<unk>  has an autosomal recessive pattern of inheritance.<unk>  is inherited in an autosomal recessive manner. People with one copy of the faulty gene are carriers of the disease and have no symptoms. As with other autosomal recessive diseases, each child born to two carriers of the disease has a 25% chance of inheriting both copies of the faulty gene and manifesting the disease. Unaffected parents of a child with<unk>  can be assumed to be carriers. Prenatal diagnosis has been made by fetal liver biopsy at 18–22 weeks of gestation, but no fetal treatment has been proposed. Prenatal diagnosis is possible with fetal DNA obtained by chorionic villus sampling when a fetus is known to be at risk. The most common forms of<unk>  are designated<unk> a and<unk> b, the former accounting for over 80% of diagnosed cases and the latter for less than 20%. A few rarer forms have been described. *<unk> a results from mutations of G6PC, the gene for glucose-6-phosphatase, located on chromosome 17q21. *<unk> b results from mutations of the gene for SLC37A4 or "G6PT1", the glucose-6-phosphate transporter. *<unk> c results from mutations of SLC17A3 or SLC37A4. Glucose-6-phosphatase is an enzyme located on the inner membrane of the endoplasmic reticulum. The catalytic unit is associated with a calcium binding protein, and three transport proteins (T1, T2, T3) that facilitate movement of glucose-6-phosphate (G6P), phosphate, and glucose (respectively) into and out of the enzyme.
Glycogen storage disease type I
Glycogen storage disease type 0
Glycogen storage disease type V
Glycogen storage disease type VI
Essential fructosuria
Inborn errors of carbohydrate metabolism
Aspartylglucosaminuria
Familial dysbetalipoproteinemia