Vitamin C contributes to an improved degradation of cholesterol

Ascorbate increases the number of low density lipoprotein receptors in cultured arterial smooth muscle cells

Cholesterol levels are influenced by several mechanisms. One of them is the uptake of cholesterol-containing lipoproteins (low-density lipoproteins, LDL) in the cells. A primary component of regulating the LDL uptake in the body – and thereby managing the amount of cholesterol in the blood – is the LDL receptor. The more LDL receptors the cell produces, the more cholesterol can be removed from the bloodstream. The present study investigated the influence of vitamin C on the number of LDL receptors on the surface of smooth muscle cells. As it turned out, vitamin C was able to significantly increase the number of LDL receptors, thereby contributing to an improved degradation of LDL molecules and cholesterol. Thus, the study clarified an important mechanism of vitamin C in regulating the cholesterol and cell metabolism. Further details can be found in the study.
Lipid disorders are characterized by imbalanced levels of fatty substances (i.e. cholesterol and triglycerides) in the bloodstream. These lipids are carried in the blood stream in form of microscopic round particles, called lipoproteins. Thus, these conditions are also called lipoprotein disorders. There are, generally speaking, two types of cholesterol-transporting lipoproteins: a) the “bad cholesterol” are those lipoproteins that carry cholesterol and other fatty substances to the sites of tissue repair, e.g. in the artery walls; the most common representatives of this group are Low-density-lipoproteins (LDL) and, a newer one, Lipoprotein(a), Lp(a). b) the “good cholesterol” are those lipoproteins that carry cholesterol and other fatty substances away from the sites of tissue repair and transport it back to the liver where it is biologically “burnt” One of the most frequent causes why “bad cholesterol” particles are elevated in the blood stream is micronutrient deficiency. This can be easily explained: A deficiency of vitamins causes structural damage to the artery walls and other organs and the body (liver) reacts with an increased production of “repair factors” like LDL and Lp(a). Because the elevation of these risk factors in the blood is already a reaction damage of our body tissue caused by vitamin deficiency, they are considered “secondary” risk factors.
Aulinskas TH, Van der Westhuyzen DR, Coetzee GA. Ascorbate increases the number of low density lipoprotein receptors in cultured arterial smooth muscle cells. Atherosclerosis. 1983 May;47(2):159-71.


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