Monounsaturated fatty acids protect against palmitate-induced lipoapoptosis in human umbilical vein endothelial cells
Diets high in saturated fatty acids are linked to increased cardiovascular disease risk, whereas monounsaturated fatty acids have been associated with improved cardiovascular outcomes. Accordingly, cell culture studies have demonstrated that saturated fatty acids, particularly long chain saturated f...
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| description | Diets high in saturated fatty acids are linked to increased cardiovascular disease risk, whereas monounsaturated fatty acids have been associated with improved cardiovascular outcomes. Accordingly, cell culture studies have demonstrated that saturated fatty acids, particularly long chain saturated fatty acids such as palmitate, induce dysfunction and cell death in a variety of cell types, and monounsaturated fatty acids may confer protection against palmitate-mediated damage. The aim of the present study was to examine whether monounsaturated fatty acids could protect against palmitate-mediated cell death in endothelial cells, to determine if AMPK inactivation and activation (via compound C and AICAR, respectively) underlies both palmitate-induced damage and monounsaturated fatty acid-mediated protection, and to explore the role of ER stress in this context. Human umbilical vein endothelial cells were examined for cell viability and apoptosis following treatment for 24 hours with palmitate (0.25 and 0.5mM) alone or in combination with the monounsaturated fatty acids oleate or palmitoleate (0.25 and 0.5mM), AICAR, compound C, 4μ8C, or TUDCA. Compared to control cells, palmitate significantly decreased cell viability and increased apoptosis in a dose-dependent manner. The monounsaturated fatty acids oleate and palmitoleate completely prevented the cytotoxic effects of palmitate. Although palmitate induced markers of ER stress, chemical inhibition of ER stress did not prevent palmitate-induced lipoapoptosis. Conversely, the AMPK activator AICAR (0.1 and 0.5mM) conferred protection from palmitate mediated-alterations in viability, apoptosis and ER stress, whereas the AMPK inhibitor compound C (20 and 40μM) significantly exacerbated palmitate-mediated damage. Lastly, co-incubation with palmitate, monounsaturated fatty acids, and compound C significantly mitigated the protective effects of both oleate and palmitoleate. In conclusion, monounsaturated fatty acids confer protection against the cytotoxic effects of palmitate in vascular endothelial cells; and palmitate-mediated damage, as well as monounsaturated-mediated protection, are due in part to inactivation and activation, respectively, of the metabolic regulator AMPK. These results may have implications for understanding the deleterious effects of high saturated fat diets on cardiovascular dysfunction and disease risk. |
| doi_str_mv | 10.1371/journal.pone.0226940 |
| format | Article |
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Accordingly, cell culture studies have demonstrated that saturated fatty acids, particularly long chain saturated fatty acids such as palmitate, induce dysfunction and cell death in a variety of cell types, and monounsaturated fatty acids may confer protection against palmitate-mediated damage. The aim of the present study was to examine whether monounsaturated fatty acids could protect against palmitate-mediated cell death in endothelial cells, to determine if AMPK inactivation and activation (via compound C and AICAR, respectively) underlies both palmitate-induced damage and monounsaturated fatty acid-mediated protection, and to explore the role of ER stress in this context. Human umbilical vein endothelial cells were examined for cell viability and apoptosis following treatment for 24 hours with palmitate (0.25 and 0.5mM) alone or in combination with the monounsaturated fatty acids oleate or palmitoleate (0.25 and 0.5mM), AICAR, compound C, 4μ8C, or TUDCA. Compared to control cells, palmitate significantly decreased cell viability and increased apoptosis in a dose-dependent manner. The monounsaturated fatty acids oleate and palmitoleate completely prevented the cytotoxic effects of palmitate. Although palmitate induced markers of ER stress, chemical inhibition of ER stress did not prevent palmitate-induced lipoapoptosis. Conversely, the AMPK activator AICAR (0.1 and 0.5mM) conferred protection from palmitate mediated-alterations in viability, apoptosis and ER stress, whereas the AMPK inhibitor compound C (20 and 40μM) significantly exacerbated palmitate-mediated damage. Lastly, co-incubation with palmitate, monounsaturated fatty acids, and compound C significantly mitigated the protective effects of both oleate and palmitoleate. In conclusion, monounsaturated fatty acids confer protection against the cytotoxic effects of palmitate in vascular endothelial cells; and palmitate-mediated damage, as well as monounsaturated-mediated protection, are due in part to inactivation and activation, respectively, of the metabolic regulator AMPK. These results may have implications for understanding the deleterious effects of high saturated fat diets on cardiovascular dysfunction and disease risk.