Acetyl coa steroid synthesis

The systematic name of this enzyme class is acetyl-CoA:acetoacetyl-CoA C-acetyltransferase (thioester-hydrolysing, carboxymethyl-forming) . Other names in common use include (S)-3-hydroxy-3-methylglutaryl-CoA acetoacetyl-CoA-lyase , (CoA-acetylating) , 3-hydroxy-3-methylglutaryl CoA synthetase , 3-hydroxy-3-methylglutaryl coenzyme A synthase , 3-hydroxy-3-methylglutaryl coenzyme A synthetase , 3-hydroxy-3-methylglutaryl-CoA synthase , 3-hydroxy-3-methylglutaryl-coenzyme A synthase , beta-hydroxy-beta-methylglutaryl-CoA synthase , HMG-CoA synthase , acetoacetyl coenzyme A transacetase , hydroxymethylglutaryl coenzyme A synthase , and hydroxymethylglutaryl coenzyme A-condensing enzyme .

Answer- Fructose does not stimulate the release of insulin. The reduced insulin/glucagon ratio stimulates gluconeogenesis and inhibits glycolysis. That is, glucagon dominates the picture, increasing fructose bisphosphatase activity and leading to formation of glucose. Gluconeogenesis occurs only if fructose in pure form is consumed. However, the more usual situation is consumption of fructose as sugar as a sweetener in a “normal” meal.  In other words, fructose is consumed together with starch or sugar. This leads to increases in blood sugar and insulin levels directly with a rapid cessation of gluconeogenesis. 

Acetyl coenzyme A or acetyl-CoA is a molecule that participates in many biochemical reactions in protein, carbohydrate and lipid metabolism . [1] Its main function is to deliver the acetyl group to the citric acid cycle (Krebs cycle) to be oxidized for energy production. Coenzyme A (CoASH or CoA) consists of a β-mercaptoethylamine group linked to the vitamin pantothenic acid through an amide linkage. [2] The acetyl group (indicated in blue in the structural diagram on the right) of acetyl-CoA is linked to the sulfhydryl substituent of the β-mercaptoethylamine group. This thioester linkage is a "high energy" bond, which is particularly reactive. Hydrolysis of the thioester bond is exergonic (− kJ/mol).

ACC1 is strictly cytosolic and is enriched in liver, adipose tissue and lactating mammary tissue. ACC2 was originally discovered in rat heart but is also expressed in liver and skeletal muscle. ACC2 has an N -terminal extension that contains a mitochondrial targeting motif and is found associated with carnitine palmitoyltransferase I (CPT I) allowing for rapid regulation of CPT I by the malonyl-CoA produced by ACC. Both isoforms of ACC are allosterically activated by citrate and inhibited by palmitoyl-CoA and other short- and long-chain fatty acyl-CoAs. Citrate triggers the polymerization of ACC1 which leads to significant increases in its activity. Although ACC2 does not undergo significant polymerization (presumably due to its mitochondrial association) it is allosterically activated by citrate. Glutamate and other dicarboxylic acids can also allosterically activate both ACC isoforms.

Acetyl coa steroid synthesis

acetyl coa steroid synthesis

ACC1 is strictly cytosolic and is enriched in liver, adipose tissue and lactating mammary tissue. ACC2 was originally discovered in rat heart but is also expressed in liver and skeletal muscle. ACC2 has an N -terminal extension that contains a mitochondrial targeting motif and is found associated with carnitine palmitoyltransferase I (CPT I) allowing for rapid regulation of CPT I by the malonyl-CoA produced by ACC. Both isoforms of ACC are allosterically activated by citrate and inhibited by palmitoyl-CoA and other short- and long-chain fatty acyl-CoAs. Citrate triggers the polymerization of ACC1 which leads to significant increases in its activity. Although ACC2 does not undergo significant polymerization (presumably due to its mitochondrial association) it is allosterically activated by citrate. Glutamate and other dicarboxylic acids can also allosterically activate both ACC isoforms.

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