Lactase

Lactase is an enzyme that hydrolyzes lactose into glucose and galactose. In humans, it is produced at the small intestine’s brush border and is often called lactase-phlorizin hydrolase.

Lactose: Lactose is a disaccharide made of glucose and galactose, naturally abundant in mammalian milk. It is the specific sugar lactase splits.
Enzyme: An enzyme is a biological catalyst that accelerates a chemical reaction without being consumed. Lactase is one enzyme whose catalytic activity enables lactose digestion.
Lactose intolerance: Lactose intolerance is the development of digestive symptoms after consuming lactose that is not adequately digested. Low lactase activity leaves lactose available for fermentation and osmotic effects in the gut.
LCT gene: The LCT gene encodes lactase-phlorizin hydrolase, the enzyme expressed on the small-intestinal brush border. It carries the instructions for producing human lactase.
Congenital lactase deficiency: Congenital lactase deficiency is a rare inherited disorder causing little or no functional lactase from birth. It is a severe, early-onset form of absent lactase activity.
Glycoside hydrolase: Glycoside hydrolases are enzymes that cleave glycosidic bonds in carbohydrates using water. Lactase belongs to this enzyme family, which explains its bond-breaking chemistry.
Protein structure: Protein structure is the arrangement of amino-acid chains into three-dimensional forms that support biological function. Lactase’s folded structure creates the sites that bind and process substrates.
Lactase persistence: Lactase persistence is continued production of intestinal lactase into adulthood. It describes the lifelong enzyme activity that permits many adults to digest lactose.
Lactase nonpersistence: Lactase nonpersistence is the normal decline in intestinal lactase production after weaning in most human populations. It contrasts with continued lactase production and accounts for low adult activity.
Secondary lactase deficiency: Secondary lactase deficiency is reduced intestinal lactase activity caused by injury to the small-intestinal lining. Unlike age-related nonpersistence, this deficiency follows damage to lactase-producing cells.

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