Perturbations of triglycerides but not of cholesterol metabolism are prevented by anti-tumour necrosis factor treatment in rats bearing an ascites hepatoma (Yoshida AH-130)
Rats transplanted with the ascites hepatoma Yoshida AH-130 developed a severely progressive cachexia, characterised by marked alterations in protein and lipid metabolism. In particular, high levels of serum triglycerides and free fatty acids were associated with altered levels and distribution of pl...
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Veröffentlicht in: | British journal of cancer 1995-11, Vol.72 (5), p.1138-1143 |
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description | Rats transplanted with the ascites hepatoma Yoshida AH-130 developed a severely progressive cachexia, characterised by marked alterations in protein and lipid metabolism. In particular, high levels of serum triglycerides and free fatty acids were associated with altered levels and distribution of plasma cholesterol, with increased total and very low-density lipoprotein-low-density lipoprotein (VLDL-LDL) cholesterol and reduced high-density lipoprotein (HDL) cholesterol. The tumour cells showed high rates of cholesterol synthesis and elevated content of free and esterified cholesterol, whereas total cholesterol synthesis was reduced in the host liver. To determine whether these perturbations could be related to the elevation of tumour necrosis factor alpha (TNF-alpha) previously shown in the AH-130 bearers (Tessitore L, Costelli P, Baccino FM 1993, Br J Cancer, 67, 15-23), either anti-TNF polyclonal antibodies or non-immune IgGs were injected daily after tumour transplantation. The anti-TNF treatment neither affected tumour growth nor prevented the serum cholesterol changes, while attenuating the hypertriglyceridaemia and the elevated serum free fatty acid levels. These data indicate that TNF does not appear to be directly involved in the altered cholesterol metabolism in AH-130 hosts, thus supporting the view that cholesterol metabolism and lipid metabolism are regulated differently during tumour growth. |
doi_str_mv | 10.1038/bjc.1995.477 |
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In particular, high levels of serum triglycerides and free fatty acids were associated with altered levels and distribution of plasma cholesterol, with increased total and very low-density lipoprotein-low-density lipoprotein (VLDL-LDL) cholesterol and reduced high-density lipoprotein (HDL) cholesterol. The tumour cells showed high rates of cholesterol synthesis and elevated content of free and esterified cholesterol, whereas total cholesterol synthesis was reduced in the host liver. To determine whether these perturbations could be related to the elevation of tumour necrosis factor alpha (TNF-alpha) previously shown in the AH-130 bearers (Tessitore L, Costelli P, Baccino FM 1993, Br J Cancer, 67, 15-23), either anti-TNF polyclonal antibodies or non-immune IgGs were injected daily after tumour transplantation. The anti-TNF treatment neither affected tumour growth nor prevented the serum cholesterol changes, while attenuating the hypertriglyceridaemia and the elevated serum free fatty acid levels. These data indicate that TNF does not appear to be directly involved in the altered cholesterol metabolism in AH-130 hosts, thus supporting the view that cholesterol metabolism and lipid metabolism are regulated differently during tumour growth.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/bjc.1995.477</identifier><identifier>PMID: 7577459</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animal tumors. Experimental tumors ; Animals ; Antibodies, Monoclonal - therapeutic use ; Ascites ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Cachexia - etiology ; Cachexia - metabolism ; Cancer Research ; Cholesterol - metabolism ; Cholesterol, HDL - metabolism ; Chromatography, High Pressure Liquid ; Drug Resistance ; Epidemiology ; Experimental digestive system and abdominal tumors ; experimental-oncology ; Immunization, Passive ; Lipoproteins - blood ; Liver - metabolism ; Liver Neoplasms, Experimental - complications ; Liver Neoplasms, Experimental - metabolism ; Liver Neoplasms, Experimental - therapy ; Male ; Medical sciences ; Molecular Medicine ; Neoplasm Proteins - antagonists & inhibitors ; Neoplasm Proteins - physiology ; Neoplasm Transplantation ; Oncology ; Rats ; Rats, Wistar ; Triglycerides - metabolism ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - physiology ; Tumors</subject><ispartof>British journal of cancer, 1995-11, Vol.72 (5), p.1138-1143</ispartof><rights>Cancer Research Campaign 