**3.1 Total cholesterol**

PUFAs have been shown to increase liver X receptor alpha (LXRα) gene expression [71, 72] via peroxisome proliferator activated receptors (PPARs) [71]. LXRα stimulates the expression of cholesterol 7 α-hydroxylase (CYP7), thereby converting cholesterol to bile acids. Therefore, by increasing CYP7 activity, PUFAs participate in cholesterol catabolism [73].

## **3.2 Triglycerides**

PUFAs interact more strongly with PPARα compared to SFAs [74]. PPARα binds to peroxisome proliferator response elements (PPREs) located in the promotor regions of genes, such as apoC-III and lipoprotein lipase (LPL) [75]. It has been proposed that LPL may demonstrate increased activity towards VLDL triglycerides containing polyunsaturated fatty acids, thereby leading to increased breakdown of triglyceride-rich lipoproteins (chylomicrons and VLDL particles) [73, 76, 77]. LPL activity is inhibited by apoC-III, and thus, increases triglyceride concentrations [78]. It has been reported that PUFAs decrease apoC-III, thereby increasing LPL activity and, indeed, VLDL catabolism [73]. Moreover, omega-3 PUFAs have been shown to reduce triglycerides by lowering diacylglycerol acyltransferase, fatty acid synthase, and acetyl coenzyme A (CoA) carboxylase [79–84].

### **3.3 LDL-C**

Intakes of linoleic acid [85] or PUFAs [73] have been demonstrated to increase LDL receptor activity, protein, and mRNA compared to SFAs. Furthermore, PUFAs increase membrane fluidity [73, 85, 86], which increases LDL receptor activity, and thus, increases LDL catabolism [87–89].

#### **3.4 LDL particle size**

It has been reported that consumption of SFAs increases large, buoyant LDL particles compared to lower SFA-containing diets [69, 90], whereas consumption of diets rich in PUFAs decreases large, buoyant LDL particles versus diets high in SFAs [70, 91]. It has been suggested that SFAs increase LPL and hepatic lipase activities [92, 93]. As such, LPL increases large, buoyant LDL particles, whereas hepatic lipase may stimulate the catabolism of triglyceride-rich lipoprotein remnants [92]. However, additional research is needed in this area regarding the mechanisms by which individual fatty acids affect LDL particle size.

#### **3.5 VLDL-C**

The sterol regulatory element-binding protein-1 (SREBP-1) is associated with lipogenesis and cholesterol synthesis in the liver [94, 95]. PUFAs have been shown to inhibit SREBP-1 gene transcription and/or protein [96], thereby lowering VLDL secretion from the liver [73, 96]. In addition, intakes of PUFAs increase VLDL catabolism and uptake [59, 81].

*The Effects of Linoleic Acid Consumption on Lipid Risk Markers for Cardiovascular Disease DOI: http://dx.doi.org/10.5772/intechopen.99894*
