**3. Summary**

Elevated serum LDL-C and low levels of HDL-C are known as major and independent risk factors for CHD. Small, dense lipoprotein sub-fractions have been reported to have atherogenic potentials, with particular reference to Lipoprotein(a) [Lp(a)], a variant of low density lipoprotein (LDL). Other atherogenic sub-fractions of lipoproteins are VLDL, LDL, and IDL. These sub-fractions are characterized by the presence of apolipoprotein B-100, with an additional apolipoprotein known as apo(a) in the Lp(a) structure. Apo(a) is structurally and functionally similar to plasminogen and it accounts for virtually all the genetic variability in plasma Lp(a) levels. Variation of length within the kringle 4-encoding region of the apo(a) gene may account for a greater proportion of the inter-individual variation in plasma Lp(a) concentrations, with a strong genetic involvement inherited as a single autosomal dominant trait.

In the course of the pathogenesis of atherosclerosis, oxidized LDL is taken up by macrophages and into endothelial cells. This leads to formation of atherosclerotic plaques which precedes development of CHD. Oxidized LDL is antigenic and titres of autoantibodies against oxidized LDL in plasma can be used as indicator of a positive association with CHD. A positive association has also been established between plasma level of LDL, specifically oxidized LDL and other risk factors contributing to development of CHD. Such risk factors were identified as hypertriglyceridemia, reduced HDL-C levels, abdominal obesity and insulin resistance. Treatment of CHD can be achieved by lowering of plasma cholesterol levels which has been achieved by cholesterol-lowering therapy, suggesting that maintenance of low cholesterol levels may sufficiently prevent or reverse an established atherosclerosis. Increasing plasma levels of HDL-C has been reported to also be of benefit. HDL-C has anti-inflammatory activity which may prevent oxidation of LDL and it plays a key role in reverse transportation of cholesterol from lipid-laden macrophages.

The enzyme Lipoprotein lipase (LpL) may be useful in chemotherapy or prophylaxis of CHD. LpL has anti-atherogenic activity by its dual functions of triglyceride hydrolysis and ligand/brigding factor for receptor-mediated lipoprotein uptake. Activation of the enzyme is dependent on the tissue, resulting in variability of its activity. Hormonal replacement therapy may also be of benefit to patients with CHD and related diseases, but reported on current findings are conflicting.

#### **Author details**

214 Lipoproteins – Role in Health and Diseases

Anuurad, 2008).

**3. Summary** 

autosomal dominant trait.

decreased high density lipoprotein activity (Clee *et al.*, 2000; Tsutsumi, 2003; Okubo *et al.*, 2007). Diets high in refined carbohydrates have been shown to cause tissue-specific overexpression of LpL. This has been implicated in tissue-specific insulin resistance and

Several studies have reported conflicting reports on the effect of hormonal replacement therapy on plasma LDL-C and Lp(a) levels (Taskinen *et al.*, 1996; Shlipak *et al.*, 2000; Vigna *et al.*, 2002). In a cohort study conducted by Danik *et al*. (2008), the effect of hormone replacement therapy (HT) on Lp(a) and cardiovascular risk was investigated. It was reported that the relationship of high Lp(a) levels with increased cardiovascular disease is modified by hormonal therapy. These data suggest that the predictive utility of Lp(a) is markedly attenuated among women taking HT and may inform clinicians' interpretation of Lp(a) values in such patients. It was noteworthy that the effect of hormonal therapy was observed only in women with high LDL cholesterol levels, in agreement with previous studies suggesting an interaction between Lp(a) and LDL cholesterol (Berglung and

Elevated serum LDL-C and low levels of HDL-C are known as major and independent risk factors for CHD. Small, dense lipoprotein sub-fractions have been reported to have atherogenic potentials, with particular reference to Lipoprotein(a) [Lp(a)], a variant of low density lipoprotein (LDL). Other atherogenic sub-fractions of lipoproteins are VLDL, LDL, and IDL. These sub-fractions are characterized by the presence of apolipoprotein B-100, with an additional apolipoprotein known as apo(a) in the Lp(a) structure. Apo(a) is structurally and functionally similar to plasminogen and it accounts for virtually all the genetic variability in plasma Lp(a) levels. Variation of length within the kringle 4-encoding region of the apo(a) gene may account for a greater proportion of the inter-individual variation in plasma Lp(a) concentrations, with a strong genetic involvement inherited as a single

In the course of the pathogenesis of atherosclerosis, oxidized LDL is taken up by macrophages and into endothelial cells. This leads to formation of atherosclerotic plaques which precedes development of CHD. Oxidized LDL is antigenic and titres of autoantibodies against oxidized LDL in plasma can be used as indicator of a positive association with CHD. A positive association has also been established between plasma level of LDL, specifically oxidized LDL and other risk factors contributing to development of CHD. Such risk factors were identified as hypertriglyceridemia, reduced HDL-C levels, abdominal obesity and insulin resistance. Treatment of CHD can be achieved by lowering of plasma cholesterol levels which has been achieved by cholesterol-lowering therapy, suggesting that maintenance of low cholesterol levels may sufficiently prevent or reverse an established atherosclerosis. Increasing plasma levels of HDL-C has been reported to also be of benefit.

consequent development of type 2 diabetes mellitus & obesity.

*2.9.3. Influence of Hormones on plasma LDL-C and Lp(a) levels* 

Adebowale Saba and Olayinka Oridupa *University of Ibadan, Nigeria* 

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