**3.6 HDL-C**

Replacing SFAs with MUFAs and/or PUFAs generates lower total cholesterol and LDL-C concentrations, with modest HDL-C reductions; however, a lower total cholesterol: HDL-C ratio results [4, 97]. It is thought that dietary fat increases the "transport rate" and decreases the "fractional catabolic rate" of HDL cholesterol ester and apolipoprotein A1 [98]. However, more research is needed to describe the mechanisms by which individual fatty acids impact HDL-C.

#### **3.7 Lipoprotein(a)**

Lipoprotein(a) is synthesized in the liver and contains apolipoprotein A, which is bound to apolipoprotein B-100 [99–101]. The biological activity of lipoprotein(a) is unknown [102]; however, high concentrations have been associated with CVD [101, 103, 104]. Genetics seem to be the primary determinant of lipoprotein(a) [105]. Hence, diet and exercise do not appear to be significant contributors to lipoprotein(a) concentrations. There have also been inconsistent findings of fatty acid consumption (including PUFAs) on lipoprotein(a) concentrations [106]. However, it has been suggested that fatty acids may affect liver apolipoprotein(a) synthesis, thereby impacting lipoprotein(a) [106–108]. As such, more research is needed to determine the effects of dietary composition on lipoprotein(a) concentrations.

#### **3.8 Apolipoprotein A1**

HDL particles contain apolipoprotein A1, which interacts with the ATP-binding cassette transporter on the surface of cells. Furthermore, apolipoprotein A1 is a cofactor for lecithin cholesterol acyl transferase, which generates mature HDL particles [43, 109]. Plasma apolipoprotein A1 concentration typically coincide with HDL-C concentrations [43]. The significance of apolipoprotein A2 is less clear [110]. Interestingly, PPARα also interacts with PPREs in the promoter region of the apolipoprotein A1 gene in the liver [75]. Hence, PUFAs may exert their effects on apolipoprotein A1 via PPARα [73].

### **3.9 Apolipoprotein B**

Apolipoprotein B also occurs in two forms: apolipoprotein B-48 and apolipoprotein B-100. The intestine synthesizes apolipoprotein B-48, which is a component of chylomicrons. The liver produces apolipoprotein B-100, which is associated with VLDL and LDL particles. Apolipoprotein B is necessary for the binding of lipoproteins to the LDL receptor. Apolipoprotein B plasma concentrations are significantly associated with LDL-C concentrations [43, 111]. It has been reported that high apolipoprotein B concentrations increase the risk for CVD, whereas apolipoprotein A1 concentrations decrease CVD risk [43, 112]. As mentioned previously, PUFAs increase LDL catabolism, thereby reducing apolipoprotein B [87].
