Endothelial cell and platelet bioenergetics: effect of glucose and nutrient composition
It has been suggested that cells that are independent of insulin for glucose uptake, when exposed to high glucose or other nutrient concentrations, manifest enhanced mitochondrial substrate oxidation with consequent enhanced potential and generation of reactive oxygen species (ROS); a paradigm that...
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| description | It has been suggested that cells that are independent of insulin for glucose uptake, when exposed to high glucose or other nutrient concentrations, manifest enhanced mitochondrial substrate oxidation with consequent enhanced potential and generation of reactive oxygen species (ROS); a paradigm that could predispose to vascular complications of diabetes. Here we exposed bovine aortic endothelial (BAE) cells and human platelets to variable glucose and fatty acid concentrations. We then examined oxygen consumption and acidification rates using recently available technology in the form of an extracellular oxygen and proton flux analyzer. Acute or overnight exposure of confluent BAE cells to glucose concentrations from 5.5 to 25 mM did not enhance or change the rate of oxygen consumption (OCR) under basal conditions, during ATP synthesis, or under uncoupled conditions. Glucose also did not alter OCR in sub-confluent cells, in cells exposed to low serum, or in cells treated with added pyruvate. Likewise, overnight exposure to fatty acids of varying saturation had no such effects. Overnight exposure of BAE cells to low glucose concentration decreased maximal uncoupled respiration, but not basal or ATP related oxygen consumption. Labeled glucose oxidation to CO(2) increased, but only marginally after high glucose exposure while oleate oxidation to CO(2) decreased. Overnight exposure to linolenic acid, but not oleic or linoleic acid increased extracellular acidification consistent with enhanced glycolytic metabolism. We were unable to detect an increase in production of reactive oxygen species (ROS) from BAE cells exposed to high medium glucose. Like BAE cells, exposure of human platelets to glucose did not increase oxygen consumption. As opposed to BAE cells, platelet mitochondria demonstrate less respiratory reserve capacity (beyond that needed for basal metabolism). Our data do not support the concept that exposure to high glucose or fatty acids accelerates mitochondrial oxidative metabolism in endothelial cells or platelets. |
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Here we exposed bovine aortic endothelial (BAE) cells and human platelets to variable glucose and fatty acid concentrations. We then examined oxygen consumption and acidification rates using recently available technology in the form of an extracellular oxygen and proton flux analyzer. Acute or overnight exposure of confluent BAE cells to glucose concentrations from 5.5 to 25 mM did not enhance or change the rate of oxygen consumption (OCR) under basal conditions, during ATP synthesis, or under uncoupled conditions. Glucose also did not alter OCR in sub-confluent cells, in cells exposed to low serum, or in cells treated with added pyruvate. Likewise, overnight exposure to fatty acids of varying saturation had no such effects. Overnight exposure of BAE cells to low glucose concentration decreased maximal uncoupled respiration, but not basal or ATP related oxygen consumption. Labeled glucose oxidation to CO(2) increased, but only marginally after high glucose exposure while oleate oxidation to CO(2) decreased. Overnight exposure to linolenic acid, but not oleic or linoleic acid increased extracellular acidification consistent with enhanced glycolytic metabolism. We were unable to detect an increase in production of reactive oxygen species (ROS) from BAE cells exposed to high medium glucose. Like BAE cells, exposure of human platelets to glucose did not increase oxygen consumption. As opposed to BAE cells, platelet mitochondria demonstrate less respiratory reserve capacity (beyond that needed for basal metabolism). Our data do not support the concept that exposure to high glucose or fatty acids accelerates mitochondrial oxidative metabolism in endothelial cells or platelets.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0039430</identifier><identifier>PMID: 22745753</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acidification ; alpha-Linolenic Acid - pharmacology ; Amino acids ; Animals ; Aorta ; ATP ; Biochemistry ; Bioenergetics ; Biology ; Blood platelets ; Blood Platelets - drug effects ; Carbon dioxide ; Cardiovascular disease ; Cattle ; Cell Line ; Complications ; Composition effects ; Diabetes ; Diabetes mellitus ; Endocrinology ; Endothelial cells ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Endothelium ; Energy consumption ; Energy Metabolism - drug effects ; Exposure ; Fatty acids ; Glucose ; Glucose - pharmacology ; Glucose metabolism ; Glycolysis ; Human subjects ; Humans ; Insulin ; Internal medicine ; Kinases ; Linoleic acid ; Linolenic acid ; Linolenic acids ; Medicine ; Metabolism ; Mitochondria ; Mortality ; Nutrient concentrations ; Nutrient uptake ; Nutrients ; Oxidation ; Oxidative metabolism ; Oxygen ; Oxygen consumption ; Oxygen Consumption - drug effects ; Phosphorylation ; Platelets ; Proton flux ; Pyruvic acid ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reserve capacity ; Rodents</subject><ispartof>PloS one, 2012-06, Vol.7 (6), p.e39430-e39430</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012. This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. 