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Review
. 2011 May;149(5):601-5.
doi: 10.1016/j.surg.2011.02.001.

Acute "adaptation" by the small intestinal enterocyte: a posttranscriptional mechanism involving apical translocation of nutrient transporters

Jeffrey S Scow  1 , Ali Tavakkolizadeh, Ye Zheng, Michael G Sarr
Affiliations
Review

Acute "adaptation" by the small intestinal enterocyte: a posttranscriptional mechanism involving apical translocation of nutrient transporters

Jeffrey S Scow et al. Surgery. 2011 May.
No abstract available

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Figures

Figure 1
Figure 1. Classic Model of Hexose Absorption by the Enterocyte
SGLT1 and GLUT5 located in the apical membrane and GLUT2 located only basolaterally. Basal Na+/K+ ATPase generates the apical gradient of sodium ions.
Figure 2
Figure 2. Proposed New Model of Glucose Transport
High luminal concentrations of glucose saturate SGLT1 causing influx of Na+, stimulating Cav1.3 causing influx of Ca2+. Through remodeling of the terminal web PKCβII is activated. Lumenal glucose also stimulates apical sweet taste receptors which activate PLCβ2 which further activates PKCβII via PIP2 and DAG. This bimodal activation of PKCβII induces apical translocation of pre-formed GLUT2 to markedly augment cellular uptake of luminal glucose. Whether PKCβII also induces basolateral translocation of GLUT2 is unknown.
See this image and copyright information in PMC

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