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HMG-CoA3-Hydroxy-3-Methyl-Glutaryl-CoA (synthase deficiency)
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3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) lyase deficiency leads to a reduced ability to synthesize ketones, which are the primary energy source of the brain when glucose is unavailable.
Statins inhibit HMG-CoA reductase, which converts HMG-CoA to mevalonate.[34],[35] In cancerous cells and noncancerous cells, statins have been reported to inhibition of the mevalonate pathway and induction of ER stress.[17],[18],[19],[20],[36] Inconsistent with these studies, our study has demonstrated that simvastatin treatment significantly inhibited ER stress in the ox-LDL-treated EC.
The mechanism by which statins can cause autoimmune necrotizing myopathy is supposed to be due to overexpression of HMG-CoA reductase in the majority of patients with class II HLA allele DRB1 * 11:01 [9].
It also has a short-elimination half-life, is cleared through both hepatic and renal routes, and is among the most hepatoselective statins available (one of the weakest inhibitors of HMG-CoA reductase).
Attenuation of Streptozotocin-Induced Lipid Profile Anomalies in the Heart, Brain, and mRNA Expression of HMG-CoA Reductase by Diosgenin in Rats.
HMG-CoA reductase catalyzes the conversion of HMG-CoA to mevalonic acid, a necessary step in cholesterol synthesis in the body.
Statins, also known as HMG-CoA reductase inhibitors are competitive inhibitor of the rate-limiting enzyme, 3-hydroxy 3-methylglutaryl coenzyme-A (HMG-CoA) reductase in cholesterol synthesis.
The liver was analyzed for HMG-CoA reductase concentration and hepatic lipase activity whiles cholesterol, LDL and HDL concentrations were measured in the blood serum.
Like statin drugs, monacolins inhibit cholesterol synthesis by inhibiting HMG-CoA reductase and also decrease C-reactive protein levels.
Currently, there are six categories of antilipidemic drugs available in the market, namely, HMG-CoA reductase inhibitors (statins), for example, lovastatin; bile acid sequestrants (anion-exchange resins), for example, cholestyramine and colestipol; fabric acid derivatives (fibrates), for example, clofibrate, gemfibrozil, fenofibrate, ciprofibrate, and bezafibrate; nicotinic acid, for example, niacin; cholesterol absorption inhibitors, for example, ezetimibe; and omega-3-fatty acids (fish oil), for example, Pulse [5].
Finally because of negative HMG-CoA reductase antibodies (IgG), associated to autoimmune statin induced rhabdomyolysis, this differential diagnosis was unlikely in our patient (Table 2).