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Labeled glucose oxidation to CO(2) increased, but only marginally after high glucose exposure while oleate oxidation to CO(2) decreased. Overnight exposure to linolenic acid, but not oleic or linoleic acid increased extracellular acidification consistent with enhanced glycolytic metabolism. We were unable to detect an increase in production of reactive oxygen species (ROS) from BAE cells exposed to high medium glucose. Like BAE cells, exposure of human platelets to glucose did not increase oxygen consumption. As opposed to BAE cells, platelet mitochondria demonstrate less respiratory reserve capacity (beyond that needed for basal metabolism). Our data do not support the concept that exposure to high glucose or fatty acids accelerates mitochondrial oxidative metabolism in endothelial cells or platelets.</description><subject>Acidification</subject><subject>alpha-Linolenic Acid - pharmacology</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Aorta</subject><subject>ATP</subject><subject>Biochemistry</subject><subject>Bioenergetics</subject><subject>Biology</subject><subject>Blood platelets</subject><subject>Blood Platelets - drug effects</subject><subject>Carbon dioxide</subject><subject>Cardiovascular disease</subject><subject>Cattle</subject><subject>Cell Line</subject><subject>Complications</subject><subject>Composition effects</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Endocrinology</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelium</subject><subject>Energy consumption</subject><subject>Energy Metabolism - 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Here we exposed bovine aortic endothelial (BAE) cells and human platelets to variable glucose and fatty acid concentrations. We then examined oxygen consumption and acidification rates using recently available technology in the form of an extracellular oxygen and proton flux analyzer. Acute or overnight exposure of confluent BAE cells to glucose concentrations from 5.5 to 25 mM did not enhance or change the rate of oxygen consumption (OCR) under basal conditions, during ATP synthesis, or under uncoupled conditions. Glucose also did not alter OCR in sub-confluent cells, in cells exposed to low serum, or in cells treated with added pyruvate. Likewise, overnight exposure to fatty acids of varying saturation had no such effects. Overnight exposure of BAE cells to low glucose concentration decreased maximal uncoupled respiration, but not basal or ATP related oxygen consumption. Labeled glucose oxidation to CO(2) increased, but only marginally after high glucose exposure while oleate oxidation to CO(2) decreased. Overnight exposure to linolenic acid, but not oleic or linoleic acid increased extracellular acidification consistent with enhanced glycolytic metabolism. We were unable to detect an increase in production of reactive oxygen species (ROS) from BAE cells exposed to high medium glucose. Like BAE cells, exposure of human platelets to glucose did not increase oxygen consumption. As opposed to BAE cells, platelet mitochondria demonstrate less respiratory reserve capacity (beyond that needed for basal metabolism). Our data do not support the concept that exposure to high glucose or fatty acids accelerates mitochondrial oxidative metabolism in endothelial cells or platelets.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22745753</pmid><doi>10.1371/journal.pone.0039430</doi><tpages>e39430</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Acidification alpha-Linolenic Acid - pharmacology Amino acids Animals Aorta ATP Biochemistry Bioenergetics Biology Blood platelets Blood Platelets - drug effects Carbon dioxide Cardiovascular disease Cattle Cell Line Complications Composition effects Diabetes Diabetes mellitus Endocrinology Endothelial cells Endothelial Cells - drug effects Endothelial Cells - metabolism Endothelium Energy consumption Energy Metabolism - drug effects Exposure Fatty acids Glucose Glucose - pharmacology Glucose metabolism Glycolysis Human subjects Humans Insulin Internal medicine Kinases Linoleic acid Linolenic acid Linolenic acids Medicine Metabolism Mitochondria Mortality Nutrient concentrations Nutrient uptake Nutrients Oxidation Oxidative metabolism Oxygen Oxygen consumption Oxygen Consumption - drug effects Phosphorylation Platelets Proton flux Pyruvic acid Reactive oxygen species Reactive Oxygen Species - metabolism Reserve capacity Rodents |
| title | Endothelial cell and platelet bioenergetics: effect of glucose and nutrient composition |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T20%3A08%3A54IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Endothelial%20cell%20and%20platelet%20bioenergetics:%20effect%20of%20glucose%20and%20nutrient%20composition&rft.jtitle=PloS%20one&rft.au=Fink,%20Brian%20D&rft.date=2012-06-22&rft.volume=7&rft.issue=6&rft.spage=e39430&rft.epage=e39430&rft.pages=e39430-e39430&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0039430&rft_dat=%3Cgale_plos_%3EA477051987%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1325027063&rft_id=info:pmid/22745753&rft_galeid=A477051987&rft_doaj_id=oai_doaj_org_article_8d4636f19da9407a85179165a467251a&rfr_iscdi=true |