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Abstract
Since Mg2+-ATP is the controlling factor for the rate-limiting enzyme in the cholesterol biosynthesis sequence that is targeted by the statin pharmaceutical drugs, comparison of the effects of Mg2+ on lipoproteins with those of the statin drugs is warranted. Formation of cholesterol in blood, as well as of cholesterol required in hormone synthesis, and membrane maintenance, is achieved in a series of enzymatic reactions that convert HMG-CoA to cholesterol. The rate-limiting reaction of this pathway is the enzymatic conversion of HMG CoA to mevalonate via HMG CoA. The statins and Mg inhibit that enzyme. Large trials have consistently shown that statins, taken by subjects with high LDL-cholesterol (LDL-C) values, lower its blood levels 35 to 65%. They also reduce the incidence of heart attacks, angina and other nonfatal cardiac events, as well as cardiac, stroke, and total mortality. These effects of statins derive less from their lowering of LDL-C than from their reduction of mevalonate formation which improves endothelial function, inhibits proliferation and migration of vascular smooth muscle cells and macrophages, promotes plaque stabilization and regression, and reduces inflammation, Mg has effects that parallel those of statins. For example, the enzyme that deactivates HMG-CoA Reductase requires Mg, making Mg a Reductase controller rather than inhibitor. Mg is also necessary for the activity of lecithin cholesterol acyl transferase (LCAT), which lowers LDL-C and triglyceride levels and raises HDL-C levels. Desaturase is another Mg-dependent enzyme involved in lipid metabolism which statins do not directly affect. Desaturase catalyzes the first step in conversion of essential fatty acids (omega-3 linoleic acid and omega-6 linolenic acid) into prostaglandins, important in cardiovascular and overall health. Mg at optimal cellular concentration is well accepted as a natural calcium channel blocker. More recent work shows that Mg also acts as a statin.
Key teaching points:
The beneficial effects of the statin drugs are paralleled and complemented by those of Mg.
Each inactivates the enzyme, HMG-CoA Reductase, which converts HMG-CoA to mevalonate—the initial step in formation of cholesterol.
Mg, additionally, activates LCAT (lecithin-cholesterol-acyl-transferase) the enzyme that lowers LDL-C and TG levels, and raises HDL-C levels.
Mg also activates a desaturase, that converts 3- and 6-omega fatty acids to prostaglandins.
Statins, like Mg, have activities important in cardiovascular and overall health.
Key teaching points:
The beneficial effects of the statin drugs are paralleled and complemented by those of Mg.
Each inactivates the enzyme, HMG-CoA Reductase, which converts HMG-CoA to mevalonate—the initial step in formation of cholesterol.
Mg, additionally, activates LCAT (lecithin-cholesterol-acyl-transferase) the enzyme that lowers LDL-C and TG levels, and raises HDL-C levels.
Mg also activates a desaturase, that converts 3- and 6-omega fatty acids to prostaglandins.
Statins, like Mg, have activities important in cardiovascular and overall health.
