How are lipid and carbohydrate metabolisms affected in liver muscle and adipose tissues during prolonged starvation?

Prolonged starvation, the liver will release glycogen in response to the glucagon secreted from the pancreas as a result of low blood glucose level. Glucagon synthesis is inhibited by glycogen by triggering cyclic AMP. In the meantime, glucose is synthesised by the hydrolysis of glucose 6-phosphate derived from glycogen. The glucose is released from the liver into the blood to increase its level of glucose.

The lipids are mobilised from adipose tissues as free fatty acids to supply energy for the muscle tissues. This involves the preparation of malonyl CoA from acetyl CoA and Co2 by acetyl CoA carboxylase. Carbons are then added in pairs to a growing fatty acyl chain in a four-step sequence by fatty acid synthase. The acetyl CoA formed can then be shunted to ketone bodies in the liver for energy production. 2 acetyl CoA are joined to release 1 CoA and 1 acetoacetyl CoA. The acetoacetyl CoA is then converted into acetoacetate where it can futher decompose into acetone or reduced into beta-hydroxybutyrate. Both acetone and beta-hydroxybutyrate are ketones that can be exported to muscle tissues to provide them with energy.