The variation of total cholesterol, triacylglycerol, HDL-cholesterol, LDL-cholesterol and total cholesterol:HDL-cholesterol ratio was primarily explained by additive genetic factors, accounting for 75, 58, 76, 78 and 79% of the total variance, respectively.
Variations of cholesterol level among the membranes of pRBC have also been suggested by spectral shifts in Nile Red as a neutral lipid indicator (Jackson et al., 2004).
The impact of this variation on cholesterol values was not considered.
[18, 19, 20]. Figure 2 d, showed the distinct variation of total cholesterol among normal, diabetes and diabetes recovered mice.
These results correlate with data in Table 4 (variation of membrane cholesterol and MDA levels) explaining the protective effect of this extract on the RBCs membrane.
Hak et al. (2004) assessed the contribution of genetic variation to cholesterol levels among postmenopausal women, and concluded that APOE genotype modifies the extent of cholesterol increase after menopause.
The wide variation in efficiency of cholesterol absorption is largely attributable to heritable factors (3, 4).
Treatment with the aqueous extract (50, 100 and 150 mg/kg) in combination with ethanol and sucrose prevented the variation of serum total cholesterol, triglycerides, atherogenic index and HDL-cholesterol as compared to the ethanol-sucrose-treated group.
No significant variation of serum creatinine, LDL cholesterol, serum triglycerides as well as liver, spleen, testicles and ovaries proteins was noted.
B12 explained 7.5% (P = 0.001) of the variation in cholesterol and 7.4% (P = 0.005) of the variation in triglycerides.
