Atherosclerotic lesion formation and triglyceride storage in obese apolipoprotein AI-deficient mice.

Atherosclerotic lesion formation and triglyceride storage in obese apolipoprotein AI-deficient mice. Research Abstract Details 

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Atherosclerotic lesion formation and triglyceride storage in obese apolipoprotein AI-deficient mice. Abstract Text:

Obese leptin-deficient (ob/ob) mice have increased levels of high-density lipoprotein (HDL) and a unique lipoprotein referred to as low-density lipoprotein (LDL)/HDL1. When crossed onto an apolipoprotein AI (apoAI)-deficient ((-/-)) background, ob/ob;apoAI(-/-) mice accumulate LDL/HDL1 in the absence of traditional HDL. To determine the role of LDL/HDL1 in atherosclerosis, C57BL/6, apoAI(-/-), ob/ob and ob/ob;apoAI(-/-) mice were placed on butterfat diet. After 20 weeks, all four groups had a significant increase in total cholesterol levels. The cholesterol in C57BL/6 mice was carried on very low-density lipoprotein (VLDL) and LDL and, in ob/ob and ob/ob;apoAI(-/-) mice, on HDL and LDL/HDL1. Atherosclerotic lesion area was similar among C57BL/6, ob/ob and ob/ob;apoAI(-/-) groups despite their dissimilar lipoprotein profiles. Hepatic triglyceride production and VLDL clearance rates were similar among the four groups. The ob/ob;apoAI(-/-) group had a significant decrease in liver weight and an increase in white adipose tissue (WAT) weight compared to the ob/ob group. Hepatic scavenger receptor class B type I (SR-BI) levels were decreased in both liver and WAT in ob/ob;apoAI(-/-) compared to ob/ob mice. Conclusions regarding the atherogenicity of LDL/HDL1 were confounded by the differences in lipoprotein profiles among the four groups. However, our studies provide support for the concept that apoAI and SR-BI assist in the partitioning of lipid from adipose tissue to the liver.

Atherosclerotic lesion formation and triglyceride storage in obese apolipoprotein AI-deficient mice. Publishing Authors By Initials

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Atherosclerotic lesion formation and triglyceride storage in obese apolipoprotein AI-deficient mice. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: The Journal of nutritional biochemistry

VOLUME: 19

Page Numbers: 664-73

Journal Abbreviation: J. Nutr. Biochem.

ISSN: 0955-2863

DAY: 14

MONTH: 02

YEAR: 2008

Atherosclerotic lesion formation and triglyceride storage in obese apolipoprotein AI-deficient mice. Information

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LANGUAGE: eng

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Grant and Affiliation Information for Atherosclerotic lesion formation and triglyceride storage in obese apolipoprotein AI-deficient mice.

AFFILIATION: Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232, USA.

Country: United States

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MEDLINETA: J Nutr Biochem

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