Glucagon
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- Glucagon secretion is stimulated under conditions of hypoglycaemia and inhibited under conditions of hyperglycaemia. Parasympathetic innervation via the vagus nerve also stimulates release of glucagon.
- Glucagon has a catabolic effect on body reserves.
- The main target tissue is the liver.
- Here it acts primarily to increase the degradation of glycogen via glycogenolysis and to increase the synthesis of glucose from amino acids via gluconeogenesis.
- Glycogen regulates the reaction in glycolysis which converts phosphoenolpyruvate (PEP) to pyruvate. This reaction is catalysed by the enzyme pyruvate kinase and produces a molecule of ATP. Glucagon inactivates this enzyme by phosphorylation via protein kinase A (PKA).
- It increases the β oxidation of fatty acids to provide energy for gluconeogenesis.
- Here it acts primarily to increase the degradation of glycogen via glycogenolysis and to increase the synthesis of glucose from amino acids via gluconeogenesis.
- Glucagon also acts on other tissues, including adipose tissue where it increases the rate of lipolysis and, skeletal muscle where it increases the rate of protein catabolism.
- Glucagon reduces basal metabolic rate.
- Glucagon predominates during fasting metabolism.
- During fasting, the citric acid cycle turns slowly as oxaloacetate is removed to make glucose. Therefore, acetyl CoA (produced from lipolyis and protein catabolism) builds up and is converted to ketone bodies. Ketosis may occur if the situation is prolonged.