Fatty acid metabolism ketone bodies

Lipid metabolism. The liver synthesizes fatty acids from acetate units. The fatty acids formed are then used to synthesize fats and phospholipids, which are released into the blood in the form of lipoproteins. The liver s special ability to convert fatty acids into ketone bodies and to release these again is also important (see p. 312). 

FIGURE 23-19 Electron micrograph of heart muscle. In the profuse mitochondria of heart tissue, pyruvate, fatty acids, and ketone bodies are oxidized to drive ATP synthesis. This steady aerobic metabolism allows the human heart to pump blood at a rate of nearly 6 IVmin, or about 350 L/hr—or 200 X 106 L over 70 years. 

The heart oxidatively metabolizes a variety of substrates, probably because it is the most essential organ in the body. The energy demands of the heart are such that it probably must rely on ATP generated in the mitochondria not enough ATP can be made anaerobically to support these demands. The heart efficiently metabolizes fatty acids and ketone bodies and may prefer those sources of energy, even to glucose. 

The liver also plays a central role in the regulation of lipid metabolism. When fuels are abundant, fatty acids derived from the diet or synthesized by the liver are esterified and secreted into the blood in the form of very low density lipoprotein (see Figure 30.15). However, in the fasting state, the liver converts fatty acids into ketone bodies. How is the fate of liver fatty acids determined The selection is made according to whether the fatty acids enter the mitochondrial... 

E. Gluconeogenesis requires ATP, which is in short supply, turning up the catabolism of glucose to lactate in the absence of an intact electron transport chain. ADP cannot be transported into the mitochondrion because ATP, its antiporter partner, isn t made by oxidative phosphorylation as a result of cyanide inhibition of cytochrome oxidase. Metabolism of fatty acids and ketone bodies requires a functional electron transport chain for their metabolism, and these possibilities are also ruled out. 

Effect of increased fatty-acid availability on muscle metabolism. The effect of fatty acids and ketone-body metabolism on glucose metabolism in the muscle is shown above. The major effect is a decrease of glucose utilization by the muscle. Negative aspects on this metabolism are shown in purple (for more detail, see the text). 

Skeletal muscles use many fuels to generate ATP. The most abundant immediate source of ATP is creatine phosphate. ATP also can be generated from glycogen stores either anaerobically (generating lactate) or aerobically, in which case pyruvate is converted to acetyl CoA for oxidation via the TCA cycle. All human skeletal muscles have some mitochondria and thus are capable of fatty acid and ketone body oxidation. Skeletal muscles are also capable of completely oxidizing the carbon skeletons of alanine, aspartate, glutamate, valine, leucine, and isoleucine, but not other amino acids. Each of these fuel oxidation pathways plays a somewhat unique role in skeletal muscle metabolism. 

Lipolysis, fatty acid oxidation, ketone body formation and cholestrol metabolism... 

Our objective was to study how TTA affect the growth and lipid metabolism in glioma cells. It is well established that normal brain tissue primarily oxidizes glucose as a source of energy, however, it is also capable of oxidizing fatty acids and ketone bodies. 

The results of experiments to be described below appear to show that anoxia and cell poisons which inhibit respiratory chain phosphorylation stimulate uptake of glucose by muscle and that under suitable conditions respiration of fatty acids and ketone bodies can lead to inhibition of glucose uptake. Since fatty acids and ketone bodies are oxidized by mitochondria and since the effects of anoxia and of these cell poisons will be exerted principally on mitochondrial metabolism it seems reasonable to accept these findings as common evidence for a regulatory effect of mitochondrial metabolism on glucose uptake. It is recognized that this concept is provisional until such time as the mechanism of this regulation has been established. 

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