期刊
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
卷 289, 期 6, 页码 G1007-G1014出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpgi.00085.2005
关键词
sodium-dependent transporter 1; adaptation; regulation; nongenomic
Adenosine modulates the intestinal functions of secretion, motility, and immunity, yet little is known about the regulation of nutrient absorption. Therefore, we measured the carrier-mediated uptake of tracer D-[C-14] glucose (2 mu M) by everted sleeves of the mouse intestine after a lumenal exposure to adenosine and a disodium salt of AMP. Rates of glucose uptake by intact tissues increased almost twofold after a 7-min exposure to 5 mM adenosine ( a physiological dose). The response was slightly more pronounced for AMP and could be induced by forskolin. The response to adenosine was blocked by theophylline and the A(2) receptor antagonist 3,7-dimethyl-1-proparglyxanthine but not by the A(1) receptor antagonist 8-phenyltheophylline. Glucose uptake by control and AMP-stimulated tissues was inhibited by phloridzin, implying that sodium- dependent glucose transporter 1 (SGLT1) is the responsive transporter, but the involvement of glucose transporter 2 (GLUT2) cannot be excluded. Of clinical relevance, AMP accelerated the systemic availability of 3-O-methylglucose after an oral administration to mice. Our results indicate that adenosine causes a rapid increase in carrier-mediated glucose uptake that is of clinical relevance and acts via receptors linked to a signaling pathway that involves intracellular cAMP production.
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