Fatty Acid Metabolism and Ketone Bodies Quiz

Metabolism of Fatty Acids and Ketone Bodies

• Fatty acids from dietary triglycerides are broken down into component fatty acids and monoglycerides in the small intestine, absorbed, converted to triglycerides, packaged into chylomicrons, and shipped out into circulation.

• Fatty acids can be cleaved into their component fatty acids through a series of enzymes and converted into acetyl-CoA in target tissues for energy.

• Fatty acids are imported into mitochondria for fatty acid oxidation pathways through a series of enzymes called Carnitine Palmitoyltransferase (CPTs).

• Acyl-CoA synthetase enzymes convert fatty acids into acyl-CoA by attaching a co-enzyme molecule to a fatty acid in the cytoplasm.

• CPT I takes the acyl-CoA, transfers the fatty acid group to a molecule of carnitine in the cytoplasm, and converts the acyl-CoA into acyl-carnitine.

• CPT II converts acyl-carnitine back into acyl-CoA in the matrix of the mitochondria.

• Beta oxidation or fatty acid oxidation converts acyl-CoA into acetyl-CoA, generating FADH2, NADH, and an acetyl-CoA molecule with each cycle.

• Beta oxidation generates a lot of energy, with 108 ATP molecules generated from a 16 carbon fatty acid.

• The brain cannot effectively use fatty acids for energy, so ketone bodies are generated from acetyl-CoA in the liver mitochondria during times of fasting/starvation.

• Ketone bodies, including Acetoacetate and Hydroxybutyrate, are four carbon molecules that can be taken up by the brain and used for energy.

• Ketones are only synthesized in the liver and released by the liver, and are used for energy during times of fasting and low blood sugar.

• Ketogenic diets are based on the generation of ketones from the release of large amounts of fatty acids, which are converted into ketones and taken up by the brain.Ketones and Ketogenesis: The Process, Function, and Complications

• Ketones are generated from acetyl-CoA in the liver during times of high fat intake, fasting, or untreated diabetes.

• The brain is heavily reliant on glucose metabolism and cannot survive in its absence.

• During fasting, the liver and muscle tissues shift from glucose to fatty acid metabolism to preserve glucose for the brain.

• Ketogenesis is similar to beta oxidation, with acetyl-CoA being converted to acetoacetyl-CoA and then to HMG-CoA.

• The liver-specific enzyme HMG-CoA lyase cleaves HMG-CoA to produce the ketone body acetoacetate and acetyl-CoA.

• Ketone bodies are transported to target tissues, where they are converted back to acetyl-CoA for energy.

• Ketone bodies lower the demand for glucose in the brain during starvation conditions and reduce the amount of protein broken down for gluconeogenesis.

• Elevated levels of ketones in the blood, as seen in diabetic ketoacidosis or severe alcoholism, can lead to acidosis and complications.

• The ketogenic diet, which involves low sugar and high fat intake, can be therapeutic for conditions such as glut1 deficiency, which reduces glucose uptake by the brain and causes seizures.

• Ketones produced during a ketogenic diet can supplement reduced glucose levels in the brain and reduce seizures in patients with glut1 deficiency.

• Fatty acid oxidation is an important way to generate energy during fasting, with the products of oxidation inhibiting glycolysis and preserving glucose for the brain.

• Ketones provide a way to transport acetyl-CoA to target tissues and reduce the demand for glucose in the brain during starvation conditions.