1994 Fiscal Year Final Research Report Summary
Regulation of apolipoprotein A-I gene expression by ascorbic acid in scurvy-prone ODS-od/od rats.
Project/Area Number |
05660136
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
食品科学・栄養科学
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Research Institution | Nagoya University |
Principal Investigator |
HORIO Fumihiko Nagoya University, School of Agricultural Sciences, Department of Applied Biological Sciences, Associate Professor, 農学部, 助教授 (20165591)
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Project Period (FY) |
1993 – 1994
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Keywords | Ascorbic acid / Apolipoprotein A-I / Atherosclerosis / Vitamin C |
Research Abstract |
Apolipoprotein A-I (Apo A-I) is a major apolipoprotein of serum high density lipoprotein (HDL) , which transports cholesterol from peripheral tissues to liver. We observed that apo A-I in serum HDL was decreased in ascorbic acid (AsA) deficiency in scurvy-prone ODS-od/od rats. In this study, we examined the mechanism how AsA deficiency causes a low level Apo A-I in serum. The Apo A-I mRNA level in the liver but not in the small intestine was decreased (50%) in AsA-deficient group compared to in the control group. As AsA deficiency did not affect the transcription rate of Apo A-I gene, AsA might be required to stabilize Apo A-I mRNA.Moreover, a lower level of albumin mRNA,a higher level of haptoglobin mRNA and a higher level of 1-acid glycoprotein mRNA in the liver was observed in ascorbic acid-deficienct rats compared to in the control rats. These changes in hepatic levels of mRNA including Apo A-I mRNA are also observed in acute phase or inflammation. At present, we are measuring the serum levels of interleukin-6, which is a major cytokine secreted in acute phase and inflammation, in ascorbic acid deficiency.
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