Ketoneogenesis

Ketoneogenesis

• Occurs when acetyl-CoA levels rise to high concentrations. Ketones can then be used as a fuel source over glucose
• Ketone bodies are made in liver mitochondria from acetyl-CoA and amino acid degradation
• Ketones can enter the blood and drop the blood pH (acidosis)

• Conversion back to acetyl-CoA can provide a lot of ATP

Ketoacidosis

• When ketone levels in the blood increase as a result of depleted glycogen stores
• Some buffering comes from blood buffering, but ketoacidosis occurs when pH drops below 7.35
• Occurs in starvation, low carb diets, and diabetes

Diabetes

• In non-diabetic individuals increased blood glucose (above 4-7mM) induces insulin release
• There are two types of diabetes: Type I and Type II
• Insulin binding to cells results in:
• Intracellular glucose
• ATP
• Glycogen
• Fat and Protein

• Autoimmune damage to pancreatic beta cells leads to deficient insulin production
• High glucose (hyperglycemia) and low glucose (hypoglycemia) can be detrimental
• Insulin injections can increase glucose intake, but also lower glucagon secretion
• The insulin injections leave glycogenolysis and gluconeogenesis unable to maintain blood glucose levels
• Low glucose levels can lead to ketone body production and ketoacidosis
• Bicarbonate injections neutralize the acidity
• Insulin treatments lead to:
• Reduced hyperglycemia
• Drop in ketone body formation
• Blood tonicity normalizes and water balance returns
• Inhibition of glycogenolysis and beta oxidation
• Glycogen and fat synthesis rises
• Glycolysis increases
• Gluconeogenesis decreases