Chronic exposure to Low dose bacterial lipopolysaccharide inhibits leptin signaling in vagal afferent neurons
Abstract Bacterially derived factors are implicated in the causation and persistence of obesity. Ingestion of a high fat diet in rodents and obesity in human subjects is associated with chronic elevation of low plasma levels of lipopolysaccharide (LPS), a breakdown product of Gram-negative bacteria....
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| Veröffentlicht in: | Physiology & behavior 2015-02, Vol.139, p.188-194 |
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| creator | de La Serre, Claire B de Lartigue, Guillaume Raybould, Helen E |
| description | Abstract Bacterially derived factors are implicated in the causation and persistence of obesity. Ingestion of a high fat diet in rodents and obesity in human subjects is associated with chronic elevation of low plasma levels of lipopolysaccharide (LPS), a breakdown product of Gram-negative bacteria. The terminals of vagal afferent neurons are positioned within the gut mucosa to convey information from the gut to the brain to regulate food intake and are responsive to LPS. We hypothesized that chronic elevation of LPS could alter vagal afferent signaling. We surgically implanted osmotic mini-pumps that delivered a constant, low-dose of LPS into the intraperitoneal cavity of rats (12.5 μg/kg/hr for 6 weeks). LPS-treated rats developed hyperphagia and showed marked changes in vagal afferent neuron function. Chronic LPS treatment reduced vagal afferent leptin signaling, characterized by a decrease in leptin-induced STAT3 phosphorylation. In addition, LPS treatment decreased cholecystokinin-induced satiety. There was no alteration in leptin signaling in the hypothalamus. These findings offer a mechanism by which a change in gut microflora can promote hyperphagia, possibly leading to obesity. |
| doi_str_mv | 10.1016/j.physbeh.2014.10.032 |
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Ingestion of a high fat diet in rodents and obesity in human subjects is associated with chronic elevation of low plasma levels of lipopolysaccharide (LPS), a breakdown product of Gram-negative bacteria. The terminals of vagal afferent neurons are positioned within the gut mucosa to convey information from the gut to the brain to regulate food intake and are responsive to LPS. We hypothesized that chronic elevation of LPS could alter vagal afferent signaling. We surgically implanted osmotic mini-pumps that delivered a constant, low-dose of LPS into the intraperitoneal cavity of rats (12.5 μg/kg/hr for 6 weeks). LPS-treated rats developed hyperphagia and showed marked changes in vagal afferent neuron function. Chronic LPS treatment reduced vagal afferent leptin signaling, characterized by a decrease in leptin-induced STAT3 phosphorylation. In addition, LPS treatment decreased cholecystokinin-induced satiety. There was no alteration in leptin signaling in the hypothalamus. These findings offer a mechanism by which a change in gut microflora can promote hyperphagia, possibly leading to obesity.</description><identifier>ISSN: 0031-9384</identifier><identifier>EISSN: 1873-507X</identifier><identifier>DOI: 10.1016/j.physbeh.2014.10.032</identifier><identifier>PMID: 25446227</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>altitude ; Animals ; Bacteria ; Blotting, Western ; chronic exposure ; digestive tract mucosa ; Eating - physiology ; food intake ; Gram-negative bacteria ; high fat diet ; humans ; Hyperphagia - physiopathology ; hypothalamus ; Immunohistochemistry ; ingestion ; intestinal microorganisms ; leptin ; Leptin - metabolism ; lipopolysaccharides ; Lipopolysaccharides - toxicity ; Male ; metabolic endotoxemia ; Neurons, Afferent - physiology ; Nodose Ganglion - physiopathology ; obesity ; overeating ; Peroxidase - metabolism ; phosphorylation ; Psychiatry ; rats ; Rats, Wistar ; Satiation - physiology ; satiety ; sensory neurons ; Sincalide - administration & dosage ; Sincalide - metabolism ; suppressor of cytokine signaling 3 ; toll-like receptor 4 ; Vagal afferent neurons ; Weight Gain - physiology</subject><ispartof>Physiology & behavior, 2015-02, Vol.139, p.188-194</ispartof><rights>2014</rights><rights>Copyright © 2014. Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c654t-2938ba0f21870dc816d19d77af3b426b994b197daf1338341bdf0d101db4ffc23</citedby><cites>FETCH-LOGICAL-c654t-2938ba0f21870dc816d19d77af3b426b994b197daf1338341bdf0d101db4ffc23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0031938414005095$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25446227$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de La Serre, Claire B</creatorcontrib><creatorcontrib>de Lartigue, Guillaume</creatorcontrib><creatorcontrib>Raybould, Helen E</creatorcontrib><title>Chronic exposure to Low dose bacterial lipopolysaccharide inhibits leptin signaling in vagal afferent neurons</title><title>Physiology & behavior</title><addtitle>Physiol Behav</addtitle><description>Abstract Bacterially derived factors are implicated in the causation and persistence of obesity. Ingestion of a high fat diet in rodents and obesity in human subjects is associated with chronic elevation of low plasma levels of lipopolysaccharide (LPS), a breakdown product of Gram-negative bacteria. The terminals of vagal afferent neurons are positioned within the gut mucosa to convey information from the gut to the brain to regulate food intake and are responsive to LPS. We hypothesized that chronic elevation of LPS could alter vagal afferent signaling. We surgically implanted osmotic mini-pumps that delivered a constant, low-dose of LPS into the intraperitoneal cavity of rats (12.5 μg/kg/hr for 6 weeks). LPS-treated rats developed hyperphagia and showed marked changes in vagal afferent neuron function. Chronic LPS treatment reduced vagal afferent leptin signaling, characterized by a decrease in leptin-induced STAT3 phosphorylation. In addition, LPS treatment decreased cholecystokinin-induced satiety. There was no alteration in leptin signaling in the hypothalamus. These findings offer a mechanism by which a change in gut microflora can promote hyperphagia, possibly leading to obesity.</description><subject>altitude</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Blotting, Western</subject><subject>chronic exposure</subject><subject>digestive tract mucosa</subject><subject>Eating - physiology</subject><subject>food intake</subject><subject>Gram-negative bacteria</subject><subject>high fat diet</subject><subject>humans</subject><subject>Hyperphagia - physiopathology</subject><subject>hypothalamus</subject><subject>Immunohistochemistry</subject><subject>ingestion</subject><subject>intestinal microorganisms</subject><subject>leptin</subject><subject>Leptin - metabolism</subject><subject>lipopolysaccharides</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Male</subject><subject>metabolic endotoxemia</subject><subject>Neurons, Afferent - physiology</subject><subject>Nodose Ganglion - physiopathology</subject><subject>obesity</subject><subject>overeating</subject><subject>Peroxidase - metabolism</subject><subject>phosphorylation</subject><subject>Psychiatry</subject><subject>rats</subject><subject>Rats, Wistar</subject><subject>Satiation - physiology</subject><subject>satiety</subject><subject>sensory neurons</subject><subject>Sincalide - administration & dosage</subject><subject>Sincalide - metabolism</subject><subject>suppressor of cytokine signaling 3</subject><subject>toll-like receptor 4</subject><subject>Vagal afferent neurons</subject><subject>Weight Gain - physiology</subject><issn>0031-9384</issn><issn>1873-507X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUk2P0zAQjRCILQs_AeQjl5TxR74ui1DFl1SJAyBxsxx70ri4cbCTLv33OGpZAZfFF0szb968mXlZ9pzCmgItX-3XY3-KLfZrBlSk2Bo4e5CtaF3xvIDq28NsBcBp3vBaXGVPYtxDelzwx9kVK4QoGatW2WHTBz9YTfDn6OMckEyebP0tMT4iaZWeMFjliLOjH707RaV1r4I1SOzQ29ZOkTgcJzuQaHeDcnbYpQw5ql2qUl2HAYeJDDinNvFp9qhTLuKzy3-dfX339svmQ7799P7j5s0212Uhppwlza2CjqVhwOialoY2pqpUx1vByrZpREubyqiOcl5zQVvTgUlrMa3oOs34dXZz5h3n9oBGJwlBOTkGe1DhJL2y8u_MYHu580cpCsahKhLBywtB8D9mjJM82KjROTWgn6OktSjTKnlT3g8tS-BNwf6HtRTAOQgQCVqcoTr4GAN2d-IpyMUAci8vBpCLAZZwMkCqe_Hn5HdVvy-eAK_PAEz7P1oMMmqLg0ZjA-pJGm_vbXHzD4NOV7daue94wrj3c0g-SNPIyCTIz4sLFxNSAVBAU_BfrX7bsA</recordid><startdate>20150201</startdate><enddate>20150201</enddate><creator>de La Serre, Claire B</creator><creator>de Lartigue, Guillaume</creator><creator>Raybould, Helen E</creator><general>Elsevier Inc</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>7QG</scope><scope>7QL</scope><scope>7TK</scope><scope>C1K</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20150201</creationdate><title>Chronic exposure to Low dose bacterial lipopolysaccharide inhibits leptin signaling in vagal afferent neurons</title><author>de