glukoneogenezde

Glukoneogeneza, also known as gluconeogenesis, is a metabolic pathway that occurs primarily in the liver and, to a lesser extent, in the kidneys. This process synthesizes glucose from non-carbohydrate precursors, such as lactate, glycerol, and certain amino acids, ensuring a steady supply of blood glucose even during periods of fasting or prolonged exercise. It serves as a critical mechanism for maintaining energy homeostasis, particularly when glycogen stores are depleted.

The pathway begins with the conversion of pyruvate, derived from lactate or amino acids, into oxaloacetate, which is then transported into the mitochondria. Oxaloacetate is subsequently converted to phosphoenolpyruvate (PEP) by the enzyme phosphoenolpyruvate carboxykinase (PEPCK), a key regulatory step in gluconeogenesis. PEP is then transported back into the cytosol, where it undergoes further transformations to produce glucose-6-phosphate, which can be released into the bloodstream as glucose after dephosphorylation by glucose-6-phosphatase.

Several amino acids, including alanine, glutamine, and glycine, can also serve as precursors for gluconeogenesis. These amino acids are transaminated to form intermediates like pyruvate or oxaloacetate, which enter the pathway. Glycerol, derived from the breakdown of triglycerides, is converted into dihydroxyacetone phosphate (DHAP), another intermediate that can be shunted into the gluconeogenic pathway.

Regulation of gluconeogenesis is tightly controlled by hormonal signals, including glucagon, cortisol, and epinephrine, which promote the process during fasting or stress. Conversely, insulin inhibits gluconeogenesis by activating enzymes that favor glycolysis, the opposite pathway. Genetic or metabolic disorders affecting key enzymes in gluconeogenesis, such as glucose-6-phosphatase deficiency (Cori disease), can lead to hypoglycemia and other metabolic complications.