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0226940</identifier><identifier>PMID: 31891641</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Adenylate Kinase - antagonists & inhibitors ; Adenylate Kinase - metabolism ; Aminoimidazole Carboxamide - analogs & derivatives ; Aminoimidazole Carboxamide - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Biochemistry ; Biology and Life Sciences ; Cardiovascular diseases ; Cardiovascular Diseases - etiology ; Cardiovascular Diseases - metabolism ; Cardiovascular Diseases - prevention & control ; Cell culture ; Cell death ; Cell Survival - drug effects ; Cell viability ; Cytotoxicity ; Damage ; Deactivation ; Diabetes ; Diet ; Dietary Fats - administration & dosage ; Dietary Fats - adverse effects ; Dietary Fats - metabolism ; Dilution ; Endothelial cells ; Endothelium ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Experiments ; Fatty acids ; Fatty Acids, Monounsaturated - administration & dosage ; Fatty Acids, Monounsaturated - metabolism ; Food science ; Gene expression ; Health risks ; High fat diet ; Homeostasis ; Human Umbilical Vein Endothelial Cells ; Humans ; Inactivation ; Incubation ; Lipids ; Medicine and Health Sciences ; Metabolic rate ; Metabolism ; Monounsaturated fatty acids ; Nutrition ; Organic chemistry ; Palmitic acid ; Palmitic Acid - adverse effects ; Palmitic Acid - metabolism ; Pyrazoles - pharmacology ; Pyrimidines - pharmacology ; Research and Analysis Methods ; Ribonucleotides - pharmacology ; Saturated fatty acids ; Stress ; Type 2 diabetes ; Umbilical vein ; Viability</subject><ispartof>PloS one, 2019-12, Vol.14 (12), p.e0226940</ispartof><rights>COPYRIGHT 2019 Public Library of Science</rights><rights>2019 Lee et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 Lee et al 2019 Lee et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-f35bed2c99cdd71da8e3661d0aa8d8fd2df3fd8cbca5ef630ecbc73da4acb36f3</citedby><cites>FETCH-LOGICAL-c758t-f35bed2c99cdd71da8e3661d0aa8d8fd2df3fd8cbca5ef630ecbc73da4acb36f3</cites><orcidid>0000-0002-5130-6160</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6938355/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6938355/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31891641$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Dustin M</creatorcontrib><creatorcontrib>Sevits, Kyle J</creatorcontrib><creatorcontrib>Battson, Micah L</creatorcontrib><creatorcontrib>Wei, Yuren</creatorcontrib><creatorcontrib>Cox-York, Kimberly A</creatorcontrib><creatorcontrib>Gentile, Christopher L</creatorcontrib><title>Monounsaturated fatty acids protect against palmitate-induced lipoapoptosis in human umbilical vein endothelial cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Diets high in saturated fatty acids are linked to increased cardiovascular disease risk, whereas monounsaturated fatty acids have been associated with improved cardiovascular outcomes. Accordingly, cell culture studies have demonstrated that saturated fatty acids, particularly long chain saturated fatty acids such as palmitate, induce dysfunction and cell death in a variety of cell types, and monounsaturated fatty acids may confer protection against palmitate-mediated damage. The aim of the present study was to examine whether monounsaturated fatty acids could protect against palmitate-mediated cell death in endothelial cells, to determine if AMPK inactivation and activation (via compound C and AICAR, respectively) underlies both palmitate-induced damage and monounsaturated fatty acid-mediated protection, and to explore the role of ER stress in this context. Human umbilical vein endothelial cells were examined for cell viability and apoptosis following treatment for 24 hours with palmitate (0.25 and 0.5mM) alone or in combination with the monounsaturated fatty acids oleate or palmitoleate (0.25 and 0.5mM), AICAR, compound C, 4μ8C, or TUDCA. Compared to control cells, palmitate significantly decreased cell viability and increased apoptosis in a dose-dependent manner. The monounsaturated fatty acids oleate and palmitoleate completely prevented the cytotoxic effects of palmitate. Although palmitate induced markers of ER stress, chemical inhibition of ER stress did not prevent palmitate-induced