La Serre, Claire B ; de Lartigue, Guillaume ; Raybould, Helen E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c654t-2938ba0f21870dc816d19d77af3b426b994b197daf1338341bdf0d101db4ffc23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>altitude</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Blotting, Western</topic><topic>chronic exposure</topic><topic>digestive tract mucosa</topic><topic>Eating - physiology</topic><topic>food intake</topic><topic>Gram-negative bacteria</topic><topic>high fat diet</topic><topic>humans</topic><topic>Hyperphagia - physiopathology</topic><topic>hypothalamus</topic><topic>Immunohistochemistry</topic><topic>ingestion</topic><topic>intestinal microorganisms</topic><topic>leptin</topic><topic>Leptin - metabolism</topic><topic>lipopolysaccharides</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Male</topic><topic>metabolic endotoxemia</topic><topic>Neurons, Afferent - physiology</topic><topic>Nodose Ganglion - physiopathology</topic><topic>obesity</topic><topic>overeating</topic><topic>Peroxidase - metabolism</topic><topic>phosphorylation</topic><topic>Psychiatry</topic><topic>rats</topic><topic>Rats, Wistar</topic><topic>Satiation - physiology</topic><topic>satiety</topic><topic>sensory neurons</topic><topic>Sincalide - administration & dosage</topic><topic>Sincalide - metabolism</topic><topic>suppressor of cytokine signaling 3</topic><topic>toll-like receptor 4</topic><topic>Vagal afferent neurons</topic><topic>Weight Gain - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de La Serre, Claire B</creatorcontrib><creatorcontrib>de Lartigue, Guillaume</creatorcontrib><creatorcontrib>Raybould, Helen E</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Neurosciences Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Physiology & behavior</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de La Serre, Claire B</au><au>de Lartigue, Guillaume</au><au>Raybould, Helen E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic exposure to Low dose bacterial lipopolysaccharide inhibits leptin signaling in vagal afferent neurons</atitle><jtitle>Physiology & behavior</jtitle><addtitle>Physiol Behav</addtitle><date>2015-02-01</date><risdate>2015</risdate><volume>139</volume><spage>188</spage><epage>194</epage><pages>188-194</pages><issn>0031-9384</issn><eissn>1873-507X</eissn><abstract>Abstract Bacterially derived factors are implicated in the causation and persistence of obesity. Ingestion of a high fat diet in rodents and obesity in human subjects is associated with chronic elevation of low plasma levels of lipopolysaccharide (LPS), a breakdown product of Gram-negative bacteria. The terminals of vagal afferent neurons are positioned within the gut mucosa to convey information from the gut to the brain to regulate food intake and are responsive to LPS. We hypothesized that chronic elevation of LPS could alter vagal afferent signaling. We surgically implanted osmotic mini-pumps that delivered a constant, low-dose of LPS into the intraperitoneal cavity of rats (12.5 μg/kg/hr for 6 weeks). LPS-treated rats developed hyperphagia and showed marked changes in vagal afferent neuron function. Chronic LPS treatment reduced vagal afferent leptin signaling, characterized by a decrease in leptin-induced STAT3 phosphorylation. In addition, LPS treatment decreased cholecystokinin-induced satiety. There was no alteration in leptin signaling in the hypothalamus. 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| subjects | altitude Animals Bacteria Blotting, Western chronic exposure digestive tract mucosa Eating - physiology food intake Gram-negative bacteria high fat diet humans Hyperphagia - physiopathology hypothalamus Immunohistochemistry ingestion intestinal microorganisms leptin Leptin - metabolism lipopolysaccharides Lipopolysaccharides - toxicity Male metabolic endotoxemia Neurons, Afferent - physiology Nodose Ganglion - physiopathology obesity overeating Peroxidase - metabolism phosphorylation Psychiatry rats Rats, Wistar Satiation - physiology satiety sensory neurons Sincalide - administration & dosage Sincalide - metabolism suppressor of cytokine signaling 3 toll-like receptor 4 Vagal afferent neurons Weight Gain - physiology |
| title | Chronic exposure to Low dose bacterial lipopolysaccharide inhibits leptin signaling in vagal afferent neurons |
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