Giby VG, Ajith TA. Role of adipokines and peroxisome proliferator-activated receptors in nonalcoholic fatty liver disease. World J Hepatol 2014; 6(8): 570-579 [PMID: 25232450 DOI: 10.4254/wjh.v6.i8.570]
Corresponding Author of This Article
Thekkuttuparambil Ananthanarayanan Ajith, PhD, Professor Biochemistry, Department of Biochemistry, Amala Institute of Medical Sciences, Amala Nagar, Thrissur-680 555, Kerala, India. taajith@rediffmail.com
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World J Hepatol. Aug 27, 2014; 6(8): 570-579 Published online Aug 27, 2014. doi: 10.4254/wjh.v6.i8.570
Role of adipokines and peroxisome proliferator-activated receptors in nonalcoholic fatty liver disease
Vettickattuparambil George Giby, Thekkuttuparambil Ananthanarayanan Ajith
Vettickattuparambil George Giby, Thekkuttuparambil Ananthanarayanan Ajith, Department of Biochemistry, Amala Institute of Medical Sciences, Thrissur-680 555, Kerala, India
Author contributions: Giby VG wrote the paragraphs: role of leptin, adiponectin, resistin, retinol binding protein-4 and pro-inflammatory cytokines in NAFLD; Ajith TA wrote the remaining paragraphs, introduction, conclusion, involved in designing, and revision of the manuscript; both authors were involved in editing the manuscript.
Correspondence to: Thekkuttuparambil Ananthanarayanan Ajith, PhD, Professor Biochemistry, Department of Biochemistry, Amala Institute of Medical Sciences, Amala Nagar, Thrissur-680 555, Kerala, India. taajith@rediffmail.com
Telephone: +91-487-2304116 Fax: +91-487-2307969
Received: March 3, 2014 Revised: April 29, 2014 Accepted: May 28, 2014 Published online: August 27, 2014
Core Tip
Core tip: Nonalcoholic fatty liver disease (NAFLD) is one of the principal causes for chronic liver disease. Recent reports suggested a positive association between cytokines secreted by the adipocytes, such as tumor necrosis factor-α, transforming growth factor-β, and interleukin (IL)-6 in NAFLD. Furthermore, hepatic natural killer T-cells produce IL-13 and IL-4; IL-13 may then activate hepatic stellate cells to produce pro-inflammatory cytokines and initiate oxidative stress, iron overload and fibrosis. Downregulation of peroxisome proliferator-activated receptors (PPAR), particularly PPAR-α in cases of hepatic steatosis, may facilitate the activity of hepatic proinflammatory cytokines. Hence, PPAR-γ and PPAR-α ligands have been considered for administration to prevent the initial inflammatory reactions and render protection to the liver cells.
