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3-Hydroxy-8-methylglutaryl CoA

As summarized in Figure 27.7, the mevalonate pathway begins with the conversion of acetate to acetyl CoA, followed by Claisen condensation to yield acetoacety) CoA. A second carbonyl condensation reaction with a third molecule of acetyl CoA, this one an aldol-like process, then yields the six-carbon compound 3-hydroxy-3-methylglutaryl CoA, which is reduced to give mevalonate. Phosphorylation, followed by loss of C02 and phosphate ion, completes the process. [Pg.1072]

Step 2 of Figure 27.7 Aldol Condensation Acetoacetyl CoA next undergoes an aldol-like addition (Section 23.1) of an acetyl CoA enolate ion in a reaction catalyzed by 3-hydroxy-3-methylglutaryl-CoA synthase. The reaction again occurs... [Pg.1072]

Most of the acetyl-CoA formed by 3-oxidation in liver is converted to acetoacetate by the 3-hydroxy-3-methylglutaryl-CoA pathway (Guzman and Gelen, 1993). Acetoacetate is reversibly converted to D-3-hydroxybutyrate by D-3-hy-droxybutyrate dehydrogenase in the mitochondrial matrix in all tissues. [Pg.116]

The ketone bodies (acetoacetate, 3-hydroxybutyrate, and acetone) are formed in hepatic mitochondria when there is a high rate of fatty acid oxidation. The pathway of ketogenesis involves synthesis and breakdown of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) by two key enzymes, HMG-CoA synthase and HMG-GoA lyase. [Pg.189]

Roberts, J.R. and Miziorko, H.M. 1997. Evidence supporting a role for histidine-235 in cation binding to human 3-hydroxy-3-methylglutaryl-CoA lyase. Biochemistry 36 7594—7600. [Pg.238]

It has been found that the 3-hydroxy-3-methylglutaryl-CoA (HMG CoA) inhibitors statins (atorvastatin, pravastatin, and cerivastatin), widely prescribed cholesterol-lowering agents, are able to inhibit phorbol ester-stimulated superoxide formation in endothelial-intact segments of the rat aorta [64] and suppress angiotensin II-mediated free radical production [65]. Delbose et al. [66] found that statins inhibited NADPH oxidase-catalyzed PMA-induced superoxide production by monocytes. It was suggested that statins can prevent or limit the involvement of superoxide in the development of atherosclerosis. It is important that statin... [Pg.920]

The therapeutic class that uniquely exemplifies lactone prodrugs are the statins, i.e., the cholesterol-lowering agents that act by inhibiting 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase (EC 1.1.1.34). This microsomal enzyme catalyzes conversion of HMG-CoA to mevalonate, an important rate-limiting step in cholesterol biosynthesis. Cholesterol synthesis occurs mainly... [Pg.510]

Hampton, R. Y., R. G. Gardner, and J. Rine, Role of 26S proteasome and HRD genes in the degradation of 3-hydroxy-3-methylglutaryl-CoA reductase, an integral endoplasmic reticulum membrane protein. Md Biol Cell, 1996, 7(12), 2029 4. [Pg.88]

In our example, EC book and Empath find an exact match to HMG-CoA reductase. The Empath link shows the metabolic step that the enzyme catalyzes (Figure 10.5 [50]). The reaction is between S-3-hydroxy-3-methylglutaryl-CoA and Mevalonate. The step summary on the right side of the chart image shows activation and regulation of the enzyme, its biological scope, direction, reversibility and stoichiometry. A pathway search... [Pg.259]

Formation of mevalonate. The conversion of acetyl CoA to acetoacetyl CoA and then to 3-hydroxy-3-methylglutaryl CoA (3-HMG CoA) corresponds to the biosynthetic pathway for ketone bodies (details on p. 312). In this case, however, the synthesis occurs not in the mitochondria as in ketone body synthesis, but in the smooth endoplasmic reticulum. In the next step, the 3-HMG group is cleaved from the CoA and at the same time reduced to mevalonate with the help of NADPH+H 3-HMG CoA reductase is the key enzyme in cholesterol biosynthesis. It is regulated by repression of transcription (effectors oxysterols such as cholesterol) and by interconversion... [Pg.172]

At high concentrations of acetyl-CoA in the liver mitochondria, two molecules condense to form acetoacetyl CoA [1]. The transfer of another acetyl group [2] gives rise to 3-hydroxy-3-methylglutaryl-CoA (HMC CoA), which after release of acetyl CoA [3] yields free acetoacetate (Lynen cycle). Acetoacetate can be converted to 3-hydroxybutyrate by reduction [4], or can pass into acetone by nonenzymatic decarboxylation [5]. These three compounds are together referred to as "ketone bodies," although in fact 3-hydroxy-butyrate is not actually a ketone. As reaction [3] releases an ion, metabolic acidosis can occur as a result of increased ketone body synthesis (see p. 288). [Pg.312]

This enzyme [EC 4.1.3.4] catalyzes the conversion of (5 )-3-hydroxy-3-methylglutaryl-CoA to acetyl-CoA and acetoacetate. [Pg.354]

