Deficiency of glycogen phosphorylase, the enzyme responsible for breaking down glycogen into glucose, conveys the inability to utilize glycogen stores. This would lead to McArdle disease (glycogen storage disease type V), characterized by exercise intolerance, muscle cramping, and myoglobinuria, but not hepatomegaly.

Von Gierke's disease (glycogen storage disease type I) is caused by a deficiency of glucose 6-phosphatase. This enzyme is primarily expressed in the liver and kidney and is responsible for the final step in both glycogenolysis and gluconeogenesis pathways, which liberate free glucose. Therefore, its absence leads to fasting hypoglycemia, lactic acidosis, hyperlipidemia, and hepatomegaly due to excessive glycogen storage.

A deficiency of fructose 1,6-bisphosphatase, which is important in gluconeogenesis, typically leads to episode of hypoglycemia that are precipitated by fasting and fructose intake. However, it doesn't lead to hyperlipidemia and hepatomegaly.

Deficiency in phosphofructokinase leads to Tarui disease (glycogen storage disease type VII), characterized by hemolytic anemia and muscle cramps, not by hepatomegaly.