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APOB is a surface molecule that travels on lipoprotein particles such as VLDL and LDL, but not HDL.
The genotypes and allele frequencies of
ApoB and ACE genes did not differ between trained and control groups (P > 0.05).
Physiologically,
apoB is arguably more relevant than LDL-C.
ApoA-I,
apoB, and apoC-III were determined by previously validated electroimmunoassays [21-23].
The distribution of S4338N polymorphism was found to be significantly different in CHD and control groups (P = 0.0008; RR (95% CI) = 0.685 (0.543, 0.864); Odds Ratio (95% CI) = 0.486 (0.319, 0.739), suggesting that S4338N polymorphism in
ApoB gene may have minor contribution in early development of coronary heart disease and therefore can be considered as a genetic marker for disease risk assessment.
No significant differences were observed for either group with
apoB concentrations.
Mice, humans and other mammals produce a directly analogous protein called apolipoprotein B (
apoB) and therapies have been developed to reduce
apoB to prevent cardiovascular disease.
Recent findings have helped to further clarify the regulatory steps in VLDL metabolism in the liver in type 2 diabetes n normal subjects, insulin inhibits the assembly and secretion of VLDL particles by increasing apolipoprotein B (
apoB) degradation and decreasing the expression of the microsomal transfer protein (MTP) in hepatocytes.
BMI, waist circumference, sum of 4 skinfolds, TG, glucose, HOMA, C-reactive protein (CRP), APOA1,
APOB, and leptin were skewed and therefore log-transformed before z-scores were constructed.
One of the most strongly selected genes is
APOB, which in mammals encodes the main protein in LDL (low density lipoprotein), known widely as "bad" cholesterol.