Role and regulation of acylethanolamides in energy balance: focus on adipocytes and β‐cells
The endocannabinoid, arachidonoylethanolamide (AEA), and the peroxisome proliferator‐activated receptor (PPAR)‐α ligand, oleylethanolamide (OEA) produce opposite effects on lipogenesis. The regulation of OEA and its anti‐inflammatory congener, palmitoylethanolamide (PEA), in adipocytes and pancreati...
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description | The endocannabinoid, arachidonoylethanolamide (AEA), and the peroxisome proliferator‐activated receptor (PPAR)‐α ligand, oleylethanolamide (OEA) produce opposite effects on lipogenesis. The regulation of OEA and its anti‐inflammatory congener, palmitoylethanolamide (PEA), in adipocytes and pancreatic β‐cells has not been investigated. We report here the results of studies on acylethanolamide regulation in these cells during obesity and hyperglycaemia, and provide an overview of acylethanolamide role in metabolic control. We analysed by liquid chromatography‐mass spectrometry OEA and PEA levels in: 1) mouse 3T3F442A adipocytes during insulin‐induced differentiation, 2) rat insulinoma RIN m5F β‐cells kept in ‘low’ or ‘high’ glucose, 3) adipose tissue and pancreas of mice with high fat diet‐induced obesity (DIO), and 4) in visceral fat or blood of obese or type 2 diabetes (T2D) patients. In adipocytes, OEA levels remain unchanged during differentiation, whereas those of PEA decrease significantly, and are under the negative control of both leptin and PPAR‐γ. PEA is significantly downregulated in subcutaneous adipose tissue of DIO mice. In RIN m5F insulinoma β‐cells, OEA and PEA levels are inhibited by ‘very high’ glucose, this effect being enhanced by insulin, whereas in cells kept for 24 h in ‘high’ glucose, they are stimulated by both glucose and insulin. Elevated OEA and PEA levels are found in the blood of T2D patients. Reduced PEA levels in hypertrophic adipocytes might play a role in obesity‐related pro‐inflammatory states. In β‐cells and human blood, OEA and PEA are down‐ or up‐regulated under conditions of transient or chronic hyperglycaemia, respectively.
British Journal of Pharmacology (2007) 152, 676–690; doi:10.1038/sj.bjp.0707424; published online 20 August 2007 |
doi_str_mv | 10.1038/sj.bjp.0707424 |
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British Journal of Pharmacology (2007) 152, 676–690; doi:10.1038/sj.bjp.0707424; published online 20 August 2007</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0707424</identifier><identifier>PMID: 17704823</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>3T3 Cells ; Adipocytes - cytology ; Adipocytes - drug effects ; Adipocytes - metabolism ; Adult ; Aged ; Amides - blood ; Amides - metabolism ; anandamide ; Animals ; Arachidonic Acids - blood ; Arachidonic Acids - metabolism ; Diabetes Mellitus, Type 2 - blood ; Endocannabinoids ; Energy Metabolism - physiology ; Ethanolamines ; fat ; Female ; Humans ; Insulin-Secreting Cells - cytology ; Insulin-Secreting Cells - drug effects ; Insulin-Secreting Cells - metabolism ; Leptin - pharmacology ; lipolysis ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Models, Biological ; Obesity - blood ; Oleic Acids - blood ; Oleic Acids - metabolism ; oleylethanolamide ; Palmitic Acids - blood ; Palmitic Acids - metabolism ; palmitoylethanolamide ; pancreas ; Polyunsaturated Alkamides - blood ; Polyunsaturated Alkamides - metabolism ; PPAR gamma - agonists ; PPAR gamma - genetics ; PPAR gamma - metabolism ; Review Literature as Topic ; Reviews ; Structure-Activity Relationship</subject><ispartof>British journal of pharmacology, 2007-11, Vol.152 (5), p.676-690</ispartof><rights>2007 British Pharmacological Society</rights><rights>Copyright 2007, Nature Publishing Group 2007 