-α immunostain were hemoglobin (r = 0.432, P <0.01), AST (r = 0.371, P <0.05), lobular inflammation (r = 0.315, P <0.05), portal inflammation (r = 0.331, P <0.05), and NAS (r = 0.365, P <0.05). Leptin immunostain was correlated with C-peptide (r = 0.356, P <0.05) and portal inflammation (r = 0.334, P <0.05). The AdipoRII immunoexpression was negatively correlated with systolic blood pressure (r = -0.481, P <0.01). Multivariate linear regressions of adipocytokine profile related mostly to age, gender, systolic blood pressure, serum uric acid, steatosis, NAS and portal inflammation. Conclusion: Although different adipocytokines may be associated with NAFLD progression in morbid obesity, their major correlations in the pathogenesis of obesity-related NASH are not clear. Additional confirmatory studies are deserved.

AB - Background: Nonalcoholic fatty liver disease (NAFLD) is associated with obesity. We retrospectively studied the clinicopathology and different hepatic adipocytokine expressions between nonalcoholic steatohepatitis (NASH) and non-NASH in morbid obesity. Methods: We enrolled 40 patients undergoing liver biopsy during bariatric surgery. We analyzed hepatic mRNA and immunohistochemistry of TNF-α, leptin, adiponectin and adiponectin receptor. Results: Thirty patients (75%) presented with NASH, including 11 with mild fibrosis and 19 with advanced fibrosis. The HbA1c (P = 0.000), AST (P = 0.000), ALT (P = 0.000), GGT (P = 0.016) and liver fibrosis (P = 0.028) have statistically difference between NASH and non-NASH groups. Steatosis was the only significant factor (r = 0.348, P <0.05) associated with TNF-α mRNA level. Adiponectin mRNA was inversely associated with C-peptide (r = -0.416, P <0.05) and uric acid level (r = -0.426, P <0.05). The best predictors for TNF-α immunostain were hemoglobin (r = 0.432, P <0.01), AST (r = 0.371, P <0.05), lobular inflammation (r = 0.315, P <0.05), portal inflammation (r = 0.331, P <0.05), and NAS (r = 0.365, P <0.05). Leptin immunostain was correlated with C-peptide (r = 0.356, P <0.05) and portal inflammation (r = 0.334, P <0.05). The AdipoRII immunoexpression was negatively correlated with systolic blood pressure (r = -0.481, P <0.01). Multivariate linear regressions of adipocytokine profile related mostly to age, gender, systolic blood pressure, serum uric acid, steatosis, NAS and portal inflammation. Conclusion: Although different adipocytokines may be associated with NAFLD progression in morbid obesity, their major correlations in the pathogenesis of obesity-related NASH are not clear. Additional confirmatory studies are deserved.

KW - Clinicopathology

KW - Hepatic adipocytokines

KW - Morbid obesity

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