Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dietary sugars are transported from the intestinal lumen into absorptive enterocytes by the sodium-dependent glucose transporter isoform 1 (SGLT1). Regulation of this protein is important for the provision of glucose to the body and avoidance of intestinal malabsorption. Although expression of SGLT1 is regulated by luminal monosaccharides, the luminal glucose sensor mediating this process was unknown. Here, we show that the sweet taste receptor subunit T1R3 and the taste G protein gustducin, expressed in enteroendocrine cells, underlie intestinal sugar sensing and regulation of SGLT1 mRNA and protein. Dietary sugar and artificial sweeteners increased SGLT1 mRNA and protein expression, and glucose absorptive capacity in wild-type mice, but not in knockout mice lacking T1R3 or alpha-gustducin. Artificial sweeteners, acting on sweet taste receptors expressed on enteroendocrine GLUTag cells, stimulated secretion of gut hormones implicated in SGLT1 up-regulation. Gut-expressed taste signaling elements involved in regulating SGLT1 expression could provide novel therapeutic targets for modulating the gut's capacity to absorb sugars, with implications for the prevention and/or treatment of malabsorption syndromes and diet-related disorders including diabetes and obesity.
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PMID:T1R3 and gustducin in gut sense sugars to regulate expression of Na+-glucose cotransporter 1. 1785 58

Necrotizing enterocolitis (NEC) causes morbidity and mortality among preterm infants and is associated with nutrient malabsorption. Therefore, a preterm pig model that spontaneously develops NEC was used to investigate the relationship between severity of NEC lesions and galactose absorption in vivo and carrier-mediated glucose absorption by intact mid small intestine. Preterm pigs collected by caesarian section at 92% of gestation received parenteral nutrition with and without minimal enteral nutrition for 48 h before conversion to enteral nutrition with colostrum or an enteral formula. Pigs were killed when symptoms of NEC were observed or after 36-40 h of enteral nutrition. NEC lesions decreased in vivo absorption of galactose and mannitol by more than 50% and abolished carrier-mediated glucose uptake by tissues with lesions. Moreover, when NEC lesions were restricted to the colon, small intestinal tissues that seemed clinically healthy had decreased in vitro glucose absorption due to reduced uptake via the sodium-dependent glucose transporter with little or no involvement of the apical facilitative glucose carrier. The present findings reveal a direct relationship between the severity of NEC lesions and the magnitude of sugar malabsorption that is detectable before clinical symptoms are evident.
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PMID:Aldohexose malabsorption in preterm pigs is directly related to the severity of necrotizing enterocolitis. 1835 43