lipoapoptosis. Conversely, the AMPK activator AICAR (0.1 and 0.5mM) conferred protection from palmitate mediated-alterations in viability, apoptosis and ER stress, whereas the AMPK inhibitor compound C (20 and 40μM) significantly exacerbated palmitate-mediated damage. Lastly, co-incubation with palmitate, monounsaturated fatty acids, and compound C significantly mitigated the protective effects of both oleate and palmitoleate. In conclusion, monounsaturated fatty acids confer protection against the cytotoxic effects of palmitate in vascular endothelial cells; and palmitate-mediated damage, as well as monounsaturated-mediated protection, are due in part to inactivation and activation, respectively, of the metabolic regulator AMPK. These results may have implications for understanding the deleterious effects of high saturated fat diets on cardiovascular dysfunction and disease risk.</description><subject>Activation</subject><subject>Adenylate Kinase - antagonists & inhibitors</subject><subject>Adenylate Kinase - metabolism</subject><subject>Aminoimidazole Carboxamide - analogs & derivatives</subject><subject>Aminoimidazole Carboxamide - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biochemistry</subject><subject>Biology and Life Sciences</subject><subject>Cardiovascular diseases</subject><subject>Cardiovascular Diseases - etiology</subject><subject>Cardiovascular Diseases - metabolism</subject><subject>Cardiovascular Diseases - prevention & control</subject><subject>Cell culture</subject><subject>Cell death</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Cytotoxicity</subject><subject>Damage</subject><subject>Deactivation</subject><subject>Diabetes</subject><subject>Diet</subject><subject>Dietary Fats - administration & dosage</subject><subject>Dietary Fats - adverse effects</subject><subject>Dietary Fats - metabolism</subject><subject>Dilution</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Experiments</subject><subject>Fatty acids</subject><subject>Fatty Acids, Monounsaturated - administration & dosage</subject><subject>Fatty Acids, Monounsaturated - metabolism</subject><subject>Food science</subject><subject>Gene expression</subject><subject>Health risks</subject><subject>High fat diet</subject><subject>Homeostasis</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humans</subject><subject>Inactivation</subject><subject>Incubation</subject><subject>Lipids</subject><subject>Medicine and Health Sciences</subject><subject>Metabolic rate</subject><subject>Metabolism</subject><subject>Monounsaturated fatty acids</subject><subject>Nutrition</subject><subject>Organic chemistry</subject><subject>Palmitic acid</subject><subject>Palmitic Acid - adverse effects</subject><subject>Palmitic Acid - metabolism</subject><subject>Pyrazoles - pharmacology</subject><subject>Pyrimidines - pharmacology</subject><subject>Research and Analysis Methods</subject><subject>Ribonucleotides - pharmacology</subject><subject>Saturated fatty acids</subject><subject>Stress</subject><subject>Type 2 diabetes</subject><subject>Umbilical vein</subject><subject>Viability</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNktuL1DAUxoso7kX_A9GCIPgwY9K0mfZFWBYvAysL3l7DaS4zGdKk5rK4__1mnO4yBQXJQ8LJ73zn8PEVxQuMlpis8LudS96CWY7OyiWqKtrV6FFxijtSLWiFyOOj90lxFsIOoYa0lD4tTghuO0xrfFqkL866ZAPE5CFKUSqI8bYErkUoR--i5LGEDWgbYjmCGXTM2EJbkXimjR4djG6MLuhQaltu0wC2TEOvjeZgyhuZi9IKF7fS6Fzg0pjwrHiiwAT5fLrPix8fP3y__Ly4uv60vry4WvBV08aFIk0vRcW7jguxwgJaSSjFAgG0olWiEooo0fKeQyMVJUjm54oIqIH3hCpyXrw66I7GBTY5FlhFCKYVbSnKxPpACAc7Nno9gL9lDjT7U3B-w8BHzY1khHPSix4DblWdt8gOKlzXmFdS9ULtp72fpqV-kIJLGz2Ymej8x-ot27gbRjvSkqbJAq8nAe9-JRniP1aeqA3krbRVLovxQQfOLihGmHZtU2Vq-RcqHyEHzXNmlM71WcPbWUNmovwdN5BCYOtvX_-fvf45Z98csVsJJm6DMylqZ8McrA8g9y4EL9WDcxixfeTv3WD7yLMp8rnt5bHrD033GSd3UxIBrA</recordid><startdate>20191231</startdate><enddate>20191231</enddate><creator>Lee, Dustin M</creator><creator>Sevits, Kyle J</creator><creator>Battson, Micah L</creator><creator>Wei, Yuren</creator><creator>Cox-York, Kimberly A</creator><creator>Gentile, Christopher L</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-5130-6160</orcidid></search><sort><creationdate>20191231</creationdate><title>Monounsaturated fatty acids protect against palmitate-induced lipoapoptosis in human umbilical vein endothelial cells</title><author>Lee, Dustin M ; Sevits, Kyle J ; Battson, Micah L ; Wei, Yuren ; Cox-York, Kimberly A ; Gentile, Christopher L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-f35bed2c99cdd71da8e3661d0aa8d8fd2df3fd8cbca5ef630ecbc73da4acb36f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Activation</topic><topic>Adenylate Kinase - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Dustin M</au><au>Sevits, Kyle J</au><au>Battson, Micah