Topic Highlight
Copyright ©2014 Baishideng Publishing Group Inc.
World J Gastroenterol. Dec 28, 2014; 20(48): 18070-18091
Published online Dec 28, 2014. doi: 10.3748/wjg.v20.i48.18070
Table 6 Studies and their findings on interleukin-6
HumanIncreased plasma IL-6 in T2DM[222]
Elevated basal IL-6 levels in healthy humans present high relative risk of developing T2DM[224]
Obese patients after bariatric surgery who lost weight had decreased IR and IL-6[225][226]
IL-6 174C polymorphism associated with NASH and IR[239]
IL-6 levels higher in NAFLD patients, especially with advance stages, compared to ones with hepatitis B[240]
Increased serum IL-6 levels in biopsy proven NAFLD compared to controls[241]
No difference in IL-6 levels among T2DM patients with NASH/advanced fibrosis compared to those without NASH or light fibrosis[242]
No difference in serum IL-6 and its intrahepatic mRNA expression between NASH and steatosis[243,244]
In morbidly obese patients serum IL-6 levels correlated with progression of steatosis but in NASH declinedIL-6 > 4.81 pg/mL predicted liver steatosis[245]
Hepatocyte IL-6 expression positively correlated with degree of inflammation, stage of fibrosis and IR[246]
Increased circulating IL-6 and its soluble receptor in NASH patients compared with steatosis and healthy volunteers[189]
Normal IL-6 values exclude NASH[247]
IL-6, total cytokeratin-18 (M65) and adiponectin - a new panel for predicting NASH[248]
Decreased IL-6 levels after lifestyle changes and vitamin E administration[249]
AnimalChronic administration of IL-6 suppressed hepatic insulin signaling without effect on skeletal muscle[231]
Lep(ob) mice neutralized with IL-6 antibody showed increased insulin receptor signaling in the liver but not in peripheral tissues[232]
IL-6 decreases overall IR and hepatic inflammation[233]
Hepatoprotective and hepatoproliferative role of short-term exposure to IL-6 in ischaemic preconditioning models[234]
Treatment of IL-6-deficient mice acutely with IL-6 restored STAT3 binding and hepatocyte proliferation[235]
Chronic liver exposure to IL-6 led to cell death via Bax induction, activation of Fas agonist derived caspase-9 and cytochrome c release[236]
IL-6 showed inflammatory and antisteatotic effects in liver on mouse NASH model[237]
Hepatoprotective role of IL-6 by STAT3 activation in severe NASH model[238]
In vitroLPS through TLR receptors stimulated macrophages to produce TNF-α that up-regulated IL-6 production in adipocytes and macrophages[220]
IL-6 inhibited insulin-induced glycogenesis in hepatocytes[227]
IL-6 promoted IR in hepatocytes and HepG2 via decreased tyrosine phosphorylation of IRS-1, impaired association of the p85 subunit of phosphatidylinositol 3-kinase with IRS-1, inhibition of Akt and glycogen synthesis[228]
IL-6 impaired insulin signaling in 3T3-L1 adipocytes through inhibition of gene transcription of IRS-1, GLUT-4 and PPARγ[229]
IL-6-dependent IR mediated by induction of SOCS-3 protein in HepG2 cells[230]