Serum Lipocalin-2 and Irisin in Non Alcoholic Fatty Liver Rat Model and their Relations to Metabolic and Inflammatory Changes
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- Category: Vol. 85, June 2017
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Serum Lipocalin-2 and Irisin in Non Alcoholic Fatty Liver Rat Model and their Relations to Metabolic and Inflammatory Changes, NAWAL K. GERGES
Abstract
Background: Non-Alcoholic Fatty Liver Disease (NAFLD) is currently the most common chronic liver disorder; however, its pathophysiology is complex and not completely elucidated. An abnormality in the balance of secretion of cytokines, and adipokines may be involved in progression from fatty infil-tration to inflammation and fibrosis. Lipocalin-2, an adipokine protein that may link obesity, insulin resistance, and metabolic syndrome; however the relation between lipo2 and NAFLD remains controversy. In addition, Irisin a newly discovered myokine, could be responsible for a better control of certain diseases related to insulin resistance, but still there are great discrepancies as regard its level in NAFLD.
Objective: This study was designed to evaluate serum lipocalin-2 and irisin levels in high fat-NAFLD (simple steatosis, NASH, and fibrosis) in relation to metabolic param-eters and inflammatory markers, and to elucidate their possible roles in the pathogenesis of NAFLD.
Material and Methods: This study was conducted on 2 groups of male albino rats: Control group (I) which was divided into 3 equal subgroups (n=8), in which rats fed normal chow for 4, 12 and 24 weeks, respectively. HFD-fed group (II) which was divided into 3 equal subgroups (n=8) in which rats were fed High Fat Diet (HFD) (%58) for 4, 12 and 24 weeks, respectively. In all groups, BMI, Abdominal Circum-ference (AC), serum levels of lipocalin-2, irisin, glucose, insulin (with calculation of HOMA-IR), lipid profile, ALT, AST, CRP, and TNF-a were measured and histopathological liver injury scoring was done.
Results: HFD-feeding for 4w, 12w, 24w resulted in simple steatosis, Non-Alcoholic Steatohepatitis (NASH) and fibrosis, respectively, as evidenced by results of the liver histopathology and significantly elevated liver enzymes. Also, there was a significant progressive increase in BMI, AC, serum glucose, insulin, cholesterol, TG, LDL, CRP, TNF-a levels and HOMA-IR in HFD/NAFLD groups. Furthermore, there was a signif-icant progressive increase in serum lipo-2 levels in the same groups, with a significant positive correlation between serum lipo-2, and all the above mentioned parameters including liver injury scoring. However, there was a significant progressive decrease in serum irisin level in the same groups, with a significant negative correlation between serum irisin, and serum glucose, insulin, cholesterol, TG, LDL, CRP, TNF-a levels, HOMA-IR, and histopatholgy liver injury scoring in HFD/NAFLD groups, while there was no significant correlation between serum irisin level and BMI or AC in the three HFD/NAFLD groups.
Conclusions: Lipocalin-2 could play a critical role in the development of NAFLD, and mediating the transition from steatosis to inflammation and fibrosis. While irisin might have a beneficial role in preventing the hepatic steatosis as a mechanism counteracting lipid accumulation, and attenuating its progression to steatohepatitis via altering the expression of inflammatory cytokines.