L</au><au>Wei, Yuren</au><au>Cox-York, Kimberly A</au><au>Gentile, Christopher L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Monounsaturated fatty acids protect against palmitate-induced lipoapoptosis in human umbilical vein endothelial cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2019-12-31</date><risdate>2019</risdate><volume>14</volume><issue>12</issue><spage>e0226940</spage><pages>e0226940-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Diets high in saturated fatty acids are linked to increased cardiovascular disease risk, whereas monounsaturated fatty acids have been associated with improved cardiovascular outcomes. Accordingly, cell culture studies have demonstrated that saturated fatty acids, particularly long chain saturated fatty acids such as palmitate, induce dysfunction and cell death in a variety of cell types, and monounsaturated fatty acids may confer protection against palmitate-mediated damage. The aim of the present study was to examine whether monounsaturated fatty acids could protect against palmitate-mediated cell death in endothelial cells, to determine if AMPK inactivation and activation (via compound C and AICAR, respectively) underlies both palmitate-induced damage and monounsaturated fatty acid-mediated protection, and to explore the role of ER stress in this context. Human umbilical vein endothelial cells were examined for cell viability and apoptosis following treatment for 24 hours with palmitate (0.25 and 0.5mM) alone or in combination with the monounsaturated fatty acids oleate or palmitoleate (0.25 and 0.5mM), AICAR, compound C, 4μ8C, or TUDCA. Compared to control cells, palmitate significantly decreased cell viability and increased apoptosis in a dose-dependent manner. The monounsaturated fatty acids oleate and palmitoleate completely prevented the cytotoxic effects of palmitate. Although palmitate induced markers of ER stress, chemical inhibition of ER stress did not prevent palmitate-induced lipoapoptosis. Conversely, the AMPK activator AICAR (0.1 and 0.5mM) conferred protection from palmitate mediated-alterations in viability, apoptosis and ER stress, whereas the AMPK inhibitor compound C (20 and 40μM) significantly exacerbated palmitate-mediated damage. Lastly, co-incubation with palmitate, monounsaturated fatty acids, and compound C significantly mitigated the protective effects of both oleate and palmitoleate. In conclusion, monounsaturated fatty acids confer protection against the cytotoxic effects of palmitate in vascular endothelial cells; and palmitate-mediated damage, as well as monounsaturated-mediated protection, are due in part to inactivation and activation, respectively, of the metabolic regulator AMPK. These results may have implications for understanding the deleterious effects of high saturated fat diets on cardiovascular dysfunction and disease risk.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>31891641</pmid><doi>10.1371/journal.pone.0226940</doi><tpages>e0226940</tpages><orcidid>https://orcid.org/0000-0002-5130-6160</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2019-12, Vol.14 (12), p.e0226940 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2331626860 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Activation Adenylate Kinase - antagonists & inhibitors Adenylate Kinase - metabolism Aminoimidazole Carboxamide - analogs & derivatives Aminoimidazole Carboxamide - pharmacology Apoptosis Apoptosis - drug effects Biochemistry Biology and Life Sciences Cardiovascular diseases Cardiovascular Diseases - etiology Cardiovascular Diseases - metabolism Cardiovascular Diseases - prevention & control Cell culture Cell death Cell Survival - drug effects Cell viability Cytotoxicity Damage Deactivation Diabetes Diet Dietary Fats - administration & dosage Dietary Fats - adverse effects Dietary Fats - metabolism Dilution Endothelial cells Endothelium Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Experiments Fatty acids Fatty Acids, Monounsaturated - administration & dosage Fatty Acids, Monounsaturated - metabolism Food science Gene expression Health risks High fat diet Homeostasis Human Umbilical Vein Endothelial Cells Humans Inactivation Incubation Lipids Medicine and Health Sciences Metabolic rate Metabolism Monounsaturated fatty acids Nutrition Organic chemistry Palmitic acid Palmitic Acid - adverse effects Palmitic Acid - metabolism Pyrazoles - pharmacology Pyrimidines - pharmacology Research and Analysis Methods Ribonucleotides - pharmacology Saturated fatty acids Stress Type 2 diabetes Umbilical vein Viability |
| title | Monounsaturated fatty acids protect against palmitate-induced lipoapoptosis in human umbilical vein endothelial cells |
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