Leptin Is a Growth Factor for Colonic Epithelial Cells
Background & Aims: Obesity increases the risk of colon cancer, whereas physical activity reduces the risk. Plasma levels of leptin increase in proportion to the level of obesity and are reduced by physical activity. Leptin acts as a growth factor for several cell types and thus may provide a bio...
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Veröffentlicht in: | Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 2001-07, Vol.121 (1), p.79-90 |
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container_title | Gastroenterology (New York, N.Y. 1943) |
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creator | Hardwick, James C.H. Van Den Brink, Gijs R. Offerhaus, G.J. Van Deventer, Sander J.H. Peppelenbosch, Maikel P. |
description | Background & Aims:
Obesity increases the risk of colon cancer, whereas physical activity reduces the risk. Plasma levels of leptin increase in proportion to the level of obesity and are reduced by physical activity. Leptin acts as a growth factor for several cell types and thus may provide a biological explanation for the observed epidemiological risk factors. The aim of this study was to investigate whether leptin is a growth factor for colonic epithelial cells.
Methods:
The presence of the leptin receptor in human colon cancer cell lines was assessed using reverse-transcription polymerase chain reaction and immunoblotting, and its presence in human colonic tissue was assessed by immunohistochemistry. The effects of leptin in vitro on HT29 cells were assessed by assessing p42/44 mitogen-activated protein kinase phosphorylation, thymidine incorporation, and cell numbers and in vivo in C57BL/6 mice by colonic bromodeoxyuridine incorporation.
Results:
The leptin receptor is expressed in human colon cancer cell lines and human colonic tissue. Stimulation with leptin leads to phosphorylation of p42/44 mitogen-activated protein kinase and increases proliferation in vitro and in vivo.
Conclusions:
Leptin is a growth factor in colonic epithelial cells and one that may provide a biological explanation for the observed associations between obesity, physical activity, and colon cancer. |
doi_str_mv | 10.1053/gast.2001.25490 |
format | Article |
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Obesity increases the risk of colon cancer, whereas physical activity reduces the risk. Plasma levels of leptin increase in proportion to the level of obesity and are reduced by physical activity. Leptin acts as a growth factor for several cell types and thus may provide a biological explanation for the observed epidemiological risk factors. The aim of this study was to investigate whether leptin is a growth factor for colonic epithelial cells.
Methods:
The presence of the leptin receptor in human colon cancer cell lines was assessed using reverse-transcription polymerase chain reaction and immunoblotting, and its presence in human colonic tissue was assessed by immunohistochemistry. The effects of leptin in vitro on HT29 cells were assessed by assessing p42/44 mitogen-activated protein kinase phosphorylation, thymidine incorporation, and cell numbers and in vivo in C57BL/6 mice by colonic bromodeoxyuridine incorporation.
Results:
The leptin receptor is expressed in human colon cancer cell lines and human colonic tissue. Stimulation with leptin leads to phosphorylation of p42/44 mitogen-activated protein kinase and increases proliferation in vitro and in vivo.
