title: Elevation of tissue α-tocopherol levels by conjugated linoleic acid in C57BL/6J mice is not associated with changes in vitamin E absorption or α-carboxyethyl hydroxychroman production.
abstract: OBJECTIVE
  Conjugated linoleic acid (CLA) decreases adipose mass and increases vitamin E levels in the liver and adipose tissue in mice. The aim of the present study was to examine the mechanism by which CLA alters vitamin E levels in tissues and antioxidant activity in mice.
  
  
  METHODS
  C57BL/6J mice were divided into three groups and fed 5% lipid as soybean oil alone (control group), 4% soybean oil supplemented with 1% CLA (CLA group), or 5% lipid with a vitamin E supplement (VE group) for 4 wk.
  
  
  RESULTS
  The CLA and VE diets resulted in a significant increase in the α-tocopherol concentration in all tissues examined, i.e., the liver, kidney, testis, spleen, heart, lung, and adipose tissue (P < 0.05). Levels of thiobarbituric acid-reactive substances in the kidney, testis, heart, lung, and adipose tissue were lower in the CLA and VE groups than in the control group (P < 0.05). CLA did not alter the absorption rate of vitamin E or α-carboxyethyl hydroxychromans levels in the liver and plasma. The CLA diet induced a significant increase in α-tocopherol transfer protein and mRNA levels in the liver. CLA resulted in a decrease in catalase and glutathione peroxidase activities and peroxisome proliferator α mRNA levels but had no effect on levels of mRNAs for other nuclear transcription factors in the liver.
  
  
  CONCLUSIONS
  The increase in vitamin E status in CLA-fed mice is not due to altered absorption and metabolism of vitamin E but might be related to the induction of α-tocopherol transfer protein expression in the liver. The regulation of the activities of catalase and glutathione peroxidase by CLA is not mediated by vitamin E accumulation in the liver.
authors.affiliation: Institute of Nutrition and Health Science, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan.
authors.forename: Wan-Hsuan
authors.initials: WH
authors.lastname: Chen
authors.forename: Yi-Jen
authors.initials: YJ
authors.lastname: Li
authors.forename: Ming-Shyong
authors.initials: MS
authors.lastname: Wang
authors.forename: Zhi-Chyang
authors.initials: ZC
authors.lastname: Kang
authors.forename: Huei-Ling
authors.initials: HL
authors.lastname: Huang
authors.forename: Huey-Mei
authors.initials: HM
authors.lastname: Shaw
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D002839:Chromans / Q000097:blood / Q000378:metabolism; D019587:Dietary Supplements; D005786:Gene Expression Regulation; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D007408:Intestinal Absorption; D044243:Linoleic Acids, Conjugated / Q000627:therapeutic use*; D008099:Liver / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010088:Oxidoreductases / Q000235:genetics / Q000378:metabolism; D047493:PPAR alpha / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014280:Triglycerides / Q000097:blood; D024502:alpha-Tocopherol / Q000097:blood / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D002352:Carrier Proteins; D002839:Chromans; D000960:Hypolipidemic Agents; D044243:Linoleic Acids, Conjugated; D047493:PPAR alpha; D012333:RNA, Messenger; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; C017763:alpha-tocopherol transfer protein; C483420:carboxyethyl-hydroxychroman; D010088:Oxidoreductases; D024502:alpha-Tocopherol