Lactase non-persistence

Milk and some dairy products contain lactose, a disaccharide hydrolyzed by the enzyme lactase-phlorizin hydrolase to glucose and galactose in the brush border of the small intestine. The differences in lactase activity are due to a genetic polymorphism. There are three genotypes: homozygous lactase persistent (LP), homozygous lactase non-persistent (LNP), and heterozygotes.

Lactase non-persistence (LNP), also known as adult-type hypolactasia, is the molecular basis of the inability to hydrolyze the lactose found in milk. It is as an autosomal recessive trait leading to down-regulation of lactase activity in the intestinal mucosa and to maldigestion of lactose. LNP is the most common phenotype in humans, estimated at 65–70%.

Humans are born with high levels of lactase activity. However, in most populations, this lactase activity declines after weaning, resulting in diminished lactase expression in the small intestine. Hypolactasia is a general term for very low activity of lactase in the jejunal mucosa due to down regulation of lactase activity after weaning (LNP) or damage to intestinal mucosa leading to secondary lactase deficiency. Total lack of lactase activity from infancy is known as congenital lactase deficiency (CLD).

Some individuals, specifically descendants from populations that have traditionally practiced dairy farming, maintain the ability to digest milk and other dairy products into adulthood.
Lactase non-persistence

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