Hyperglycaemia and apoptosis of microglial cells in human septic shock
The effect of hyperglycaemia on the brain cells of septic shock patients is unknown. The objective of this study was to evaluate the relationship between hyperglycaemia and apoptosis in the brains of septic shock patients. In a prospective study of 17 patients who died from septic shock, hippocampal...
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| Veröffentlicht in: | Critical care (London, England) England), 2011-01, Vol.15 (3), p.R131-R131, Article R131 |
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| creator | Polito, Andrea Brouland, Jean-Philippe Porcher, Raphael Sonneville, Romain Siami, Shidasp Stevens, Robert D Guidoux, Céline Maxime, Virginie de la Grandmaison, Geoffroy Lorin Chrétien, Fabrice C Gray, Françoise Annane, Djillali Sharshar, Tarek |
| description | The effect of hyperglycaemia on the brain cells of septic shock patients is unknown. The objective of this study was to evaluate the relationship between hyperglycaemia and apoptosis in the brains of septic shock patients.
In a prospective study of 17 patients who died from septic shock, hippocampal tissue was assessed for neuronal ischaemia, neuronal and microglial apoptosis, neuronal Glucose Transporter (GLUT) 4, endothelial inducible Nitric Oxide Synthase (iNOS), microglial GLUT5 expression, microglial and astrocyte activation. Blood glucose (BG) was recorded five times a day from ICU admission to death. Hyperglycaemia was defined as a BG 200 mg/dL g/l and the area under the BG curve (AUBGC) > 2 g/l was assessed.
Median BG over ICU stay was 2.2 g/l. Neuronal apoptosis was correlated with endothelial iNOS expression (rho = 0.68, P = 0.04), while microglial apoptosis was associated with AUBGC > 2 g/l (rho = 0.70; P = 0.002). Neuronal and microglial apoptosis correlated with each other (rho = 0.69, P = 0.006), but neither correlated with the duration of septic shock, nor with GLUT4 and 5 expression. Neuronal apoptosis and ischaemia tended to correlate with duration of hypotension.
In patients with septic shock, neuronal apoptosis is rather associated with iNOS expression and microglial apoptosis with hyperglycaemia, possibly because GLUT5 is not downregulated. These data provide a mechanistic basis for understanding the neuroprotective effects of glycemic control. |
| doi_str_mv | 10.1186/cc10244 |
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In a prospective study of 17 patients who died from septic shock, hippocampal tissue was assessed for neuronal ischaemia, neuronal and microglial apoptosis, neuronal Glucose Transporter (GLUT) 4, endothelial inducible Nitric Oxide Synthase (iNOS), microglial GLUT5 expression, microglial and astrocyte activation. Blood glucose (BG) was recorded five times a day from ICU admission to death. Hyperglycaemia was defined as a BG 200 mg/dL g/l and the area under the BG curve (AUBGC) > 2 g/l was assessed.
Median BG over ICU stay was 2.2 g/l. Neuronal apoptosis was correlated with endothelial iNOS expression (rho = 0.68, P = 0.04), while microglial apoptosis was associated with AUBGC > 2 g/l (rho = 0.70; P = 0.002). Neuronal and microglial apoptosis correlated with each other (rho = 0.69, P = 0.006), but neither correlated with the duration of septic shock, nor with GLUT4 and 5 expression. Neuronal apoptosis and ischaemia tended to correlate with duration of hypotension.
In patients with septic shock, neuronal apoptosis is rather associated with iNOS expression and microglial apoptosis with hyperglycaemia, possibly because GLUT5 is not downregulated. These data provide a mechanistic basis for understanding the neuroprotective effects of glycemic control.</description><identifier>ISSN: 1364-8535</identifier><identifier>EISSN: 1466-609X</identifier><identifier>EISSN: 1364-8535</identifier><identifier>DOI: 10.1186/cc10244</identifier><identifier>PMID: 21612615</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Aged ; Apoptosis ; Blood Glucose - analysis ; Brain - metabolism ; Brain - pathology ; Female ; Health aspects ; Human health and pathology ; Humans ; Hyperglycemia ; Life Sciences ; Male ; Microglia - metabolism ; Microglia - pathology ; Middle Aged ; Patient outcomes ; Physiological aspects ; Prospective Studies ; Risk factors ; Septic shock ; Shock, Septic - metabolism ; Shock, Septic - pathology ; Tissues and Organs</subject><ispartof>Critical care (London, England), 2011-01, Vol.15 (3), p.R131-R131, Article R131</ispartof><rights>COPYRIGHT 2011 BioMed Central Ltd.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>Copyright ©2011 Polito et al.; licensee BioMed Central Ltd. 2011 Polito et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b590t-5476a99c709ffaa6acdc49f34c95f7634b31cf5cfda76bdead67a57e9955c2283</citedby><cites>FETCH-LOGICAL-b590t-5476a99c709ffaa6acdc49f34c95f7634b31cf5cfda76bdead67a57e9955c2283</cites><orcidid>0000-0001-6805-8944</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/PMC3218997/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3218997/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21612615$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://pasteur.hal.science/pasteur-00629084$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Polito, Andrea</creatorcontrib><creatorcontrib>Brouland, Jean-Philippe</creatorcontrib><creatorcontrib>Porcher, Raphael</creatorcontrib><creatorcontrib>Sonneville, Romain</creatorcontrib><creatorcontrib>Siami, Shidasp</creatorcontrib><creatorcontrib>Stevens, Robert D</creatorcontrib><creatorcontrib>Guidoux, Céline</creatorcontrib><creatorcontrib>Maxime, Virginie</creatorcontrib><creatorcontrib>de la Grandmaison, Geoffroy Lorin</creatorcontrib><creatorcontrib>Chrétien, Fabrice C</creatorcontrib><creatorcontrib>Gray, Françoise</creatorcontrib><creatorcontrib>Annane, Djillali</creatorcontrib><creatorcontrib>Sharshar, Tarek</creatorcontrib><title>Hyperglycaemia and apoptosis of microglial cells in human septic shock</title><title>Critical care (London, England)</title><addtitle>Crit Care</addtitle><description>The effect of hyperglycaemia on the brain cells of septic shock patients is unknown. The objective of this study was to evaluate the relationship between hyperglycaemia and apoptosis in the brains of septic shock patients.
