1. Intestinal glucose transport: Evidence for a membrane traffic–based pathway in humans 
René Santer, Georg Hillebrand, Beat Steinmann, Jürgen Schaub 
Gastroenterology 
Volume 124, Issue 1, Pages (January 2003)
DOI: /gast
Copyright © 2003 American Gastroenterological Association Terms and Conditions

2. Fig. 1
(A) Classical model of intestinal glucose absorption: glucose is transported at the apical membrane of enterocytes against its gradient by coupling of its transport to the transport of sodium. Sodium follows its electrochemical gradient, which is maintained by the action of the sodium-potassium-ATPase at the basolateral membrane. Glucose exits the enterocyte at the basolateral side along its gradient by facilitative diffusion mediated by the transporter protein GLUT2. (B) Proposed mechanism of intestinal glucose transport including the suggested membrane traffic-based pathway. This pathway seems to be a major route for glucose transport because congenital GLUT2 deficiency was not found to be associated with any impairment of glucose absorption. Conversely, congenital G6PT1 deficiency only results in slightly impaired glucose transport; presumably because of the fact that facilitative diffusion mediated by GLUT2 can serve as a salvage pathway.
Gastroenterology  , 34-39DOI: ( /gast )
Copyright © 2003 American Gastroenterological Association Terms and Conditions

3. Fig. 2
Results of oral monosaccharide and lactose tolerance tests. (A) In a normal individual, both the ingestion of monosaccharides (Glc + Gal) and lactose (Lac) resulted in a marked increase of plasma glucose (>1.4 mmol/L) within a few minutes (upper panel). Plasma galactose concentration remained within normal limits (<0.8 mmol/L) (middle panel). In the breath samples, a normal basal H2 concentration (<16 ppm)25 and no increase of H2 after carbohydrate ingestion was found both in the Glc + Gal test and in the Lac test. (B) In congenital GLUT2 deficiency (FBS), the oral administration of monosaccharides resulted in an exaggerated plasma glucose increase, a known phenomenon in patients with this condition.7 It can be explained by diminished hepatic uptake; furthermore, an inappropriately low insulin secretion because of an impairment of the glucose sensing mechanism of beta cells has been suggested to contribute to this phenomenon (upper panel). Likewise, galactose ingestion resulted in an elevated plasma galactose concentration, which is explained by the fact that GLUT2 is both a glucose and a galactose carrier (middle panel; note the logarithmic scale). The main finding is that no impairment of the intestinal transport of monosaccharides was detected by the H2 breath test in congenital GLUT2 deficiency (lower panel). The fact that Lac resulted in a marked H2 increase shows that the patient investigated was indeed able to produce H2, which means that the bacterial flora of his large intestine was able to convert undigested carbohydrates to H2. This finding has to be interpreted in the sense that this patient is also lactase deficient. This had already been known from his medical history, and it well explains the different results obtained for plasma glucose and galactose concentrations after the ingestion of the different carbohydrate solutions (upper and middle panel). (C) In congenital G6PT1 deficiency (GSD 1 non-A), the fasting period of 8 hours before the tests resulted in a marked decrease of plasma glucose concentration (upper panel), which is explained by an impairment of hepatic glycogen breakdown and gluconeogenesis because of the defect of the glucose-6-phosphatase system in these patients. This decrease was more pronounced than in GLUT2 deficiency, and it was accompanied by compensated metabolic acidosis (pHmin 7.4, BEmax −13.4). The main finding in G6PT1 deficiency is the elevation of basal H2 concentrations, which were reproducible in both breath tests (lower panel). This observation is generally interpreted as the result of bacterial overgrowth of the small intestine, which in the absence of other known causes is suggestive for chronic malabsorption of carbohydrates.25 Certainly, absorption of monosaccharides cannot be severely impaired because plasma glucose concentration markedly increased on Glc + Gal. This patient, like the FBS patient in Figure 2B, has additional signs of mild lactase deficiency such as the diminished increase of plasma glucose after Lac, and the increase of H2 at the expected time interval when unabsorbed lactose enters the colon, which is colonized by H2-producing bacteria.
Gastroenterology  , 34-39DOI: ( /gast )
Copyright © 2003 American Gastroenterological Association Terms and Conditions