Liver glycogen exhaustion

Fuels used when liver glycogen is exhausted... 

In the early stage of starvation, noradrenahne and cortisol induce breakdown of protein. Generation of KBs from FAs takes place in the Hver, while glycerol and amino acids are used for gluconeogenesis. In starvation, uric acid excretion falls by about 50 per cent. Liver glycogen is exhausted after 12—24 hours without food. 

Glycogen stores in liver and kidney are exhausted in about 24 hours. After this, the body must find glucose equivalents somewhere. The major metabolic adaptations of starvation are the result of having to maintain glucose levels without any direct source of it (Fig. 17-8). 

When the blood glucose level falls and the liver s glycogen reserves are also exhausted, the liver still has the capacity to synthesize glucose via gluconeogenesis from amino acids that are supplied from protein breakdown. Under starvation conditions the liver forms increasing amounts of ketone bodies (see fig. 18.7). This is due to elevated concentrations of acetyl-CoA, which favor the formation of ketone bodies. The ketone bodies are secreted and used as a source of energy by other tissues, especially those tissues like the brain that cannot catabolize fatty acids directly. 

When food intake decreases, the utilization of fat and protein reserves in the body enables various essential metabolic processes to continue during the nutritional inadequacy. In the early stage of fasting or starvation, glucose requirements of the brain and nervous system are fulfilled by mobilization of glycogen in the liver. This short-term adaptation lasts only a day until glycogen stores are exhausted. Gluconeogenesis... 

Muscle pyridoxal phosphate is released into the circulation (as pyridoxal) in starvation as muscle glycogen reserves are exhausted and there is less requirement for glycogen phosphorylase activity. Under these conditions, it is potentially available for redistribution to other tissues, especially the liver and kidneys, to meet the increased requirement for gluconeogenesis from amino acids (Black et al., 1978). However, during both starvation and prolonged bed rest, there is a considerable increase in urinary excretion of 4-pyridoxic acid, suggesting that much of the vitamin Be released as a result of depletion of muscle glycogen and atrophy of muscle is not redistributed, but rather is ca-tabolized and excreted (Cobum et al., 1995). 

Gluconeogenesis is activated when the glycogen reserves are exhausted. There are three alternative substrates available in the liver cells for glucose synthesis ... 

The glycogen stores in the fetus at term are twice those in the adult in the liver and ten times those in adult muscle. After birth the liver stores of glycogen are almost exhausted within hours because of conversion to glucose. The muscle stores take longer to be depleted. 

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