<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li Y</submitter><funding>Key R &amp;amp; D projects of Xinjiang Autonomous Region</funding><funding>Taishan Industry Leadership Project</funding><funding>Shandong Post-doctoral Innovation Project</funding><funding>Key R &amp; D projects of Xinjiang Autonomous Region</funding><funding>Natural Science Foundation of Shandong Province</funding><funding>National Natural Science Foundation of China</funding><funding>Special Economic Animal Industry Technology System of Shandong Province</funding><funding>Modern Agro-industry Technology Research system</funding><pagination>1444-1453</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9449403</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>35(9)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>Acetate plays an important role in host lipid metabolism. However, the network of acetate-regulated lipid metabolism remains unclear. Previous studies show that mitogen-activated protein kinases (MAPKs) and mechanistic target of rapamycin (mTOR) play a crucial role in lipid metabolism. We hypothesize that acetate could affect MAPKs and/or mTOR signaling and then regulate lipid metabolism. The present study investigated whether any cross talk occurs among MAPKs, mTOR and acetate in regulating lipid metabolism.&lt;h4>Methods&lt;/h4>The ceramide C6 (an extracellular signaling-regulated kinases 1 and 2 [ERK1/2] activator) and MHY1485 (a mTOR activator) were used to treat rabbit adipose-derived stem cells (ADSCs) with or without acetate, respectively.&lt;h4>Results&lt;/h4>It indicated tha</pubmed_abstract><journal>Animal bioscience</journal><pubmed_title>Mechanistic target of rapamycin and an extracellular signaling-regulated kinases 1 and 2 signaling participate in the process of acetate regulating lipid metabolism and hormone-sensitive lipase expression.</pubmed_title><pmcid>PMC9449403</pmcid><funding_grant_id>CARS-43-B-1</funding_grant_id><funding_grant_id>ZR2021MC043</funding_grant_id><funding_grant_id>TSCY20190107</funding_grant_id><funding_grant_id>SDAIT-21-16</funding_grant_id><funding_grant_id>31972594</funding_grant_id><funding_grant_id>2020B01004-1-3</funding_grant_id><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Fu C</pubmed_authors><pubmed_authors>Liu L</pubmed_authors><pubmed_authors>Li F</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mechanistic target of rapamycin and an extracellular signaling-regulated kinases 1 and 2 signaling participate in the process of acetate regulating lipid metabolism and hormone-sensitive lipase expression.</name><description>&lt;h4>Objective&lt;/h4>Acetate plays an important role in host lipid metabolism. However, the network of acetate-regulated lipid metabolism remains unclear. Previous studies show that mitogen-activated protein kinases (MAPKs) and mechanistic target of rapamycin (mTOR) play a crucial role in lipid metabolism. We hypothesize that acetate could affect MAPKs and/or mTOR signaling and then regulate lipid metabolism. The present study investigated whether any cross talk occurs among MAPKs, mTOR and acetate in regulating lipid metabolism.&lt;h4>Methods&lt;/h4>The ceramide C6 (an extracellular signaling-regulated kinases 1 and 2 [ERK1/2] activator) and MHY1485 (a mTOR activator) were used to treat rabbit adipose-derived stem cells (ADSCs) with or without acetate, respectively.&lt;h4>Results&lt;/h4>It indicated tha</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Sep</publication><modification>2026-05-28T00:33:53.099Z</modification><creation>2025-04-06T01:52:13.3Z</creation></dates><accession>S-EPMC9449403</accession><cross_references><pubmed>34727637</pubmed><doi>10.5713/ab.21.0341</doi></cross_references></HashMap>