1995</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3867-2baae8cb6b4dbc1e0efbd2524f09546de4a014fe998cf040eb56bca20357e31e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033925/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033925/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,2727,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2896819$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7577459$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dessì, S</creatorcontrib><creatorcontrib>Batetta, B</creatorcontrib><creatorcontrib>Spano, O</creatorcontrib><creatorcontrib>Bagby, GJ</creatorcontrib><creatorcontrib>Tessitore, L</creatorcontrib><creatorcontrib>Costelli, P</creatorcontrib><creatorcontrib>Baccino, FM</creatorcontrib><creatorcontrib>Pani, P</creatorcontrib><creatorcontrib>Argilès, JM</creatorcontrib><title>Perturbations of triglycerides but not of cholesterol metabolism are prevented by anti-tumour necrosis factor treatment in rats bearing an ascites hepatoma (Yoshida AH-130)</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Rats transplanted with the ascites hepatoma Yoshida AH-130 developed a severely progressive cachexia, characterised by marked alterations in protein and lipid metabolism. In particular, high levels of serum triglycerides and free fatty acids were associated with altered levels and distribution of plasma cholesterol, with increased total and very low-density lipoprotein-low-density lipoprotein (VLDL-LDL) cholesterol and reduced high-density lipoprotein (HDL) cholesterol. The tumour cells showed high rates of cholesterol synthesis and elevated content of free and esterified cholesterol, whereas total cholesterol synthesis was reduced in the host liver. To determine whether these perturbations could be related to the elevation of tumour necrosis factor alpha (TNF-alpha) previously shown in the AH-130 bearers (Tessitore L, Costelli P, Baccino FM 1993, Br J Cancer, 67, 15-23), either anti-TNF polyclonal antibodies or non-immune IgGs were injected daily after tumour transplantation. The anti-TNF treatment neither affected tumour growth nor prevented the serum cholesterol changes, while attenuating the hypertriglyceridaemia and the elevated serum free fatty acid levels. These data indicate that TNF does not appear to be directly involved in the altered cholesterol metabolism in AH-130 hosts, thus supporting the view that cholesterol metabolism and lipid metabolism are regulated differently during tumour growth.</description><subject>Animal tumors. Experimental tumors</subject><subject>Animals</subject><subject>Antibodies, Monoclonal - therapeutic use</subject><subject>Ascites</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cachexia - etiology</subject><subject>Cachexia - metabolism</subject><subject>Cancer Research</subject><subject>Cholesterol - metabolism</subject><subject>Cholesterol, HDL - metabolism</subject><subject>Chromatography, High Pressure Liquid</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Experimental digestive system and abdominal tumors</subject><subject>experimental-oncology</subject><subject>Immunization, Passive</subject><subject>Lipoproteins - blood</subject><subject>Liver - metabolism</subject><subject>Liver Neoplasms, Experimental - complications</subject><subject>Liver Neoplasms, Experimental - metabolism</subject><subject>Liver Neoplasms, Experimental - therapy</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Molecular Medicine</subject><subject>Neoplasm Proteins - antagonists & inhibitors</subject><subject>Neoplasm Proteins - physiology</subject><subject>Neoplasm Transplantation</subject><subject>Oncology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Triglycerides - metabolism</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1ks2KFDEUhYMoYzu6cytkIaJgtUn9pbIZGIYZRxjQhS5chZvUre40VUmbpAb6nXxIU3TT6MJVCPfLOZdzQshrztacVd0nvTNrLmWzroV4Qla8qcqCd6V4SlaMMVEwWbLn5EWMu3yVrBMX5EI0QtSNXJHf3zCkOWhI1rtI_UBTsJvxYDDYHiPVc6LOp2Vgtn7EmDD4kU6YQPvRxolCQLoP-IguYU_1gYJLtkjz5OdAHZrgo410AJN8yOIIacootY4GSNkAIVi3ya8oRGNT9tziHpKfgL7_6ePW9kCv7wtesQ8vybMBxoivTucl-XF3-_3mvnj4-vnLzfVDYaquFUWpAbAzutV1rw1HhoPuy6asByabuu2xBsbrAaXszMBqhrpptYGSVY3AimN1Sa6OuvtZT9ibvG-AUe2DnSAclAer_p04u1Ub_6iyRCXLJgu8OwkE_2vOoanJRoPjCA79HJUQbddWnczgxyO4xBQDDmcTztTSrsrtqqVdldvN-Ju_FzvDpzrz_O1pnrOEcQjgjI1nrOxk2_EFK45Y3C_ZY1C7XJbLkf7Plh55B_mv4FkvQwuzIH8A5nfMzQ</recordid><startdate>19951101</startdate><enddate>19951101</enddate><creator>Dessì, S</creator><creator>Batetta, B</creator><creator>Spano, O</creator><creator>Bagby, GJ</creator><creator>Tessitore, L</creator><creator>Costelli, P</creator><creator>Baccino, FM</creator><creator>Pani, P</creator><creator>Argilès, JM</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19951101</creationdate><title>Perturbations of triglycerides but not of cholesterol metabolism are prevented by anti-tumour necrosis factor treatment in rats bearing an ascites hepatoma (Yoshida AH-130)</title><author>Dessì, S ; Batetta, B ; Spano, O ; Bagby, GJ ; Tessitore, L ; Costelli, P ; Baccino, FM ; Pani, P ; Argilès, JM</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3867-2baae8cb6b4dbc1e0efbd2524f09546de4a014fe998cf040eb56bca20357e31e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animal