In horses: it has been reported in American Quarter Horses and related breeds.

In cats: the disease has been reported in the Norwegian Forest Cat, where it causes skeletal muscle, heart, and CNS degeneration in animals greater than 5 months old. It has not been associated with cirrhosis or liver failure.

No sexual predilection is observed because the deficiency of glycogen synthetase activity is inherited as an autosomal recessive trait.

Glycogen storage disease type IX can be inherited via:

- X-linked recessive inheritance due to mutations at either PHKA1 or the PHKA2 (most common) gene

- Autosomal recessive could be the inheritance pattern for an affected individual when the genes PHKB or PHKG2 have a mutation.

Prognosis strongly depends on which subtype of disease it is. Some are deadly in infancy but most are late onset and mostly manageable.

The overall frequency of glycogen-storage disease is approximately 1 case per 20,000–25,000 people. Glycogen-storage disease type 0 is a rare form, representing less than 1% of all cases. The identification of asymptomatic and oligosymptomatic siblings in several glycogen-storage disease type 0 families has suggested that glycogen-storage disease type 0 is underdiagnosed.

Overall, according to a study in British Columbia, approximately 2.3 children per 100,000 births (1 in 43,000) have some form of glycogen storage disease. In the United States, they are estimated to occur in 1 per 20,000–25,000 births. Dutch incidence rate is estimated to be 1 per 40,000 births.

Glycogen storage disease type IX is a hereditary deficiency of glycogen phosphorylase kinase B that affects the liver and skeletal muscle tissue. It is inherited in an X-linked or autosomal recessive manner.

Neutral lipid storage disease (also known as Chanarin–Dorfman syndrome) is an autosomal recessive disorder characterized by accumulation of triglycerides in the cytoplasm of leukocytes, muscle, liver, fibroblasts, and other tissues.

It can be associated with "CGI58".

Life expectancy with Fabry disease for males was 58.2 years, compared with 74.7 years in the general population, and for females 75.4 years compared with 80.0 years in the general population, according to registry data from 2001 to 2008. The most common cause of death was cardiovascular disease, and most of those had received kidney replacements.

It is also known as:

- Glycogenosis type IV

- Glycogen branching enzyme deficiency

- Polyglucosan body disease

- Amylopectinosis

The eponym "Andersen's disease" is sometimes used, for Dorothy Hansine Andersen.

Mutations in GBE1 can also cause a milder disease in adults called adult polyglucosan body disease.

Gangliosidosis contains different types of lipid storage disorders caused by the accumulation of lipids known as gangliosides. There are two distinct genetic causes of the disease. Both are autosomal recessive and affect males and females equally.

Canine phosphofructokinase deficiency is found mostly in English Springer Spaniels and American Cocker Spaniels, but has also been reported in Whippets and Wachtelhunds. Mixed-breed dogs descended from any of these breeds are also at risk to inherit PFK deficiency.

Although no cure currently exists, there is hope in treatment for this class of hereditary diseases with the use of an embryonic mitochondrial transplant.

Phosphofructokinase deficiency, also known as glycogen storage disease type VII or Tarui's disease, is a muscular metabolic disorder, with an autosomal recessive inheritance pattern.

It may affect humans as well as other mammals (especially dogs). In humans, it is the least common type of glycogen storage disease. It was named after the Japanese physician, Seiichiro Tarui (1927– ) who first observed the condition in 1965.

PSSM is most prevalent in American Quarter Horses and their related breeds (Paint horse, Appaloosa, Appendix Quarter Horse), Draft horse breeds (especially Belgian Draft and Percherons), and Warmblood breeds. The Belgian Draft been shown to have a 36% prevalence of PSSM. Other breeds that have been diagnosed with PSSM include the Arabian, Lipizzaner, Morgan, Mustang, Peruvian Paso, Rocky Mountain Horse, Standardbred, Tennessee Walking Horse, Thoroughbred, and National Show Horse. It has been suggested that the GSY1 mutation provided some benefit to hard working animals with poor-quality diets, and is now damaging members of those "thrifty" breeds that are managed with moderate to low levels of work and diets high in non-structural carbohydrates.