In a prospective study of 17 patients who died from septic shock, hippocampal tissue was assessed for neuronal ischaemia, neuronal and microglial apoptosis, neuronal Glucose Transporter (GLUT) 4, endothelial inducible Nitric Oxide Synthase (iNOS), microglial GLUT5 expression, microglial and astrocyte activation. Blood glucose (BG) was recorded five times a day from ICU admission to death. Hyperglycaemia was defined as a BG 200 mg/dL g/l and the area under the BG curve (AUBGC) > 2 g/l was assessed.
Median BG over ICU stay was 2.2 g/l. Neuronal apoptosis was correlated with endothelial iNOS expression (rho = 0.68, P = 0.04), while microglial apoptosis was associated with AUBGC > 2 g/l (rho = 0.70; P = 0.002). Neuronal and microglial apoptosis correlated with each other (rho = 0.69, P = 0.006), but neither correlated with the duration of septic shock, nor with GLUT4 and 5 expression. Neuronal apoptosis and ischaemia tended to correlate with duration of hypotension.
In patients with septic shock, neuronal apoptosis is rather associated with iNOS expression and microglial apoptosis with hyperglycaemia, possibly because GLUT5 is not downregulated. These data provide a mechanistic basis for understanding the neuroprotective effects of glycemic control.</description><subject>Aged</subject><subject>Apoptosis</subject><subject>Blood Glucose - analysis</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Female</subject><subject>Health aspects</subject><subject>Human health and pathology</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Microglia - metabolism</subject><subject>Microglia - pathology</subject><subject>Middle Aged</subject><subject>Patient outcomes</subject><subject>Physiological aspects</subject><subject>Prospective Studies</subject><subject>Risk factors</subject><subject>Septic shock</subject><subject>Shock, Septic - metabolism</subject><subject>Shock, Septic - pathology</subject><subject>Tissues and Organs</subject><issn>1364-8535</issn><issn>1466-609X</issn><issn>1364-8535</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1Uk2LFDEUDKK46yr-Awl48NRrvtPxIAyL6wgDXhS8hdfpZCba3Wk73Qvz780447IjSg4JeVX1ilcPoZeUXFNaq7fOUcKEeIQuqVCqUsR8e1zeXImqllxeoGc5fyeE6lrxp-iCUUWZovIS3a73o5-23d6B7yNgGFoMYxrnlGPGKeA-uiltuwgddr7rMo4D3i09DDj7cY4O511yP56jJwG67F-c7iv09fbDl5t1tfn88dPNalM10pC5kkIrMMZpYkIAUOBaJ0zgwhkZtOKi4dQF6UILWjWth1ZpkNobI6VjrOZX6P1Rd1ya3rfOD_MEnR2n2MO0twmiPa8McWe36c5yRmtjdBGojgK7v2jr1caOkGe_TJYQxQypxR0t-HdHfBPTfxqeV1zq7SmNQn5zcjuln4vPs-1jPkwRBp-WbGttlFZSHmy9PiK30Hkbh5CKmDug7YopRo2Sv_Wu_4Eqpy3ZuTT4EMv_GeFkoGSY8-TDvXFK7GFxHlh99XCw97g_m8J_AcVdvyk</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Polito, Andrea</creator><creator>Brouland, Jean-Philippe</creator><creator>Porcher, Raphael</creator><creator>Sonneville, Romain</creator><creator>Siami, Shidasp</creator><creator>Stevens, Robert D</creator><creator>Guidoux, Céline</creator><creator>Maxime, Virginie</creator><creator>de la Grandmaison, Geoffroy Lorin</creator><creator>Chrétien, Fabrice C</creator><creator>Gray, Françoise</creator><creator>Annane, Djillali</creator><creator>Sharshar, Tarek</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6805-8944</orcidid></search><sort><creationdate>20110101</creationdate><title>Hyperglycaemia and apoptosis of microglial cells in human septic shock</title><author>Polito, Andrea ; Brouland, Jean-Philippe ; Porcher, Raphael ; Sonneville, Romain ; Siami, Shidasp ; Stevens, Robert D ; Guidoux, Céline ; Maxime, Virginie ; de la Grandmaison, Geoffroy Lorin ; Chrétien, Fabrice C ; Gray, Françoise ; Annane, Djillali ; Sharshar, Tarek</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b590t-5476a99c709ffaa6acdc49f34c95f7634b31cf5cfda76bdead67a57e9955c2283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Aged</topic><topic>Apoptosis</topic><topic>Blood Glucose - analysis</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Female</topic><topic>Health aspects</topic><topic>Human health and pathology</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Microglia - metabolism</topic><topic>Microglia - pathology</topic><topic>Middle Aged</topic><topic>Patient outcomes</topic><topic>Physiological aspects</topic><topic>Prospective Studies</topic><topic>Risk factors</topic><topic>Septic shock</topic><topic>Shock, Septic - metabolism</topic><topic>Shock, Septic - pathology</topic><topic>Tissues and Organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Polito, Andrea</creatorcontrib><creatorcontrib>Brouland, Jean-Philippe</creatorcontrib><creatorcontrib>Porcher, Raphael</creatorcontrib><creatorcontrib>Sonneville, Romain</creatorcontrib><creatorcontrib>Siami, Shidasp</creatorcontrib><creatorcontrib>Stevens, Robert D</creatorcontrib><creatorcontrib>Guidoux, Céline</creatorcontrib><creatorcontrib>Maxime, Virginie</creatorcontrib><creatorcontrib>de la Grandmaison, Geoffroy Lorin</creatorcontrib><creatorcontrib>Chrétien, Fabrice C</creatorcontrib><creatorcontrib>Gray, Françoise</creatorcontrib><creatorcontrib>Annane, Djillali</creatorcontrib><creatorcontrib>Sharshar, Tarek</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Critical care (London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Polito, Andrea</au><au>Brouland, Jean-Philippe</au><au>Porcher, Raphael</au><au>Sonneville, Romain</au><au>Siami, Shidasp</au><au>Stevens, Robert D</au><au>Guidoux, Céline</au><au>Maxime, Virginie</au><au>de la Grandmaison, Geoffroy Lorin</au><au>Chrétien, Fabrice C</au><au>Gray, Françoise</au><au>Annane, Djillali</au><au>Sharshar, Tarek</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperglycaemia and apoptosis of microglial cells in human septic shock</atitle><jtitle>Critical care (London, England)</jtitle><addtitle>Crit Care</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>15</volume><issue>3</issue><spage>R131</spage><epage>R131</epage><pages>R131-R131</pages><artnum>R131</artnum><issn>1364-8535</issn><eissn>1466-609X</eissn><eissn>1364-8535</eissn><abstract>The effect of hyperglycaemia on the brain cells of septic shock patients is unknown. The objective of this study was to evaluate the relationship between hyperglycaemia and apoptosis in the brains of septic shock patients.
In a prospective study of 17 patients who died from septic shock, hippocampal tissue was assessed for neuronal ischaemia, neuronal and microglial apoptosis, neuronal Glucose Transporter (GLUT) 4, endothelial inducible Nitric Oxide Synthase (iNOS), microglial GLUT5 expression, microglial and astrocyte activation. Blood glucose (BG) was recorded five times a day from ICU admission to death. Hyperglycaemia was defined as a BG 200 mg/dL g/l and the area under the BG curve (AUBGC) > 2 g/l was assessed.
Median BG over ICU stay was 2.2 g/l. Neuronal apoptosis was correlated with endothelial iNOS expression (rho = 0.68, P = 0.04), while microglial apoptosis was associated with AUBGC > 2 g/l (rho = 0.70; P = 0.002). Neuronal and microglial apoptosis correlated with each other (rho = 0.69, P = 0.006), but neither correlated with the duration of septic shock, nor with GLUT4 and 5 expression. Neuronal apoptosis and ischaemia tended to correlate with duration of hypotension.
In patients with septic shock, neuronal apoptosis is rather associated with iNOS expression and microglial apoptosis with hyperglycaemia, possibly because GLUT5 is not downregulated. These data provide a mechanistic basis for understanding the neuroprotective effects of glycemic control.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>21612615</pmid><doi>10.1186/cc10244</doi><orcidid>https://orcid.org/0000-0001-6805-8944</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Apoptosis Blood Glucose - analysis Brain - metabolism Brain - pathology Female Health aspects Human health and pathology Humans Hyperglycemia Life Sciences Male Microglia - metabolism Microglia - pathology Middle Aged Patient outcomes Physiological aspects Prospective Studies Risk factors Septic shock Shock, Septic - metabolism Shock, Septic - pathology Tissues and Organs |
| title | Hyperglycaemia and apoptosis of microglial cells in human septic shock |
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