Abstract
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 (apoB48/48) or apoB-100 only (apoB100/100). Cholesterol levels were higher in apoB48/48 mice than in apoB100/100 mice but triglyceride levels were similar. Lipid levels were increased by the apoC-III transgene. However, triglyceride levels were significantly higher in apoB100/100C-III than in apoB48/48C-III mice (895 +/- 395 mg/dl vs. 690 +/- 252 mg/dl; P <0.01), whereas cholesterol levels were higher in the apoB48/48C-III mice than in apoB100/100C-III (144 +/- 35 mg/dl vs. 94 +/- 30 mg/dl; P <0.00001). Triglyceride clearance from VLDL was impaired to a greater extent in apoB100/100C-III vs. apoB100/100 mice than in apoB48/48C-III vs. apoB48/48 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 apoB48/48 mice vs. apoB100/100 mice, perhaps on the basis of metabolic competition.
Highlights
The adaptive value of apolipoprotein B-48, the truncated form of apoB produced by the intestine, in lipid metabolism remains unclear
We have applied the method of metabolic characterization of genetically modified mice to the study of the effects of Apolipoprotein B-48 (apoB-48) and apoB-100 on plasma cholesterol and TG metabolism
ApoC-III, which impairs both lipolysis and remnant lipoprotein clearance [28], was introduced as a variable via a human apoC-III transgene to highlight the relevant differences between apoB-48 and apoB-100
Summary
The adaptive value of apolipoprotein B-48 (apoB48), 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 (apoB48/48) or apoB-100 only (apoB100/100). Cholesterol levels were higher in apoB48/48 mice than in apoB100/100 mice but triglyceride levels were similar. Lipid levels were increased by the apoC-III transgene. Triglyceride levels were significantly higher in apoB100/100C-III than in apoB48/48C-III mice (895 ؎ 395 mg/dl vs 690 ؎ 252 mg/dl; P Ͻ 0.01), whereas cholesterol levels were higher in the apoB48/48C-III mice than in apoB100/100C-III (144 ؎ 35 mg/dl vs 94 ؎ 30 mg/dl; P Ͻ 0.00001). 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 apoB48/48 mice vs apoB100/100 mice, perhaps on the basis of metabolic competition.—Conde-Knape, K., K.
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