Intestinal absorption of sucrose in man: interrelation of hydrolysis and monosaccharide product absorption.

Gut-training: the impact of two weeks repetitive gut-challenge during exercise on gastrointestinal status, glucose availability, fuel kinetics, and running performance

“…It is possible that the repetitive multiple-transportable carbohydrate challenge on CHO-S may have promoted upregulation of specific transport carriers (e.g., GLUT5 facilitated transporter for fructose and (or) SGLT1 active transporter for glucose at the enterocyte apical border, with or without upregulation of GLUT2 at the basolateral border) (Ferraris and Diamond 1997;Gray and Ingelfinger 1966;Nguyen et al 2014;Shi et al 1997). Indeed, increased circulatory glucose availability was seen on CHO-S in GC2 (7.2 (6.3-8.1) mMol·L -1 ) compared with GC1 (6.1 (5.5-6.7) mMol·L -1 ), and in adjunct with the reduction in breath H 2 , provides some evidence of upregulated carbohydrate intestinal absorption.…”

Functional characterization of a putative disaccharide membrane transporter in crustacean intestine

“…This is the accepted model in other mammals as well (Miller and Crane, 1963). In humans, sucrose hydrolysis was studied and compared to monosaccharide absorption to reveal sucrose hydrolysis rates that exceeded the monosaccharide product absorption rates (Gray, 1966). Therefore, in animal cells sucrose was accepted to be hydrolyzed into glucose and fructose which subsequently passed across the plasma membrane.…”

“…The α-amylase in decapod crustaceans has been shown to be similar to amylolytic activity associated with mammals. Food (Gray, 1966).…”

“…The concentrations of monosaccharide to disaccharide in the lumen can also affect sucrose transport across the epithelium. After sucrose hydrolysis by sucrase, the glucose product by a feedback inhibition system saturates the glucose transporter's active transport mechanism (Gray, 1966). Therefore, as glucose was being produced, the intestinal sucrase enzyme reacted at a reduced rate increasing the amount of intact sucrose molecules available for MS transport.…”

Intestinal β-galactosidases

“…In fact lactose is split so slowly that the hydrolysis step is rate limiting for the over-all process of hydrolysis-transport in both normal adults (3) and children.' This is in contrast to the hydrolysis of other oligosaccharides by intestinal mucosal enzymes which occurs rapidly enough to provide for saturation of the intestinal monosaccharide transport mechanism (3,4). Perhaps partly because of the relatively low lactase levels in normal man, frank deficiency of intestinal lactase, and consequent intolerance to lactose-containing foods has been found to be frequent in individuals from certain population groups (5,6) as well as in healthy people who appear to retain this defect as a permanent residual of previous intestinal disease (7,8).…”