<?xml version="1.0" encoding="UTF-8"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-10-30T06:27:36Z</responseDate><request verb="GetRecord" identifier="oai:bayburt-rdlopen.rawdatalibrary.net:bayburt/12874" metadataPrefix="oai_dc">https://bayburt-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:bayburt-rdlopen.rawdatalibrary.net:bayburt/12874</identifier><datestamp>2026-10-29T19:42:51Z</datestamp><setSpec>openaire</setSpec><setSpec>driver</setSpec><setSpec>com_bayburt_10000</setSpec><setSpec>col_bayburt_10001</setSpec><setSpec>com_bayburt_10010</setSpec><setSpec>col_bayburt_10222</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:title>Interleukin-27 as a novel player in alleviating hepatic steatosis: Mechanistic insights from an in vitro analysis</dc:title><dc:creator>Cho, Wonjun</dc:creator><dc:creator>Oh, Heeseung</dc:creator><dc:creator>Abd El-Aty, A.M.</dc:creator><dc:creator>Özten, Ömer</dc:creator><dc:creator>Jeong, Ji Hoon</dc:creator><dc:creator>Jung, Tae Woo</dc:creator><dc:subject>AMPK</dc:subject><dc:subject>Autophagy</dc:subject><dc:subject>ER stress</dc:subject><dc:subject>IL-27</dc:subject><dc:subject>NAFLD</dc:subject><dc:subject>Obesity</dc:subject><dc:description>Interleukin-27 (IL-27) is a recently discovered cytokine that has been implicated in inflammatory and metabolic conditions, such as atherosclerosis and insulin resistance. However, the mechanisms by which IL-27 attenuates hepatic lipid accumulation in hyperlipidemic conditions and counteracts endoplasmic reticulum (ER) stress, a known risk factor for impaired hepatic lipid metabolism, have not been elucidated. This in vitro study was designed to examine the effect of IL-27 on hepatic lipid metabolism. The study included the evaluation of lipogenesis-associated proteins and ER stress markers by Western blotting, the determination of hepatic lipid accumulation by Oil Red O staining, and the examination of autophagosome formation by MDC staining. The results showed that IL-27 treatment reduced lipogenic lipid deposition and the expression of ER stress markers in cultured hepatocytes exposed to palmitate. Moreover, treatment with IL-27 suppressed CD36 expression and enhanced fatty acid oxidation in palmitate-treated hepatocytes. The effects of IL-27 on hyperlipidemic hepatocytes were attenuated when adenosine monophosphate-activated protein kinase (AMPK) or 3-methyladenine (3 MA) were inhibited by small interfering RNA (siRNA). These results suggest that IL-27 attenuates hepatic ER stress and fatty acid uptake and stimulates fatty acid oxidation via AMPK/autophagy signaling, thereby alleviating hepatic steatosis. In conclusion, this study identified IL-27 as a promising therapeutic target for nonalcoholic fatty liver disease (NAFLD).</dc:description><dc:publisher>Elsevier B.V.</dc:publisher><dc:date>2024</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/bayburt/12874</dc:identifier><dc:identifier>https://doi.org/10.1016/j.bbrc.2024.149671</dc:identifier><dc:identifier>0006-291X</dc:identifier><dc:language>en</dc:language><dc:relation>Biochemical and Biophysical Research Communications</dc:relation><dc:rights>info:eu-repo/semantics/openAccess</dc:rights><dc:type>info:eu-repo/semantics/article</dc:type><dc:identifier>https://bayburt-rdlopen.rawdatalibrary.net/tr/items/bayburt/12874</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>