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4317-108c004a6982a872112e77ce35530d9d26baf2b9e76627a839888ab451962f653</citedby><cites>FETCH-LOGICAL-c4317-108c004a6982a872112e77ce35530d9d26baf2b9e76627a839888ab451962f653</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190005/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190005/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17704823$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matias, I</creatorcontrib><creatorcontrib>Gonthier, M‐P</creatorcontrib><creatorcontrib>Petrosino, S</creatorcontrib><creatorcontrib>Docimo, L</creatorcontrib><creatorcontrib>Capasso, R</creatorcontrib><creatorcontrib>Hoareau, L</creatorcontrib><creatorcontrib>Monteleone, P</creatorcontrib><creatorcontrib>Roche, R</creatorcontrib><creatorcontrib>Izzo, A A</creatorcontrib><creatorcontrib>Di Marzo, V</creatorcontrib><title>Role and regulation of acylethanolamides in energy balance: focus on adipocytes and β‐cells</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>The endocannabinoid, arachidonoylethanolamide (AEA), and the peroxisome proliferator‐activated receptor (PPAR)‐α ligand, oleylethanolamide (OEA) produce opposite effects on lipogenesis. The regulation of OEA and its anti‐inflammatory congener, palmitoylethanolamide (PEA), in adipocytes and pancreatic β‐cells has not been investigated. We report here the results of studies on acylethanolamide regulation in these cells during obesity and hyperglycaemia, and provide an overview of acylethanolamide role in metabolic control. We analysed by liquid chromatography‐mass spectrometry OEA and PEA levels in: 1) mouse 3T3F442A adipocytes during insulin‐induced differentiation, 2) rat insulinoma RIN m5F β‐cells kept in ‘low’ or ‘high’ glucose, 3) adipose tissue and pancreas of mice with high fat diet‐induced obesity (DIO), and 4) in visceral fat or blood of obese or type 2 diabetes (T2D) patients. In adipocytes, OEA levels remain unchanged during differentiation, whereas those of PEA decrease significantly, and are under the negative control of both leptin and PPAR‐γ. PEA is significantly downregulated in subcutaneous adipose tissue of DIO mice. In RIN m5F insulinoma β‐cells, OEA and PEA levels are inhibited by ‘very high’ glucose, this effect being enhanced by insulin, whereas in cells kept for 24 h in ‘high’ glucose, they are stimulated by both glucose and insulin. Elevated OEA and PEA levels are found in the blood of T2D patients. Reduced PEA levels in hypertrophic adipocytes might play a role in obesity‐related pro‐inflammatory states. In β‐cells and human blood, OEA and PEA are down‐ or up‐regulated under conditions of transient or chronic hyperglycaemia, respectively.
British Journal of Pharmacology (2007) 152, 676–690; doi:10.1038/sj.bjp.0707424; published online 20 August 2007</description><subject>3T3 Cells</subject><subject>Adipocytes - cytology</subject><subject>Adipocytes - drug effects</subject><subject>Adipocytes - metabolism</subject><subject>Adult</subject><subject>Aged</subject><subject>Amides - blood</subject><subject>Amides - metabolism</subject><subject>anandamide</subject><subject>Animals</subject><subject>Arachidonic Acids - blood</subject><subject>Arachidonic Acids - metabolism</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Endocannabinoids</subject><subject>Energy Metabolism - physiology</subject><subject>Ethanolamines</subject><subject>fat</subject><subject>Female</subject><subject>Humans</subject><subject>Insulin-Secreting Cells - cytology</subject><subject>Insulin-Secreting Cells - drug effects</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>Leptin - pharmacology</subject><subject>lipolysis</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Middle Aged</subject><subject>Models, Biological</subject><subject>Obesity - blood</subject><subject>Oleic Acids - blood</subject><subject>Oleic Acids - metabolism</subject><subject>oleylethanolamide</subject><subject>Palmitic Acids - blood</subject><subject>Palmitic Acids - metabolism</subject><subject>palmitoylethanolamide</subject><subject>pancreas</subject><subject>Polyunsaturated Alkamides - blood</subject><subject>Polyunsaturated Alkamides - metabolism</subject><subject>PPAR gamma - agonists</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>Review Literature as