Both GLP-1 agonism and DPP4 inhibition reduce postprandial triacylglycerol and ApoB-48
in rodents [111, 112].
was quantitated from plasma using a Western Blotting/Enhanced Chemiluminescence procedure described previously (23).
Similarly, chylomicrons and their remnants contain a single molecule of apoB-48
. Hence, plasma apoB concentrations reflect the total number of atherogenic particles present in the circulation (4, 5).
Chylomicrons contain apoA, apoC, and apoB-48
and lack apoB-100.
Hypertriglyceridemia attributable to increased plasma concentrations of VLDL apolipoprotein (apo) B-100 and chylomicron apoB-48
is the most consistent lipid disorder in obesity (3, 4).
The human apoB gene (APOB) is located on chromosome 2, and the same gene produces two forms of apoB in circulating lipoproteins, apoB-48
Higher non-HDL cholesterol in the obese, a known correlate with apoB (27, 28), supports an increased apoB concentration, composed of apoB-100 and apoB-48
, both of which are increased in obese men (29).
Hypertriglyceridemia attributable to increased plasma concentrations of hepatic apolipoprotein (apo)4 B-100 and intestinal apoB-48
is the most consistent lipid disorder in visceral obesity and a risk factor for coronary artery disease (1, 2).
Apolipoprotein B-48 (apoB-48
)  is an excellent marker of postprandial lipoproteins because it is associated exclusively in humans with intestinally derived chylomicrons (CMs) and their remnants, circulating particles that have been described as atherogenic (1).
Use of a monoclonal antibody that recognizes an epitope within the apoB-51 region distal to the C-terminus of apoB-48
(7) allows apo B-48-containing lipoproteins to be selectively enriched in the RLP fraction compared with the VLDL fraction isolated by the UC.
Because the mean VLDL-C concentration in the plasma of control C57BL/6 and apoE(-) mice was 3.03 and 4.52 mmol/L, respectively, it is very likely that intermediate-density lipoprotein and LDL, which in mice are also largely remnant-like particles containing apoB-48
, also cause interference with the PEGME measurement of HDL-C.
Contribution of apoB-48
and apoB-100 triglyceride-rich lipoproteins (TRL) to postprandial increases in the plasma concentration of TRL triglycerides and retinyl esters.