Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice

<p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p< Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Teivainen Päivi A [verfasserIn] Eliassen Knut A [verfasserIn] Rubin Edward M [verfasserIn] Djurovic Srdjan [verfasserIn] Berg Kåre [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2004

Übergeordnetes Werk:	In: Lipids in Health and Disease - BMC, 2003, 3(2004), 1, p 8
Übergeordnetes Werk:	volume:3 ; year:2004 ; number:1, p 8

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1476-511X-3-8

Katalog-ID:	DOAJ030848288

Internformat


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520			\|a <p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p<
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700	0		\|a Berg Kåre \|e verfasserin \|4 aut
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912			\|a GBV_ILN_4325
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author_variant	t p a tpa e k a eka r e m rem d s ds b k bk
matchkey_str	article:1476511X:2004----::uaaocnrbtsonraesrmoaaolvlnt
hierarchy_sort_str	2004
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publishDate	2004
allfields	10.1186/1476-511X-3-8 doi (DE-627)DOAJ030848288 (DE-599)DOAJc05aab68fda1477f84c1f3df984641a1 DE-627 ger DE-627 rakwb eng RC620-627 Teivainen Päivi A verfasserin aut Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p< Nutritional diseases. Deficiency diseases Eliassen Knut A verfasserin aut Rubin Edward M verfasserin aut Djurovic Srdjan verfasserin aut Berg Kåre verfasserin aut In Lipids in Health and Disease BMC, 2003 3(2004), 1, p 8 (DE-627)355987694 (DE-600)2091381-3 1476511X nnns volume:3 year:2004 number:1, p 8 https://doi.org/10.1186/1476-511X-3-8 kostenfrei https://doaj.org/article/c05aab68fda1477f84c1f3df984641a1 kostenfrei http://www.lipidworld.com/content/3/1/8 kostenfrei https://doaj.org/toc/1476-511X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2004 1, p 8
spelling	10.1186/1476-511X-3-8 doi (DE-627)DOAJ030848288 (DE-599)DOAJc05aab68fda1477f84c1f3df984641a1 DE-627 ger DE-627 rakwb eng RC620-627 Teivainen Päivi A verfasserin aut Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p< Nutritional diseases. Deficiency diseases Eliassen Knut A verfasserin aut Rubin Edward M verfasserin aut Djurovic Srdjan verfasserin aut Berg Kåre verfasserin aut In Lipids in Health and Disease BMC, 2003 3(2004), 1, p 8 (DE-627)355987694 (DE-600)2091381-3 1476511X nnns volume:3 year:2004 number:1, p 8 https://doi.org/10.1186/1476-511X-3-8 kostenfrei https://doaj.org/article/c05aab68fda1477f84c1f3df984641a1 kostenfrei http://www.lipidworld.com/content/3/1/8 kostenfrei https://doaj.org/toc/1476-511X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2004 1, p 8
allfields_unstemmed	10.1186/1476-511X-3-8 doi (DE-627)DOAJ030848288 (DE-599)DOAJc05aab68fda1477f84c1f3df984641a1 DE-627 ger DE-627 rakwb eng RC620-627 Teivainen Päivi A verfasserin aut Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p< Nutritional diseases. Deficiency diseases Eliassen Knut A verfasserin aut Rubin Edward M verfasserin aut Djurovic Srdjan verfasserin aut Berg Kåre verfasserin aut In Lipids in Health and Disease BMC, 2003 3(2004), 1, p 8 (DE-627)355987694 (DE-600)2091381-3 1476511X nnns volume:3 year:2004 number:1, p 8 https://doi.org/10.1186/1476-511X-3-8 kostenfrei https://doaj.org/article/c05aab68fda1477f84c1f3df984641a1 kostenfrei http://www.lipidworld.com/content/3/1/8 kostenfrei https://doaj.org/toc/1476-511X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2004 1, p 8
allfieldsGer	10.1186/1476-511X-3-8 doi (DE-627)DOAJ030848288 (DE-599)DOAJc05aab68fda1477f84c1f3df984641a1 DE-627 ger DE-627 rakwb eng RC620-627 Teivainen Päivi A verfasserin aut Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p< Nutritional diseases. Deficiency diseases Eliassen Knut A verfasserin aut Rubin Edward M verfasserin aut Djurovic Srdjan verfasserin aut Berg Kåre verfasserin aut In Lipids in Health and Disease BMC, 2003 3(2004), 1, p 8 (DE-627)355987694 (DE-600)2091381-3 1476511X nnns volume:3 year:2004 number:1, p 8 https://doi.org/10.1186/1476-511X-3-8 kostenfrei https://doaj.org/article/c05aab68fda1477f84c1f3df984641a1 kostenfrei http://www.lipidworld.com/content/3/1/8 kostenfrei https://doaj.org/toc/1476-511X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2004 1, p 8
allfieldsSound	10.1186/1476-511X-3-8 doi (DE-627)DOAJ030848288 (DE-599)DOAJc05aab68fda1477f84c1f3df984641a1 DE-627 ger DE-627 rakwb eng RC620-627 Teivainen Päivi A verfasserin aut Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p< Nutritional diseases. Deficiency diseases Eliassen Knut A verfasserin aut Rubin Edward M verfasserin aut Djurovic Srdjan verfasserin aut Berg Kåre verfasserin aut In Lipids in Health and Disease BMC, 2003 3(2004), 1, p 8 (DE-627)355987694 (DE-600)2091381-3 1476511X nnns volume:3 year:2004 number:1, p 8 https://doi.org/10.1186/1476-511X-3-8 kostenfrei https://doaj.org/article/c05aab68fda1477f84c1f3df984641a1 kostenfrei http://www.lipidworld.com/content/3/1/8 kostenfrei https://doaj.org/toc/1476-511X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2004 1, p 8
