Glucose movements across the wall of the rat small intestine

Abstract

This paper describes further work on the absorption of glucose from the surviving preparation of rat small intestine which we have previously described (Fisher & Parsons, 1949, 1950a. It was tacitly assumed in the earlier work that as the mucosa, the most active tissue of the intestinal wall, was directly in contact with the fluid in the lumen, it would draw its nourishment from this fluid. Consequently, it was supposed that disappearance of glucose from the fluid in the lumen was due to two processes: translocation of glucose into the submucosal space by some of the cells, and utilization of glucose for metabolic purposes by all of the cells. The work to be described suggests that this is not so. The intestine behaves as though glucose were translocated across the mucosa by relatively few cells, and as though the lumenal borders of the remaining mucosal cells were impermeable to glucose. The glucose concentration in the fluid in the submucosal space of the surviving intestine rises sharply during glucose absorption, and most of the glucose supply of the mucosa is presumably derived from this source.The general relation existing between glucose concentration in the lumen and the rate of absorption is described and discussed. METHODS(Glucose concentrations are expressed as percentages; the meaning here is g of glucose/100 ml.)The isolated intestine preparation of Fisher & Parsons (1949) was used. The technique of sampling circulating fluids was modified. Towards the end of the period of observation most of the circulgtiny fluid wis drainal into a voluamtric fhsk without interruption of the circulation.At the end of the period, approximately 50 ml. of glucose-free, warm, oxygenated Ringer were introduced, allowed to circulate briefly, and withdrawn as far as po33ible. The circulation was not interrupted. A further 50 ml. of Ringer were introduced and again as much fluid as possible

The absorption of sucrose, maltose and higher oligosaccharides from the isolated rat small intestine

“…The rate of glucose absorption from a solution containing initially 0-5 % (w/v) was 2-54 mg/cm/hr in the first 30 min but only 1 18 mg/cm/hr in the second 30 min (Fisher & Parsons, 1953). With starch hydrolysate the corresponding rates were 2-70 mg/cm/hr and 1*54 mg/cm/hr (Table 3).…”

“…With a 0-16% (w/v) glucose concentration in the lumen, the rate of disappearance from the lumen of glucose would be expected to be around 1 mg/cm/hr. As this 1 mg/cm/hr of glucose corresponds to the glucose utilization rate for the intestine (Fisher & Parsons, 1953) practically no glucose would be expected on the serosal side under these conditions. The appearance of 1-32 mg/cm/hr (Table 2) of glucose on the serosal side in the second half hour of the starch hydrolysate perfusions, when the glucose concentration was at most 0 16 % (w/v), cannot therefore be accounted for solely by glucose absorption.…”

“…The observation of Fisher & Parsons (1950) Table 2 The rate of disappearance of carbohydrate from the lumen of the isolated rat small intestine was certainly not less when starch hydrolysate was used than when 0-5 % (w/v) glucose was used, although with starch hydrolysate the concentration of glucose in the lumen never rose above 0*16 % (w/v). It is of interest to compare the observed rates of disappearance from the lumen and appearance on the serosal side with the results of Fisher & Parsons (1953) using various glucose concentrations in the inner circuit. With a 0-16% (w/v) glucose concentration in the lumen, the rate of disappearance from the lumen of glucose would be expected to be around 1 mg/cm/hr.…”

Intestinal absorption of carbohydrates in man

“…Holdsworth & Dawson, 1964). Glucose absorption behaves in accordance with ordinary enzyme kinetics (Fisher & Parsons, 1953).…”

Structure of, and functional insight into the GLUT family of membrane transporters

“…Initial explanations of how glucose is transported across the cell membrane were based on mathematical analysis of the transport activities of hexose utilizing erythrocyte preparations. The fluxes were best fit with the Michaelis-Menten enzyme kinetics model [89][90] which predicts that the rate of hexose absorption depends on both the initial hexose concentrations and the binding affinity of the protein for the substrate and that there is a maximum rate of transfer (rate of transfer is saturable). 91 The earliest mechanistic theory, ie, the "simple carrier model", was proposed by …”