ketogenesis

The four where he was the sole author were on ketogenesis.

Usually, these amounts of insulin are sufficient to suppress ketogenesis.

However, when ketogenesis is happening at higher-than-normal levels, the body is said to be in a state of ketosis.

Ketogenesis may or may not occur, depending on levels of available carbohydrates in the cell or body.

Basically, they are water soluble, undergo b-oxidation, do not induce ketogenesis but rather promote gluconeogenesis.

Ketone bodies are formed by ketogenesis when liver glycogen stores are depleted.

HMG-CoA is an intermediate in both cholesterol synthesis and ketogenesis.

DHA is formed by ketogenesis of glycerol.

Unable to be used in the citric acid cycle, the excess acetyl-CoA is therefore rerouted to ketogenesis.

Specifically, the enzyme is required for ketogenesis in the liver, and is also responsible for processing the amino acid leucine.

Edson also befriended Luis Federico Leloir and collaborated with him on ketogenesis.

Triglycerides are too hydrophobic to cross into brain cells, so the liver must convert fatty acids into ketones through ketogenesis.

PPAR-alpha is activated under conditions of energy deprivation and is necessary for the process of ketogenesis, a key adaptive response to prolonged fasting.

They have potentially beneficial attributes in protein metabolism but may be contraindicated in some situations due to their tendency to induce ketogenesis and metabolic acidosis.

For example, restricting dietary carbohydrates increases the plasma concentration of B-hydroxybutyrate (that is, ketogenesis), a shift that may counteract life-span extension in mammals.

With his colleague, J. Denis McGarry, he discovered the malonyl-CoA regulatory system for fatty acid oxidation and ketogenesis.

Mice lacking FGF21 fail to fully induce PGC-1α expression in response to a prolonged fast and have impaired gluconeogenesis and ketogenesis.

A ketogenic amino acid is an amino acid that can be degraded directly into Acetyl CoA through ketogenesis.

The most severe neuroglycopenic symptoms occur with hypoglycemia caused by excess insulin because insulin reduces the availability of other fuels by suppressing ketogenesis and gluconeogenesis.

It is a mitochondrial enzyme that catalyzes the first reaction of ketogenesis, a metabolic pathway that provides lipid-derived energy for various organs during times of carbohydrate deprivation, such as fasting.

Ketone bodies are produced from acetyl-CoA (see ketogenesis) mainly in the mitochondrial matrix of hepatocytes when carbohydrates are so scarce that energy must be obtained from fatty acid metabolisms.

Initially, the level of insulin in circulation drops and the levels of glucagon and epinephrine rise, degrading high amounts of glycogen and upregulating gluconeogenesis, lipolysis, and ketogenesis.

Acute FGF21 treatment induced hepatic expression of key regulators of gluconeogenesis, lipid metabolism, and ketogenesis including glucose-6-phosphatase, phosphoenol pyruvate carboxykinase, 3-hydroxybutyrate dehydrogenase type 1, and carnitine palmitoyltransferase 1α.

In mice FGF21 is strongly induced in liver by prolonged fasting via PPAR-alpha and in turn induces the transcriptional coactivator PGC-1α and stimulates hepatic gluconeogenesis, fatty acid oxidation, and ketogenesis.

Acetyl-CoA is not being recycled through the citric acid cycle because the citric acid cycle intermediates (mainly oxaloacetate) have been depleted to feed the gluconeogenesis pathway, and the resulting accumulation of acetyl-CoA activates ketogenesis.