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Publication : Overexpression of apoC-III produces lesser hypertriglyceridemia in apoB-48-only gene-targeted mice than in apoB-100-only mice.

First Author  Conde-Knape K Year  2004
Journal  J Lipid Res Volume  45
Issue  12 Pages  2235-44
PubMed ID  15342689 Mgi Jnum  J:94159
Mgi Id  MGI:3511398 Doi  10.1194/jlr.M400185-JLR200
Citation  Conde-Knape K, et al. (2004) Overexpression of apoC-III produces lesser hypertriglyceridemia in apoB-48-only gene-targeted mice than in apoB-100-only mice. J Lipid Res 45(12):2235-44
abstractText  The adaptive value of apolipoprotein B-48 (apoB-48), the truncated form of apoB produced by the intestine, in lipid metabolism remains unclear. We crossed human apoC-III transgenic mice with mice expressing either apoB-48 only (apoB(48/48)) or apoB-100 only (apoB(100/100)). Cholesterol levels were higher in apoB(48/48) mice than in apoB(100/100) mice but triglyceride levels were similar. Lipid levels were increased by the apoC-III transgene. However, triglyceride levels were significantly higher in apoB(100/100)C-III than in apoB(48/48)C-III mice (895 +/- 395 mg/dl vs. 690 +/- 252 mg/dl; P < 0.01), whereas cholesterol levels were higher in the apoB(48/48)C-III mice than in apoB(100/100)C-III (144 +/- 35 mg/dl vs. 94 +/- 30 mg/dl; P < 0.00001). Triglyceride clearance from VLDL was impaired to a greater extent in apoB(100/100)C-III vs. apoB(100/100) mice than in apoB(48/48)C-III vs. apoB(48/48) mice. Triglyceride secretion rates were no different in apoC-III transgenic mice than in their nontransgenic littermates. ApoB-48 triglyceride-rich lipoproteins were more resistant to the triglyceride-increasing effects of apoC-III but appeared more sensitive to the remnant clearance inhibition. Our findings support a coordinated role for apoB-48 in facilitating the delivery of dietary triglycerides to the periphery. Consistent with such a mechanism, glucose levels were significantly higher in apoB(48/48) mice vs. apoB(100/100) mice, perhaps on the basis of metabolic competition.
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