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Lactose can not be absorbed by the intestine and needs to be split in the small intestine into galactose and glucose by the enzyme called lactase; unabsorbed lactose can cause abdominal pain, bloating, diarrhea, gas, and nausea. [citation needed] In most mammals, production of lactase diminishes after infants are weaned from maternal milk.
Glucose-galactose malabsorption is a rare condition in which the cells lining the intestine cannot take in the sugars glucose and galactose, which prevents proper digestion of these molecules and larger molecules made from them. Glucose and galactose are called simple sugars, or monosaccharides.
After the ingestion of lactose, most commonly from breast milk for an infant or cow milk and any milk from an animal, the enzyme lactase hydrolyzes the sugar into its monosaccharide constituents, glucose and galactose. In the first step of galactose metabolism, galactose is converted to galactose-1-phosphate (Gal-1-P) by the enzyme galactokinase.
After separation from glucose, galactose travels to the liver for conversion to glucose. [12] Galactokinase uses one molecule of ATP to phosphorylate galactose. [ 2 ] The phosphorylated galactose is then converted to glucose-1-phosphate, and then eventually glucose-6-phosphate, which can be broken down in glycolysis.
The development of early cataracts in homozygous affected infants is fully preventable through early diagnosis and treatment with a galactose-restricted diet. Some studies have suggested that, depending on milk consumption later in life, heterozygous carriers of galactokinase deficiency may be prone to presenile cataracts at 20–50 years of age.
Infants with classic galactosemia cannot be breast-fed due to lactose in human breast milk which consists of both galactose and glucose and are usually fed a soy-based formula. [ 24 ] Galactosemia is sometimes confused with lactose intolerance , but galactosemia is a more serious condition.
Because glucose is the primary source of fuel for the brain, patients with GLUT1 deficiency have insufficient cellular energy to permit normal brain growth and function. [ 8 ] Around 90% of cases of GLUT1 deficiency syndrome are de novo mutations of the SLC2A1 gene (a mutation not present in the parents, but present in one of the two copies of ...
Guidelines in the UK, however, recommend pre-feed screening of at-risk infants at 2–4 hours of age (to avoid false positives when blood glucose is, ordinarily, at its lowest at 2–3 hours of age) and at the subsequent feed until a blood glucose level of >2.0 mmol/L (36 mg/dL) on at least two consecutive occasions and is feeding well.