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Fructose intestinal absorption

The handicap of slower intestinal absorption is overcome when fructose is given... [Pg.122]

Glucose and galactose enter the absorptive cells by way of secondary active transport. Cotransport carrier molecules associated with the disaccharidases in the brush border transport the monosaccharide and a Na+ ion from the lumen of the small intestine into the absorptive cell. This process is referred to as "secondary" because the cotransport carriers operate passively and do not require energy. However, they do require a concentration gradient for the transport of Na+ ions into the cell. This gradient is established by the active transport of Na+ ions out of the absorptive cell at the basolateral surface. Fructose enters the absorptive cells by way of facilitated diffusion. All monosaccharide molecules exit the absorptive cells by way of facilitated diffusion and enter the blood capillaries. [Pg.300]

Source and kinds of disaccharidases The final digestive processes occur at the mucosal lining of the small intestine. Several disaccharidases [for example, lactase (p-galactosidase), sucrase, maltase, and isomal-tase] produce monosaccharides (glucose, galactose, and fructose). These enzymes are secreted by and remain associated with the luminal side of the brush border membranes of intestinal mucosal cells. Absorption of the monosaccharides requires specific trans porters. [Pg.476]

When sorbitol and fructose are taken by mouth, the increase in blood fructose is modulated by their rates of absorption from the intestine, preventing the serious... [Pg.297]

The reduction of carbohydrate absorption from the intestine of rats with a saccharide supplemented by EGCG or green tea is based upon suppression of the activity of intestinal a-amylase, sucrase, or a-glucosidase. Also, green tea enhances insulin sensitivity of normal and fructose-fed rats as demonstrated by increased glucose uptake by muscle cells. ... [Pg.249]

Fructose is found in many plants and is an important portion of dietary carbohydrate. Most commonly it is ingested as free fructose or sucrose. Fructose is not actively transported by the intestinal mucosa, and variable proportions are converted to glucose in the process of absorption in man, about one-sixth is converted (Ml). Most of the metabolism of fructose occurs in the liver. If a renal threshold for fructose exists, it is very low. [Pg.42]

Glucose, galactose, and fructose formed by the digestive enzymes are transported into the absorptive epithelial cells of the small intestine by protein-mediated Na -dependent active transport and facilitative diffusion. Monosaccharides are transported from these cells into the blood and circulate to the liver and peripheral tissues, where they are taken up by facilitative transporters. Facilitative transport of glucose across epithelial cells and other cell membranes is mediated by a family of tissue-specific glucose transport proteins (GLUT I-V). The type of transporter found in each cell reflects the role of glucose metabolism in that cell. [Pg.494]

Fig. 27.12. Na -dependent and facilitative transporters in the intestinal epithelial cells. Both glucose and fructose are transported by the facilitated glucose transpxrrters on the luminal and serosal sides of the absorptive cells. Glucose and galactose are transported by the Na -glucose cotransporters on the luminal (mucosal) side of the absorptive cells. Fig. 27.12. Na -dependent and facilitative transporters in the intestinal epithelial cells. Both glucose and fructose are transported by the facilitated glucose transpxrrters on the luminal and serosal sides of the absorptive cells. Glucose and galactose are transported by the Na -glucose cotransporters on the luminal (mucosal) side of the absorptive cells.
Sucrase is associated with the brush border of the intestinal mucosal cells. It catalyzed the hydrolysis of sucrose to D-glucose and D-fructose. Its absence means that sucrose passes through the small intestine where it enters the large intestine. There it interferes with water absorption because it is osmotically active and leads to the retention of water in the bowel lumen. This gives rise to abdominal cramps and watery diarrhea. Treatment involves limiting sucrose in the diet and more recently the ingesting of a proprietary enzyme, Sucraid. [Pg.367]

There are numerous reports of interactions of dietary elements that cause variation in the absorption of chromium. Amino acids, which chelate chromium, prevent precipitation at the basic pH in the small intestine, which increases its absorption [13]. Other chelating agents have mixed effects. Phytates significantly decrease absorption whereas oxalates lead to increased absorption [15]. Certain vitamins such as nicotinic acid and ascorbic acid have been shown to increase absorption [16]. Starch has also been shown to increase absorption to a greater degree than glucose, fructose, and sucrose. Some metals can compete with chromium and decrease its absorption. Studies show that zinc, vanadium, and iron have a common intestinal transport mechanism with chromium and can decrease the absorption of chromium [9]. [Pg.325]

Absorption of the major monosaccharides, n-glucose, n-fructose, and D-galactose, apparently involves phosphorylation in the intestinal mucosa and liberation of the sugar in the blood stream 2). The mechanism is believed to be analogous to the formation of urine in the renal tubules. Mannose and the pentoses seem to be absorbed only by diffusion (S). [Pg.781]

Other monosaccharides are absorbed by carrier-mediated diffusion there are at least three distinct carrier proteins one for fructose, one for other monosaccharides and one for sugar alcohols. Because they are not actively transported, fructose and sugar alcohols are absorbed only to a limited extent, and after a moderately high intake a significant amount will avoid absorption and remain in the intestinal lumen, acting as a substrate for colon bacteria and, like unabsorbed disaccharides in people with disaccharidase deficiency, causing abdominal pain and diarrhoea. [Pg.92]

Inorganic iron is absorbed only in the Fe (reduced) form. This means that a variety of reducing agents present in the intestinal lumen together with dietary iron will enhance its absorption. The most effective such compound is vitamin C (section 11.14.4.1) and, although intakes of 40-60 mg of vitamin C per day are more than adequate to meet requirements, an intake of 25-50 mg per meal is sometimes recommended to enhance iron absorption. Alcohol and fructose also enhance iron absorption. [Pg.112]


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See also in sourсe #XX -- [ Pg.141 ]




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