This enzyme [EC 2.7.1.109], also known simply as reductase kinase, catalyzes the reaction of ATP with the enzyme 3-hydroxy-3-methylglutaryl-CoA reductase (NADPH) producing ADP and the phosphorylated form of the reductase. This phosphorylation inactivates the reductase. Histones can substitute for the reductase as substrates. [Pg.355]

Figure 9-4. Metabolism of the branched-chain amino acids. The first two reactions, transamination and oxidative decarboxylation, are catalyzed by the same enzyme in all cases. Details are provided only for isoleucine. Further metabolism of isoleucine and valine follows a common pathway to propionyl CoA. Subsequent steps in the leucine degradative pathway diverge to yield acetoacetate. An intermediate in the pathway is 3-hydroxy-3-methylglutaryl CoA (HMG-CoA), which is a precursor for cytosolic cholesterol biosynthesis. Figure 9-4. Metabolism of the branched-chain amino acids. The first two reactions, transamination and oxidative decarboxylation, are catalyzed by the same enzyme in all cases. Details are provided only for isoleucine. Further metabolism of isoleucine and valine follows a common pathway to propionyl CoA. Subsequent steps in the leucine degradative pathway diverge to yield acetoacetate. An intermediate in the pathway is 3-hydroxy-3-methylglutaryl CoA (HMG-CoA), which is a precursor for cytosolic cholesterol biosynthesis.
Figure 12.1. HMG-CoA catalyzed conversion of 3-hydroxy-3-methylglutaryl CoA into mevalonate as the rate-limiting step of cholesterol biosynthesis. Figure 12.1. HMG-CoA catalyzed conversion of 3-hydroxy-3-methylglutaryl CoA into mevalonate as the rate-limiting step of cholesterol biosynthesis.
Zapata R., D. Martin, M-D. Kulachs, and X. Belles (2002). Effects of h3fpocholesterolaemic agents on the expression and activity of 3-hydroxy-3-methylglutaryl-CoA reductase in the fat body of the German Cockroach. Archives of Insect Biochemistry and Physiology 49 177-186. [Pg.292]

Zapata R., M-D. Piulachs, and X. Belles (2(X)3). Inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase lower fecundity in the German cockroach Correlation between the effects on fecundity in vivo with the inhibition of enzymatic activity in embryo cells. Pest Management Science 59 1111-1117. [Pg.292]

Healthy, well-nourished individuals produce ketone bodies at a relatively low rate. When acetyl-CoA accumulates (as in starvation or untreated diabetes, for example), thiolase catalyzes the condensation of two acetyl-CoA molecules to acetoacetyl-CoA, the parent compound of the three ketone bodies The reactions of ketone body formation occur in the matrix of liver mitochondria. The six-carbon compound /3-hydroxy-/3-methylglutaryl-CoA (HMG-CoA) is also an intermediate of sterol biosynthesis, but the enzyme that forms HMG-CoA in that pathway is cytosolic. HMG-CoA lyase is present only in the mitochondrial matrix. [Pg.651]

Cholesterol is formed from acetyl-CoA in a complex series of reactions, through the intermediates /3-hydroxy-/3-methylglutaryl-CoA, mevalonate, and two activated isoprenes, dimethylallyl pyrophosphate and isopentenyl pyrophosphate. Condensation of isoprene units produces the noncyclic squalene, which is cyclized to yield the steroid ring system and side chain. [Pg.829]


See other pages where 3-Hydroxy-8-methylglutaryl CoA is mentioned: [Pg.833]    [Pg.833]    [Pg.833]    [Pg.101]    [Pg.818]    [Pg.1074]    [Pg.1074]    [Pg.1074]    [Pg.674]    [Pg.793]    [Pg.220]    [Pg.521]    [Pg.112]    [Pg.355]    [Pg.149]    [Pg.170]    [Pg.170]    [Pg.132]    [Pg.66]    [Pg.293]    [Pg.82]    [Pg.174]    [Pg.125]   
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See also in sourсe #XX -- [ Pg.388 ]

See also in sourсe #XX -- [ Pg.699 , Pg.701 ]

See also in sourсe #XX -- [ Pg.699 , Pg.701 , Pg.946 , Pg.992 ]

See also in sourсe #XX -- [ Pg.699 , Pg.701 , Pg.946 , Pg.992 ]

See also in sourсe #XX -- [ Pg.407 , Pg.418 , Pg.436 , Pg.599 ]

See also in sourсe #XX -- [ Pg.313 ]

See also in sourсe #XX -- [ Pg.448 ]




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3 -Hydroxy-3 -methylglutaryl

3- Hydroxy-3-methylglutaryl CoA lyase deficiency

3- Hydroxy-3-methylglutaryl-CoA (HMG

3-Hydroxy-3-methylglutaryl-CoA lyase

3-Hydroxy-3-methylglutaryl-CoA synthase (HMG

3-Hydroxy-3-methylglutaryl-CoA synthesis

3-Hydroxy-3-methylglutaryl-CoA synthetase

3-methylglutaryl

Hydroxy methylglutaryl-CoA reductase

Hydroxy-3-methylglutaryl-CoA synthetase (EC

S-3-Hydroxy-3-methylglutaryl-CoA

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