Ketone bodies contain ketone group that is produced by the liver from fatty acids, during fasting carbohydrate restriction, starvation, prolonged intense exercise alcoholism, type 1 diabetes mellitus <\/div><\/p>\n\n\n\n When oxidation of fatty acyl CoA to acetyl CoA produces enough NADH and FADH2<\/sub>\u00a0to provide the ATP needs of the liver, acetyl CoA is redirected from the TCA cycle into ketogenesis and oxaloacetate in the TCA cycle is diverted toward malate and into glucose synthesis (gluconeogenesis<\/a>). <\/p>\n\n\n\n This phenomenon is regulated by the NADH\/NAD+<\/sup>\u00a0ratio, which is rather high during \u03b2-oxidation.<\/p>\n\n\n\n As the length of time of fasting continues, elevated transcription of the gene for mitochondrial\u00a0HMG-CoA synthase<\/strong>\u00a0supports high rates of ketone body generation.<\/p>\n\n\n<\/span>\n Snider MDS. Devlin\u2019s Textbook of Biochemistry with Clinical Correlations<\/strong>, the 8th Edition. John Wiley & Sons, Incorporated, 2020; 2019.<\/span> <\/p>\n<\/span>Regulation of Ketone Body Synthesis<\/h2>\n<\/span>\n\n\n
Liver<\/h2>\n<\/span>\n\n\n
glycogen digestion (75% of blood glucose) with inactivation of glycogen synthesis<\/td><\/tr> lactate, alanine, glycerol (25% of glucose) <\/td><\/tr> F-1.6-BP-active<\/td><\/tr> glycolysis PFK2\/kinase and pyruvate kinase phosphorylated, inactivated<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n<\/span>\n Metabolic processes in long-term hunger \u2013 Insulin vs. glucagon<\/h2>\n<\/span>\n\n<\/span>\n
Glucagon effect is strong when:<\/h2>\n<\/span>\n\n\n
Liver\/muscle glycogen storage is empty<\/td><\/tr> Glucose absence in RBC, brain (25%)<\/td><\/tr> LIVER: fatty acid, ketone body synthesis increase<\/td><\/tr> GLUCONEOGESIS INCREASED<\/td><\/tr> KETOGENESIS<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n<\/span>\n References<\/h2>\n<\/span>\n\n\n