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Sucrose intolerance or genetic sucrase-isomaltase deficiency (GSID) is the condition in which sucrase-isomaltase, an enzyme needed for proper metabolism of sucrose (sugar) and starch (e.g., grains), is not produced or the enzyme produced is either partially functional or non-functional in the small intestine.
Lactose intolerance is the ancestral state of all humans before the recent evolution of lactase persistence in some cultures, which extends lactose tolerance into adulthood. [9] Lactase persistence evolved in several populations independently, probably as an adaptation to the domestication of dairy animals around 10,000 years ago.
Food intolerance reactions can include pharmacologic, metabolic, and gastro-intestinal responses to foods or food compounds. Food intolerance does not include either psychological responses [3] or foodborne illness. A non-allergic food hypersensitivity is an abnormal physiological response.
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Apples. The original source of sweetness for many of the early settlers in the United States, the sugar from an apple comes with a healthy dose of fiber.
Fructose malabsorption, formerly named dietary fructose intolerance (DFI), is a digestive disorder [1] in which absorption of fructose is impaired by deficient fructose carriers in the small intestine's enterocytes. This results in an increased concentration of fructose. Intolerance to fructose was first identified and reported in 1956. [2]
This is an accepted version of this page This is the latest accepted revision, reviewed on 18 February 2025. Diets restricting carbohydrate consumption This article is about low-carbohydrate dieting as a lifestyle choice or for weight loss. For information on low-carbohydrate dieting as a therapy for epilepsy, see Ketogenic diet. An example of a low-carbohydrate dish, cooked kale and poached ...
Some FODMAPs, such as fructose, are readily absorbed in the small intestine of humans via GLUT receptors. [19] Absorption thus depends on the appropriate expression and delivery of these receptors in the intestinal enterocyte to both the apical surface, contacting the lumen of the intestine (e.g., GLUT5), and to the basal membrane, contacting the blood (e.g., GLUT2). [19]
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