tumors. Experimental tumors</topic><topic>Animals</topic><topic>Antibodies, Monoclonal - therapeutic use</topic><topic>Ascites</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cachexia - etiology</topic><topic>Cachexia - metabolism</topic><topic>Cancer Research</topic><topic>Cholesterol - metabolism</topic><topic>Cholesterol, HDL - metabolism</topic><topic>Chromatography, High Pressure Liquid</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>Experimental digestive system and abdominal tumors</topic><topic>experimental-oncology</topic><topic>Immunization, Passive</topic><topic>Lipoproteins - blood</topic><topic>Liver - metabolism</topic><topic>Liver Neoplasms, Experimental - complications</topic><topic>Liver Neoplasms, Experimental - metabolism</topic><topic>Liver Neoplasms, Experimental - therapy</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Molecular Medicine</topic><topic>Neoplasm Proteins - antagonists & inhibitors</topic><topic>Neoplasm Proteins - physiology</topic><topic>Neoplasm Transplantation</topic><topic>Oncology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Triglycerides - metabolism</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dessì, S</creatorcontrib><creatorcontrib>Batetta, B</creatorcontrib><creatorcontrib>Spano, O</creatorcontrib><creatorcontrib>Bagby, GJ</creatorcontrib><creatorcontrib>Tessitore, L</creatorcontrib><creatorcontrib>Costelli, P</creatorcontrib><creatorcontrib>Baccino, FM</creatorcontrib><creatorcontrib>Pani, P</creatorcontrib><creatorcontrib>Argilès, JM</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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dessì, S</au><au>Batetta, B</au><au>Spano, O</au><au>Bagby, GJ</au><au>Tessitore, L</au><au>Costelli, P</au><au>Baccino, FM</au><au>Pani, P</au><au>Argilès, JM</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Perturbations of triglycerides but not of cholesterol metabolism are prevented by anti-tumour necrosis factor treatment in rats bearing an ascites hepatoma (Yoshida AH-130)</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>1995-11-01</date><risdate>1995</risdate><volume>72</volume><issue>5</issue><spage>1138</spage><epage>1143</epage><pages>1138-1143</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Rats transplanted with the ascites hepatoma Yoshida AH-130 developed a severely progressive cachexia, characterised by marked alterations in protein and lipid metabolism. In particular, high levels of serum triglycerides and free fatty acids were associated with altered levels and distribution of plasma cholesterol, with increased total and very low-density lipoprotein-low-density lipoprotein (VLDL-LDL) cholesterol and reduced high-density lipoprotein (HDL) cholesterol. The tumour cells showed high rates of cholesterol synthesis and elevated content of free and esterified cholesterol, whereas total cholesterol synthesis was reduced in the host liver. To determine whether these perturbations could be related to the elevation of tumour necrosis factor alpha (TNF-alpha) previously shown in the AH-130 bearers (Tessitore L, Costelli P, Baccino FM 1993, Br J Cancer, 67, 15-23), either anti-TNF polyclonal antibodies or non-immune IgGs were injected daily after tumour transplantation. The anti-TNF treatment neither affected tumour growth nor prevented the serum cholesterol changes, while attenuating the hypertriglyceridaemia and the elevated serum free fatty acid levels. These data indicate that TNF does not appear to be directly involved in the altered cholesterol metabolism in AH-130 hosts, thus supporting the view that cholesterol metabolism and lipid metabolism are regulated differently during tumour growth.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>7577459</pmid><doi>10.1038/bjc.1995.477</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animal tumors. Experimental tumors Animals Antibodies, Monoclonal - therapeutic use Ascites Biological and medical sciences Biomedical and Life Sciences Biomedicine Cachexia - etiology Cachexia - metabolism Cancer Research Cholesterol - metabolism Cholesterol, HDL - metabolism Chromatography, High Pressure Liquid Drug Resistance Epidemiology Experimental digestive system and abdominal tumors experimental-oncology Immunization, Passive Lipoproteins - blood Liver - metabolism Liver Neoplasms, Experimental - complications Liver Neoplasms, Experimental - metabolism Liver Neoplasms, Experimental - therapy Male Medical sciences Molecular Medicine Neoplasm Proteins - antagonists & inhibitors Neoplasm Proteins - physiology Neoplasm Transplantation Oncology Rats Rats, Wistar Triglycerides - metabolism Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - physiology Tumors |
title | Perturbations of triglycerides but not of cholesterol metabolism are prevented by anti-tumour necrosis factor treatment in rats bearing an ascites hepatoma (Yoshida AH-130) |
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