title: The prime role of HDL to transport lutein into the retina: evidence from HDL-deficient WHAM chicks having a mutant ABCA1 transporter.
abstract: OBJECTIVE
  Lutein and zeaxanthin are largely transported in plasma by high-density lipoprotein (HDL). The Wisconsin hypoalpha mutant (WHAM) chicken has a recessive sex-linked mutation in the ABCA1 transporter gene that results in a severe deficiency of HDL. In this study, the transport and tissue distribution of lutein and zeaxanthin were examined in newly hatched and 28-day-old WHAM chicks compared with control chicks.
  
  
  METHODS
  One-day-old WHAM and control chicks were randomized to be fed a high-lutein or a control diet for 28 days. The plasma and tissues were analyzed for lutein, zeaxanthin, and lipoproteins on days 1 and 28.
  
  
  RESULTS
  The WHAM chicks had very low plasma levels of HDL cholesterol (5.3% of normal). They also had very low concentrations of lutein in the plasma and all other tissues compared with control chicks. The plasma and retina were only 9% and 6% of control levels (P < 0.01), respectively. Zeaxanthin levels were similarly low (9% of control, P < 0.01). The high-lutein diet increased the content of lutein in the plasma and tissues of control chicks (P < 0.01). In contrast, in WHAM chicks, lutein increased greatly in the plasma, liver, and heart, but little in the retina (6% of control).
  
  
  CONCLUSIONS
  HDL deficiency in the WHAM chicks was associated with a deficiency of lutein and zeaxanthin in the tissues, especially in the retina. The high-lutein diet increased the lutein content of some tissues via LDL and VLDL transport, but retinal lutein remained very low. These data support the prime role of HDL as the specific transporter of lutein and zeaxanthin into the retina. The WHAM chick provides an excellent model for the study of the role of HDL in the retinal uptake of lutein and zeaxanthin.
authors.affiliation: Division of Endocrinology, Metabolism, and Clinical Nutrition, Department of Medicine, Oregon Health and Science University, Portland, Oregon 97239, USA. connorw@ohsu.edu
authors.forename: William E
authors.initials: WE
authors.lastname: Connor
authors.forename: P Barton
authors.initials: PB
authors.lastname: Duell
authors.forename: Ron
authors.initials: R
authors.lastname: Kean
authors.forename: Yingming
authors.initials: Y
authors.lastname: Wang
mesh_terms: D064286:ATP Binding Cassette Transporter 1; D018528:ATP-Binding Cassette Transporters / Q000235:genetics*; D000818:Animals; D030801:Animals, Genetically Modified; D000831:Animals, Newborn; D002645:Chickens; D008076:Cholesterol, HDL / Q000097:blood / Q000172:deficiency / Q000502:physiology*; D002851:Chromatography, High Pressure Liquid; D004032:Diet; D004530:Egg Yolk / Q000737:chemistry; D008099:Liver / Q000378:metabolism; D014975:Lutein / Q000008:administration & dosage / Q000378:metabolism*; D009154:Mutation; D009206:Myocardium / Q000378:metabolism; D021381:Protein Transport; D012160:Retina / Q000378:metabolism*; D014018:Tissue Distribution; D024341:Xanthophylls / Q000008:administration & dosage / Q000378:metabolism*; D065146:Zeaxanthins
chemical_list: D064286:ATP Binding Cassette Transporter 1; D018528:ATP-Binding Cassette Transporters; D008076:Cholesterol, HDL; D024341:Xanthophylls; D065146:Zeaxanthins; D014975:Lutein