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The relationship between nonfasting and fasting lipid measurements in patients with or without type 2 diabetes mellitus receiving treatment with 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors. Weiss R1, Harder M, Rowe J.
Mutations in the HMGCL gene cause HMG-CoA lyase deficiency. The HMGCL gene provides instructions for making an enzyme known as 3-hydroxymethyl-3-methylglutaryl-coenzyme A lyase (HMG-CoA lyase). This enzyme plays a critical role in breaking down dietary proteins and fats for energy. Specifically, it is responsible for processing leucine, an amino acid that is part of many proteins. HMG-CoA lyase also produces ketones during the breakdown of fats.
HMG-CoA (or 3-hydroxy-3-methylglutaryl-coenzyme A) is an intermediate in the mevalonate and ketogenesis pathways. It is formed from acetyl CoA and acetoacetyl CoA by HMG-CoA synthase.
108. Bargossi AM, Battino M, Gaddi A, et al. Exogenous CoQ10 preserves plasma ubiquinone levels in patients treated with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Int J Clin Lab Res. 1994;24(3):171-176.
Hyperlipidemia is a major risk factor for coronary artery disease (CAD). A higher level of low density lipoprotein-cholesterol (LDL-C) can increase the incidence of CAD . The 3-hydroxy-3-methylglutaryl coenzyme.