title: Apolipoprotein A-V deficiency results in marked hypertriglyceridemia attributable to decreased lipolysis of triglyceride-rich lipoproteins and removal of their remnants.
abstract: OBJECTIVE
  ApoAV, a newly discovered apoprotein, affects plasma triglyceride level. To determine how this occurs, we studied triglyceride-rich lipoprotein (TRL) metabolism in mice deficient in apoAV.
  
  
  RESULTS
  No significant difference in triglyceride production rate was found between apoa5(-/-) mice and controls. The presence or absence of apoAV affected TRL catabolism. After the injection of 14C-palmitate and 3H-cholesterol labeled chylomicrons and (125)I-labeled chylomicron remnants, the disappearance of 14C, 3H, and (125)I was significantly slower in apoa5(-/-) mice relative to controls. This was because of diminished lipolysis of TRL and the reduced rate of uptake of their remnants in apoa5(-/-) mice. Observed elevated cholesterol level was caused by increased high-density lipoprotein (HDL) cholesterol in apoa5(-/-) mice. VLDL from apoa5(-/-) mice were poor substrate for lipoprotein lipase, and did not bind to the low-density lipoprotein (LDL) receptor as well as normal very-low-density lipoprotein (VLDL). LDL receptor levels were slightly elevated in apoa5(-/-) mice consistent with lower remnant uptake rates. These alterations may be the result of the lower apoE-to-apoC ratio found in VLDL isolated from apoa5(-/-) mice.
  
  
  CONCLUSIONS
  These results support the hypothesis that the absence of apoAV slows lipolysis of TRL and the removal of their remnants by regulating their apoproteins content after secretion.
authors.affiliation: Department of Medicine, School of Medicine, Stanford University, California, USA. itamarg@stanford.edu
authors.forename: Itamar
authors.initials: I
authors.lastname: Grosskopf
authors.forename: Nadine
authors.initials: N
authors.lastname: Baroukh
authors.forename: Sung-Joon
authors.initials: SJ
authors.lastname: Lee
authors.forename: Yehuda
authors.initials: Y
authors.lastname: Kamari
authors.forename: Dror
authors.initials: D
authors.lastname: Harats
authors.forename: Edward M
authors.initials: EM
authors.lastname: Rubin
authors.forename: Len A
authors.initials: LA
authors.lastname: Pennacchio
authors.forename: Allen D
authors.initials: AD
authors.lastname: Cooper
mesh_terms: D000818:Animals; D000072040:Apolipoprotein A-V; D001053:Apolipoproteins / Q000235:genetics* / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood / Q000737:chemistry; D002914:Chylomicrons / Q000378:metabolism; D006868:Hydrolysis; D015228:Hypertriglyceridemia / Q000235:genetics* / Q000378:metabolism* / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology; D008066:Lipolysis / Q000502:physiology; D008074:Lipoproteins / Q000097:blood; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D010316:Particle Size; D011973:Receptors, LDL / Q000378:metabolism; D014280:Triglycerides / Q000097:blood* / Q000378:metabolism
chemical_list: C499058:Apoa5 protein, mouse; D000072040:Apolipoprotein A-V; D001053:Apolipoproteins; D008076:Cholesterol, HDL; D015243:Cholesterol, VLDL; D002914:Chylomicrons; D008074:Lipoproteins; D011973:Receptors, LDL; D014280:Triglycerides; C112017:remnant-like particle cholesterol; D002784:Cholesterol