language	English
source	In Lipids in Health and Disease 3(2004), 1, p 8 volume:3 year:2004 number:1, p 8
sourceStr	In Lipids in Health and Disease 3(2004), 1, p 8 volume:3 year:2004 number:1, p 8
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Nutritional diseases. Deficiency diseases
isfreeaccess_bool	true
container_title	Lipids in Health and Disease
authorswithroles_txt_mv	Teivainen Päivi A @@aut@@ Eliassen Knut A @@aut@@ Rubin Edward M @@aut@@ Djurovic Srdjan @@aut@@ Berg Kåre @@aut@@
publishDateDaySort_date	2004-01-01T00:00:00Z
hierarchy_top_id	355987694
id	DOAJ030848288
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ030848288</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230307153254.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230226s2004 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/1476-511X-3-8</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ030848288</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJc05aab68fda1477f84c1f3df984641a1</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC620-627</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Teivainen Päivi A</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2004</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a"><p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p<</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Nutritional diseases. 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callnumber-first	R - Medicine
author	Teivainen Päivi A
spellingShingle	Teivainen Päivi A misc RC620-627 misc Nutritional diseases. Deficiency diseases Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice
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topic_title	RC620-627 Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice
topic	misc RC620-627 misc Nutritional diseases. Deficiency diseases
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title	Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice
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title_full	Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice
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journal	Lipids in Health and Disease
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author_browse	Teivainen Päivi A Eliassen Knut A Rubin Edward M Djurovic Srdjan Berg Kåre
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title_sort	human apob contributes to increased serum total apo(a) level in <it<lpa </it<transgenic mice
callnumber	RC620-627
title_auth	Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice
abstract	<p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p<
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title_short	Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice
url	https://doi.org/10.1186/1476-511X-3-8 https://doaj.org/article/c05aab68fda1477f84c1f3df984641a1 http://www.lipidworld.com/content/3/1/8 https://doaj.org/toc/1476-511X
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up_date	2024-07-03T17:18:38.008Z
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Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the <it<LPA </it<gene and mice capable of forming Lp(a) particles, <it<LPA</it<-YAC transgenic mice and <it<hAPOB </it<transgenic mice were crossed and their offspring examined.</p< <p<Results</p< <p<Comparison of <it<LPA</it<-YAC with <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice showed that <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the <it<hAPOB </it<gene. However, hepatic apo(a) mRNA level was higher in <it<LPA</it<-YAC transgenic mice than in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice. Feeding of a high-cholesterol/high-fat diet to male <it<LPA</it<-YAC transgenic mice with or without the <it<hAPOB </it<gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level.</p< <p<Conclusion</p< <p<In conclusion, the higher serum total apo(a) level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than in <it<LPA</it<-YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in <it<LPA</it<-YAC/<it<hAPOB </it<than in <it<LPA</it<-YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in <it<LPA</it<-YAC/<it<hAPOB </it<transgenic mice than either in wild type or <it<LPA</it<-YAC transgenic mice may further suggest that human <it<APOB </it<transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male <it<LPA</it<-YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding.</p<</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Nutritional diseases. 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Human apoB contributes to increased serum total apo(a) level in <it<LPA </it<transgenic mice

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