PSSM Type 1 (homozygous or heterozygous for the GSY1 mutation) is more common in Quarter Horses and their related breeds, and draft breeds, while PSSM Type 2 (negative for the GSY1 mutation) is more commonly seen in other breeds, including warmbloods. There is no sex predilection to the disease.

Glycogen storage disease type III is an autosomal recessive metabolic disorder and inborn error of metabolism (specifically of carbohydrates) characterized by a deficiency in glycogen debranching enzymes. It is also known as Cori's disease in honor of the 1947 Nobel laureates Carl Cori and Gerty Cori. Other names include Forbes disease in honor of clinician Gilbert Burnett Forbes (1915–2003), an American Physician who further described the features of the disorder, or limit dextrinosis, due to the limit dextrin-like structures in cytosol. Limit dextrin is the remaining polymer produced after hydrolysis of glycogen. Without glycogen debranching enzymes to further convert these branched glycogen polymers to glucose, limit dextrinosis abnormally accumulates in the cytoplasm.

Glycogen is a molecule the body uses to store carbohydrate energy. Symptoms of GSD-III are caused by a deficiency of the enzyme amylo-1,6 glucosidase, or debrancher enzyme. This causes excess amounts of an abnormal glycogen to be deposited in the liver, muscles and, in some cases, the heart.

The GM1 gangliosidoses (or GM1 gangliosidos"i"s) are caused by a deficiency of beta-galactosidase, with resulting abnormal storage of acidic lipid materials in cells of the central and peripheral nervous systems, but particularly in the nerve cells.

GM1 Gangliosidoses are inherited, autosomal recessive sphingolipidoses, resulting from marked deficiency of Acid Beta Galactosidase.

Metabolic myopathies are myopathies that result from defects in biochemical metabolism that primarily affect muscle. They include:

- Glycogen storage diseases

- Lipid storage disorder

- Phosphocreatine stores disorder

Central core disease (CCD), also known as central core myopathy, is an autosomal dominant congenital myopathy (inborn muscle disorder). It was first described by Shy and Magee in 1956. It is characterized by the appearance of the myofibril under the microscope.

There is no specific treatment but triggering anesthetics are avoided and relatives are screened for "RYR1" mutations as these may make them susceptible to MH.

There are two autosomal recessive forms of this disease, childhood-onset and adult-onset. The gene for myophosphorylase, PYGM (the muscle-type of the glycogen phosphorylase gene), is located on chromosome 11q13. According to the most recent publications, 95 different mutations have been reported. The forms of the mutations may vary between ethnic groups. For example, the R49X (Arg49Stop) mutation is most common in North America and western Europe, and the Y84X mutation is most common among central Europeans.

The exact method of protein disruption has been elucidated in certain mutations. For example, R138W is known to disrupt to pyridoxal phosphate binding site. In 2006, another mutation (c.13_14delCT) was discovered which may contribute to increased symptoms in addition to the common Arg50Stop mutation.

Glycogen storage disease type V (GSD-V) is a metabolic disorder, more specifically a glycogen storage disease, caused by a deficiency of myophosphorylase. Its incidence is reported as 1 in 100,000, approximately the same as glycogen storage disease type I.

The disease was first reported in 1951 by Dr. Brian McArdle of Guy's Hospital, London.

Treatment for glycogen storage disease type III may involve a high-protein diet, in order to facilitate gluconeogenesis. Additionally the individual may need:

- IV glucose (if oral route is inadvisable)

- Nutritional specialist

- Vitamin D (for osteoporosis/secondary complication)

- Hepatic transplant (if complication occurs)

Brody myopathy is a genetic disease.

It can be associated with "ATP2A1".

It was characterized in 1969.

Glycogen storage disease type VI (GSD VI) is a type of glycogen storage disease caused by a deficiency in liver glycogen phosphorylase or other components of the associated phosphorylase cascade system. It is also known as "Hers' disease", after Henri G. Hers, who characterized it in 1959. The scope of GSD VI now also includes glycogen storage disease type VIII, IX (caused by phosphorylase b kinase deficiency) and X (deficiency protein kinase A).

The incidence of GSD VI is approximately 1 case per 65,000–85,000 births, representing approximately 30% all cases of glycogen storage disease. Approximately 75% of these GSD VI cases result from the X-linked recessive forms of phosphorylase kinase deficiency, all other forms are autosomal recessive.