Conclusions:
Leptin is a growth factor in colonic epithelial cells and one that may provide a biological explanation for the observed associations between obesity, physical activity, and colon cancer.</description><identifier>ISSN: 0016-5085</identifier><identifier>EISSN: 1528-0012</identifier><identifier>DOI: 10.1053/gast.2001.25490</identifier><identifier>PMID: 11438496</identifier><identifier>CODEN: GASTAB</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adenocarcinoma - etiology ; Adenocarcinoma - metabolism ; Adenocarcinoma - pathology ; Animals ; Biological and medical sciences ; Bromodeoxyuridine - metabolism ; Carrier Proteins - drug effects ; Carrier Proteins - isolation & purification ; Colonic Neoplasms - etiology ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Epithelium - drug effects ; Epithelium - metabolism ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Growth Substances - pharmacology ; Humans ; Leptin - isolation & purification ; Leptin - pharmacology ; Medical sciences ; Mice ; Obesity - complications ; Protein Kinases - metabolism ; Receptors, Cell Surface ; Receptors, Leptin ; Reverse Transcriptase Polymerase Chain Reaction ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Thymidine - metabolism ; Tumor Cells, Cultured ; Tumors</subject><ispartof>Gastroenterology (New York, N.Y. 1943), 2001-07, Vol.121 (1), p.79-90</ispartof><rights>2001 The American Gastroenterological Association</rights><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-c0fd9b7cb86de27314b50dd6e83aef7b133f56c9feefc909222ec7a1971ff1473</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0016508501199580$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1055521$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11438496$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hardwick, James C.H.</creatorcontrib><creatorcontrib>Van Den Brink, Gijs R.</creatorcontrib><creatorcontrib>Offerhaus, G.J.</creatorcontrib><creatorcontrib>Van Deventer, Sander J.H.</creatorcontrib><creatorcontrib>Peppelenbosch, Maikel P.</creatorcontrib><title>Leptin Is a Growth Factor for Colonic Epithelial Cells</title><title>Gastroenterology (New York, N.Y. 1943)</title><addtitle>Gastroenterology</addtitle><description>Background & Aims:
Obesity increases the risk of colon cancer, whereas physical activity reduces the risk. Plasma levels of leptin increase in proportion to the level of obesity and are reduced by physical activity. Leptin acts as a growth factor for several cell types and thus may provide a biological explanation for the observed epidemiological risk factors. The aim of this study was to investigate whether leptin is a growth factor for colonic epithelial cells.
Methods:
The presence of the leptin receptor in human colon cancer cell lines was assessed using reverse-transcription polymerase chain reaction and immunoblotting, and its presence in human colonic tissue was assessed by immunohistochemistry. The effects of leptin in vitro on HT29 cells were assessed by assessing p42/44 mitogen-activated protein kinase phosphorylation, thymidine incorporation, and cell numbers and in vivo in C57BL/6 mice by colonic bromodeoxyuridine incorporation.
Results:
The leptin receptor is expressed in human colon cancer cell lines and human colonic tissue. Stimulation with leptin leads to phosphorylation of p42/44 mitogen-activated protein kinase and increases proliferation in vitro and in vivo.
Conclusions:
Leptin is a growth factor in colonic epithelial cells and one that may provide a biological explanation for the observed associations between obesity, physical activity, and colon cancer.</description><subject>Adenocarcinoma - etiology</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - pathology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bromodeoxyuridine - metabolism</subject><subject>Carrier Proteins - drug effects</subject><subject>Carrier Proteins - isolation & purification</subject><subject>Colonic Neoplasms - etiology</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Epithelium - drug effects</subject><subject>Epithelium - metabolism</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Growth Substances - pharmacology</subject><subject>Humans</subject><subject>Leptin - isolation & purification</subject><subject>Leptin - pharmacology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Obesity - complications</subject><subject>Protein Kinases - metabolism</subject><subject>Receptors, Cell Surface</subject><subject>Receptors, Leptin</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Thymidine - metabolism</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0016-5085</issn><issn>1528-0012</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kL1PwzAQxS0EoqUws6EMrGn9EcfxiKK2VKrEArPlOGdq5CaRHUD897i0EiwMpyedfu907yF0S_CcYM4WrzqOc4oxmVNeSHyGpoTTKk8Leo6mScqc44pP0FWMbxhjySpyiSaEFKwqZDlF5RaG0XXZJmY6W4f-c9xlK23GPmQ2Td37vnMmWw5u3IF32mc1eB-v0YXVPsLNSWfoZbV8rh_z7dN6Uz9sc1MIOeYG21Y2wjRV2QIVjBQNx21bQsU0WNEQxiwvjbQA1kgsKaVghCZSEGtJIdgMLY53TehjDGDVENxehy9FsDo0oA4NqEMD6qeB5Lg7Oob3Zg_tL3-KnID7E6Cj0d4G3RkX_9zlnFOSMHnEIMX7cBBUNA46A60LYEbV9u7fH74BWql2gw</recordid><startdate>20010701</startdate><enddate>20010701</enddate><creator>Hardwick, James C.H.