Topic</subject><subject>Reviews</subject><subject>Structure-Activity Relationship</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkb9uFDEQhy0EIkegpUSu6O7wv117KZBIBAQpUhCCFmvWO3vxyWcf613QdjwCz5IHyUPwJPh0JyAV1RTzzTdj_wh5ytmKM2le5M2q3exWTDOthLpHFlzpellJw--TBWNMLzk35oQ8ynnDWGnq6iE54VozZYRckC8fU0AKsaMDrqcAo0-Rpp6CmwOO1xBTgK3vMFMfKUYc1jNtIUB0-JL2yU2ZlgHo_C65eSzYXnV78-vHT4ch5MfkQQ8h45NjPSWf3775dH6xvLx69_789eXSKcnLjcw4xhTUjRFgtOBcoNYOZVVJ1jWdqFvoRdugrmuhwcjGGAOtqnhTi76u5Cl5dfDupnaLncM4DhDsbvBbGGabwNu7neiv7Tp9s4I35Zf2gudHwZC-TphHu_V5_wSImKZsa6MUZ0IUcHUA3ZByHrD_s4Qzu4_E5o0tkdhjJGXg2b-n_cWPGRRAHIDvPuD8H509-3BRaS1_A143mpE</recordid><startdate>200711</startdate><enddate>200711</enddate><creator>Matias, I</creator><creator>Gonthier, M‐P</creator><creator>Petrosino, S</creator><creator>Docimo, L</creator><creator>Capasso, R</creator><creator>Hoareau, L</creator><creator>Monteleone, P</creator><creator>Roche, R</creator><creator>Izzo, A A</creator><creator>Di Marzo, V</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing Group</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>200711</creationdate><title>Role and regulation of acylethanolamides in energy balance: focus on adipocytes and β‐cells</title><author>Matias, I ; 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The regulation of OEA and its anti‐inflammatory congener, palmitoylethanolamide (PEA), in adipocytes and pancreatic β‐cells has not been investigated. We report here the results of studies on acylethanolamide regulation in these cells during obesity and hyperglycaemia, and provide an overview of acylethanolamide role in metabolic control. We analysed by liquid chromatography‐mass spectrometry OEA and PEA levels in: 1) mouse 3T3F442A adipocytes during insulin‐induced differentiation, 2) rat insulinoma RIN m5F β‐cells kept in ‘low’ or ‘high’ glucose, 3) adipose tissue and pancreas of mice with high fat diet‐induced obesity (DIO), and 4) in visceral fat or blood of obese or type 2 diabetes (T2D) patients. In adipocytes, OEA levels remain unchanged during differentiation, whereas those of PEA decrease significantly, and are under the negative control of both leptin and PPAR‐γ. PEA is significantly downregulated in subcutaneous adipose tissue of DIO mice. In RIN m5F insulinoma β‐cells, OEA and PEA levels are inhibited by ‘very high’ glucose, this effect being enhanced by insulin, whereas in cells kept for 24 h in ‘high’ glucose, they are stimulated by both glucose and insulin. Elevated OEA and PEA levels are found in the blood of T2D patients. Reduced PEA levels in hypertrophic adipocytes might play a role in obesity‐related pro‐inflammatory states. In β‐cells and human blood, OEA and PEA are down‐ or up‐regulated under conditions of transient or chronic hyperglycaemia, respectively.
British Journal of Pharmacology (2007) 152, 676–690; doi:10.1038/sj.bjp.0707424; published online 20 August 2007</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17704823</pmid><doi>10.1038/sj.bjp.0707424</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 3T3 Cells Adipocytes - cytology Adipocytes - drug effects Adipocytes - metabolism Adult Aged Amides - blood Amides - metabolism anandamide Animals Arachidonic Acids - blood Arachidonic Acids - metabolism Diabetes Mellitus, Type 2 - blood Endocannabinoids Energy Metabolism - physiology Ethanolamines fat Female Humans Insulin-Secreting Cells - cytology Insulin-Secreting Cells - drug effects Insulin-Secreting Cells - metabolism Leptin - pharmacology lipolysis Male Mice Mice, Inbred C57BL Middle Aged Models, Biological Obesity - blood Oleic Acids - blood Oleic Acids - metabolism oleylethanolamide Palmitic Acids - blood Palmitic Acids - metabolism palmitoylethanolamide pancreas Polyunsaturated Alkamides - blood Polyunsaturated Alkamides - metabolism PPAR gamma - agonists PPAR gamma - genetics PPAR gamma - metabolism Review Literature as Topic Reviews Structure-Activity Relationship |
title | Role and regulation of acylethanolamides in energy balance: focus on adipocytes and β‐cells |
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