Gluconeogenesis (1)
Gluconeogenesis Overview
Definition: Group of metabolic reactions in cytosol and mitochondria to maintain blood glucose levels during fasting.
Regulation: Local and global regulation through hormones such as insulin, glucagon, and cortisol. Some reactions are highly exergonic and irreversible.
Key Organs: Liver is the primary organ for blood glucose supply; kidneys play a secondary role during prolonged fasting.
Importance of Glucose Supply
Continuous glucose supply is essential for several tissues:
Brain: Primarily relies on glucose, using 70% of the total glucose produced during fasting.
Erythrocytes, Renal Medulla, Lens and Cornea, Testes, Skeletal Muscles: Also require glucose.
Initial Energy Sources: Hepatic glycogenolysis (up to 190 g of glucose available) covers energy needs for roughly one day. The daily requirement is approximately 160 g.
Shift to Gluconeogenesis
After several hours of fasting, gluconeogenesis starts contributing significantly to glucose production:
54% from gluconeogenesis after 14 hours of starvation.
64% after 22 hours and up to 84% after 42 hours.
Alternative Glucose Sources
With depleted glycogen storage, alternative sources for gluconeogenesis include:
Lactate
Glycerol: Derived from triglyceride catabolism.
Glucogenic Amino Acids: Such as alanine, methionine, and valine.
Odd-chain Fatty Acids: Converted during beta-oxidation to propionyl CoA, then to succinyl CoA, an intermediate in the TCA cycle that can enter gluconeogenesis.
Mechanism and Reactions
Initiation: Pyruvate carboxylase converts pyruvate to oxaloacetate, which is then phosphorylated to phosphoenolpyruvate (PEP) through PEP carboxykinase.
Key Enzymes:
Pyruvate Carboxylase (PC): Requires ATP and biotin, found in mitochondria.
Phosphoenolpyruvate Carboxykinase (PEPCK): Uses GTP as a phosphate donor, induced by glucocorticoids.
Subsequent Steps:
Enolase converts PEP to 2-phosphoglycerate, followed by a series of reversible reactions leading to fructose-1,6 bisphosphate.
Rate-Limiting Step: Conversion of fructose-1,6 bisphosphate to fructose-6 phosphate via fructose-1,6 bisphosphatase, regulated by ATP, citrate, AMP, and fructose-2,6 bisphosphate.
Final Conversion to Glucose
The last irreversible step is catalyzed by glucose-6 phosphatase, converting glucose-6 phosphate to glucose, primarily in the liver and kidneys.
Muscle cells do not express this enzyme, as their glucose use is primarily for energy needs.
Clinical Significance
Glycogen Storage Disease Type 1 - Von Gierke Disease
Characteristics: Inherited metabolic disorder with poor fasting tolerance due to lack of glucose-6 phosphatase.
Symptoms:
Hepatomegaly and kidney enlargement.
Severe fasting hypoglycemia.
Lactic acidosis due to accumulation of glucose-6 phosphate.
Hypertriglyceridemia and hyperuricemia due to disrupted metabolic pathways.
Pyruvate Carboxylase Deficiency
Implications: Lack of pyruvate carboxylase leads to lactic acidosis, hyperammonemia, and hypoglycemia.
Hyperammonemia caused by reduced oxaloacetate levels affecting the urea cycle.