</creator><creator>Van Den Brink, Gijs R.</creator><creator>Offerhaus, G.J.</creator><creator>Van Deventer, Sander J.H.</creator><creator>Peppelenbosch, Maikel P.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20010701</creationdate><title>Leptin Is a Growth Factor for Colonic Epithelial Cells</title><author>Hardwick, James C.H. ; Van Den Brink, Gijs R. ; Offerhaus, G.J. ; Van Deventer, Sander J.H. ; Peppelenbosch, Maikel P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c479t-c0fd9b7cb86de27314b50dd6e83aef7b133f56c9feefc909222ec7a1971ff1473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adenocarcinoma - etiology</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - pathology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bromodeoxyuridine - metabolism</topic><topic>Carrier Proteins - drug effects</topic><topic>Carrier Proteins - isolation & purification</topic><topic>Colonic Neoplasms - etiology</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colonic Neoplasms - pathology</topic><topic>Epithelium - drug effects</topic><topic>Epithelium - metabolism</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Growth Substances - pharmacology</topic><topic>Humans</topic><topic>Leptin - isolation & purification</topic><topic>Leptin - pharmacology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Obesity - complications</topic><topic>Protein Kinases - metabolism</topic><topic>Receptors, Cell Surface</topic><topic>Receptors, Leptin</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Thymidine - metabolism</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hardwick, James C.H.</creatorcontrib><creatorcontrib>Van Den Brink, Gijs R.</creatorcontrib><creatorcontrib>Offerhaus, G.J.</creatorcontrib><creatorcontrib>Van Deventer, Sander J.H.</creatorcontrib><creatorcontrib>Peppelenbosch, Maikel P.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hardwick, James C.H.</au><au>Van Den Brink, Gijs R.</au><au>Offerhaus, G.J.</au><au>Van Deventer, Sander J.H.</au><au>Peppelenbosch, Maikel P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leptin Is a Growth Factor for Colonic Epithelial Cells</atitle><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle><addtitle>Gastroenterology</addtitle><date>2001-07-01</date><risdate>2001</risdate><volume>121</volume><issue>1</issue><spage>79</spage><epage>90</epage><pages>79-90</pages><issn>0016-5085</issn><eissn>1528-0012</eissn><coden>GASTAB</coden><abstract>Background & Aims:
Obesity increases the risk of colon cancer, whereas physical activity reduces the risk. Plasma levels of leptin increase in proportion to the level of obesity and are reduced by physical activity. Leptin acts as a growth factor for several cell types and thus may provide a biological explanation for the observed epidemiological risk factors. The aim of this study was to investigate whether leptin is a growth factor for colonic epithelial cells.
Methods:
The presence of the leptin receptor in human colon cancer cell lines was assessed using reverse-transcription polymerase chain reaction and immunoblotting, and its presence in human colonic tissue was assessed by immunohistochemistry. The effects of leptin in vitro on HT29 cells were assessed by assessing p42/44 mitogen-activated protein kinase phosphorylation, thymidine incorporation, and cell numbers and in vivo in C57BL/6 mice by colonic bromodeoxyuridine incorporation.
Results:
The leptin receptor is expressed in human colon cancer cell lines and human colonic tissue. Stimulation with leptin leads to phosphorylation of p42/44 mitogen-activated protein kinase and increases proliferation in vitro and in vivo.
Conclusions:
Leptin is a growth factor in colonic epithelial cells and one that may provide a biological explanation for the observed associations between obesity, physical activity, and colon cancer.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>11438496</pmid><doi>10.1053/gast.2001.25490</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adenocarcinoma - etiology Adenocarcinoma - metabolism Adenocarcinoma - pathology Animals Biological and medical sciences Bromodeoxyuridine - metabolism Carrier Proteins - drug effects Carrier Proteins - isolation & purification Colonic Neoplasms - etiology Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Epithelium - drug effects Epithelium - metabolism Female Gastroenterology. Liver. Pancreas. Abdomen Growth Substances - pharmacology Humans Leptin - isolation & purification Leptin - pharmacology Medical sciences Mice Obesity - complications Protein Kinases - metabolism Receptors, Cell Surface Receptors, Leptin Reverse Transcriptase Polymerase Chain Reaction Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Thymidine - metabolism Tumor Cells, Cultured Tumors |
title | Leptin Is a Growth Factor for Colonic Epithelial Cells |
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