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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 7 Studies and their findings on interleukin-1α, interleukin-1β, interleukin-1Ra and interleukin-18
IL-1αAcute treatment of 3T3-L1 adipocytes with IL-1α led to transient IR at IRS-1 level, mediated by its serine phosphorylation[254]
HumanWeight loss in severely obese patients led to decreased IL-1β in subcutaneous adipose tissue and in liver without effect on adipose IL-1α IL-1β was significantly higher in subcutaneous/visceral adipose tissue than in liver[253]
IL1-β genetic variants in Japanese population associated with NASH[259]
AnimalHepatic IL-1α and IL-1β increased in NASH animal models Mice deficient in either cytokine not prone to NASH and fibrosis development[255]
In experimental models TLR2 and palmitic acid activated inflammasome in Kupffer cells and produced IL-1α and IL-1β[257]
IL-1β/ApoE-deficient mice had less pronounced atherosclerosis[262]
Treatment with an IL-1β antibody improved glycemic control and β cell function in diet-induced obese mice[263]
Animal NASH model showed increased macrophage infiltration in adipose tissue as well as in liver accompanied with increased expression of IL-1β[264]
Hepatic steatosis partially mediated by Kupffer cells that produced IL-1β which suppressed PPAR-α[266]
In diet induced NASH mice probiotics decreased hepatic IL-1β mRNA[268]
In vitroIL-1β inhibited insulin-induced phosphorylation of the insulin receptor beta subunit, IRS1, protein kinase B and extracellular regulated kinase 1/2 in murine and human adipocytes that lead to IR and inhibition of lipogenesis IL-1β decreased adiponectin[260]
IL-1β promoted hepatic fibrosis by upregulating TIMMP-1 in rat HSC mediated by p38 mitogen-activated protein kinases and JNK[267]
IL-1RaIL-1Ra decreased glucose uptake in muscle and was upregulated in WAT of diet-induce obese mice[270]
Atherogenic diet in IL-1Ra deficient mice caused severe liver steatosis, inflammation and portal fibrosis[272]
IL-18In obese women IL-18 positively correlated with body weight and visceral fat[275]
In T2DM patients and non-diabetic controls IL-18 plasma levels positively correlated with HOMA-IR[276]
In male patients with NAFLD, IL-18 alone in the absence of metabolic risks cannot contribute to evolution of NAFLD[278]
IL-18 enhanced cytokine production by stimulating TNF-α synthesis in immune cells[279]
Il-18 administrated with IL-12 induced mouse fatty liver in an IFN-γ dependent manner[280]
Rosiglitazone in NAFLD rat model reduced IL-18 and caspase-1 in liver as well as improved histology[277]