What is the difference between HMG-CoA formation in ketone bodies synthesis and cholesterol synthesis?

What is the difference between HMG-CoA formation in ketone bodies synthesis and cholesterol synthesis?

Unlike the HMG-CoA formed during ketone body synthesis in the mitochondrial matrix, the other isoenzyme HMG-CoA synthase, this form is synthesized in the cytoplasm for cholesterol synthesis. HMGR absolutely requires NADPH as a cofactor and two moles of NADPH are consumed during the conversion of HMG-CoA to mevalonate.

How are ketone bodies synthesis?

Ketone bodies are synthesized from acetyl-coenzyme A (acetyl-CoA) which is a product of mitochondrial β-oxidation of fatty acids. This adenosine triphosphate (ATP)-dependent catabolism of fatty acids is associated with breakdown of two carbon fragments at a time and results in formation of acetyl-CoA.

How is cholesterol synthesized?

Biosynthesis of cholesterol generally takes place in the endoplasmic reticulum of hepatic cells and begins with acetyl- CoA, which is mainly derived from an oxidation reaction in the mitochondria. However, acetyl-CoA can also be derived from the cytoplasmic oxidation of ethanol by acetyl-CoA synthetase.

What is the mechanism of ketosis?

Ketosis is a metabolic state characterized by elevated levels of ketone bodies in the blood or urine. Physiologic ketosis is a normal response to low glucose availability, such as low-carbohydrate diets or fasting, that provides an additional energy source for the brain in the form of ketones.

What are the three major ketone bodies produced in the body?

A carbonyl compound produced as a water-soluble byproduct when fatty acids are broken down for energy in the liver. There are three endogenous ketone bodies: acetone, acetoacetic acid, and (R)-3-hydroxybutyric acid; others may be produced as a result of the metabolism of synthetic triglycerides.

Is acetone a ketone body?

Ketone bodies are produced by the liver and used peripherally as an energy source when glucose is not readily available. The two main ketone bodies are acetoacetate (AcAc) and 3-beta-hydroxybutyrate (3HB), while acetone is the third, and least abundant, ketone body.

What enzyme makes cholesterol?

In eukaryotes, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase is a key enzyme that catalyses the synthesis of a precusor of cholesterol as well as non-sterol isoprenoids, mevalonate.

Where are ketone bodies metabolized?

The ketone bodies are efficiently metabolized in peripheral tissues except in the brain. Hepatic ketogenesis is suppressed and upregulated by insulin and glucagon, respectively. The ketone bodies and AMP suppress ChREBP transactivity and de novo lipogenesis in the liver.

Where in the body are ketone bodies produced?

the liver
Ketone bodies are produced by the liver and used peripherally as an energy source when glucose is not readily available.

How is the synthesis of a ketone body?

Just like cholesterol synthesis, ketone body synthesis begins with the thiolase reaction, a reversible reaction that combines two acetyl-CoA into one acetoacetyl-CoA. Then, acetoacetyl-CoA and acetyl-CoA are combined by HMG-CoA synthase to yield HMG-CoA.

How are the ketone bodies of cholesterol broken down?

During the breakdown of ketone bodies, D-β-hydroxybutyrate is oxidized to acetoacetate, which receives a CoA from succinyl-CoA in the β -ketoacyl-CoA transferase reaction. Acetoacetyl-CoA is then broken down into two acetyl-CoA by thiolase.

Where are ketone bodies produced in the liver?

Ketone bodies are only produced in the mitochondria of the liver cells. It uses acetyl-CoA yielded from beta-oxidation (which also occurs in the mitochondria). This means that citrate plays no role in ketone body synthesis, because there is no need to transport acetyl-CoA across the mitochondrial membrane.

How does insulin affect the formation of ketone bodies?

The rate of formation of ketone bodies depends on the concentration of fatty acids derived from hydrolysis of adipose tissue triacylglycerol by hormone-sensitive lipase. Insulin depresses lipolysis and promotes triacylglycerol synthesis and storage, while glucagon has the opposite effects.

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