151 Æ 31 to 142 Æ 31 mg/dL), 27% in VLDL-C level (from 23 Æ 12 to 17 Æ 8 mg/
dL), and 9% in total cholesterol level (from 233 Æ 35 to 213 Æ 36 mg/dL). However,
no significant (P > 0.05) change was observed in the levels of HDL-C (Gulesserian
and Widhalm 2002). A lot of literature is available on the cholesterol and triglycerides lowering effects of rapeseed or canola oil (Gylling et al. 1999; Chisholm et al.
2005; Ferguson et al. 2016; Kruse et al. 2015), but the mechanism behind
hypotriacyglycerolemic and/or hypocholesterolemic effect is still not well understood (Gulesserian and Widhalm 2002). It is suggested that there are some compositional changes in VLDL or in the expressed activities of the enzymes and proteins
involved in intravascular processing and catabolism of VLDL, which could play an
important role in lowering serum triacylglycerides level (McNamara 1992; RuizGutierrez et al. 1998; Campos et al. 1996; Montalto and Bensadoun 1993). Fumeron
et al. (2017) reviewed the possible mechanisms for cholesterol-lowering effects of
plant stanols/phytosterols. It was suggested that phytosterols (which are present in
appreciable amount in canola oil) compete with cholesterol in the micelles of lecithin
and bile salts, which causes a reduction in cholesterol solubilization. When the
concentration of phytosterols is high in diet, cholesterol almost loses its solubility
for intestinal absorption and excreted out through feces (De Smet et al. 2012; Ikeda
et al. 1989).
2.4.2 In Cardiovascular Diseases
There are evidences suggesting that consumption of MUFA-rich oils such as canola
can reduce the risk factors related to cardiovascular diseases, which have comprehensively reviewed by Hammad et al. (2016) and Baum et al. (2012). American
Heart Association has recommended a diet that provides <10% of calories from
SFA, up to 10% from PUFA, and as much as 15% from MUFA for cardiovascular
health (Kris-Etherton 1999). The serum levels of LDL and HDL are directly
correlated with the risk of heart diseases, which have already been discussed in
previous section. Currently, there is an increased interest in the relation of
thrombogenesis and MUFA-rich diet. A few studies have suggested that MUFA
decreases the platelet aggregation (Sirtori et al. 1986), increases bleeding time
(McDonald et al. 1989), and increases fibrinolysis (Lopez-Segura et al. 1996),
thereby protecting against thrombogenesis. Several researchers observed a slight
protective effect against CHD on replacing energy from complex carbohydrates with
MUFAs (Hu et al. 1997; Kris-Etherton 1999). In 1997, a prospective study was
conducted on 80,082 women (age 34–59 years), who had no known coronary
disease, stroke, cancer, hypercholesterolemia, or diabetes in 1980. During 14 years
of follow-up, it was observed that for a 5% increment in energy from monounsaturated fats, the risk of coronary disease was reduced to 0.81 (95% confidence
interval, 0.65–1.00; P ¼ 0.05) (Hu et al. 1997). A wide range of literature has
suggested that MUFA reduced the level of LDL-cholesterol, triglycerides, and total
cholesterol, whereby increased the HDL-cholesterol and, thus, played a positive role
60
A. Goyal et al.
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