| Literature DB >> 8889271 |
A B Thomson1, M Keelan, G E Wild.
Abstract
The authors review the physiological, cellular and molecular aspects of the patterns, mechanisms and signals of the adaptation of intestinal transport of sugars and lipids, especially in response to manipulations of dietary lipid content. In models of intestinal adaptation, nutrient uptake is enhanced by an up- or down-regulation of the maximal rate of carrier-mediated transport or by alterations in the passive permeability properties (Pd) of the intestinal brush border membrane (BBM). The importance of unstirred water layers has been demonstrated. Alterations in the Pd for lipid uptake are due to changes in the lipid content of the BBM, which in turn are associated with alterations in the activity of lipid-metabolizing enzymes in the enterocyte microsomal membrane (EMM), and, therefore, alterations in the lipid composition of the EMM. Lipid uptake is also mediated by at least two proteins in the BBM, the sodium-hydrogen exchangers and the membrane-fatty-acid-binding protein. Alterations in the maximal transport rate for glucose and fructose transporters are associated with variations in the abundance of their transporters (including sodium-dependent glucose transporter, glucose and fructose transporter and fructose transporter) in the basolateral membrane sodium-potassium adenosine triphosphatase, and in the abundance of the messenger RNA of the transporters. Isocaloric changes in dietary lipids, such as switching from a saturated to a polyunsaturated diet, within the range seen in human consumption, leads to major alterations in passive and active transport processes. In a proposed model, changes in dietary lipids stimulate intracellular second messengers, modifying gene expression of the transporter carriers and of the EMM lipid-metabolizing enzymes. Thus, an understanding of the mechanisms of intestinal adaptation lays the groundwork for future studies of dietary manipulations. It may also lead to dietary interventions to prevent unwanted or to enhance desirable intestinal adaptation, thereby preventing disease.Entities:
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Year: 1996 PMID: 8889271
Source DB: PubMed Journal: Clin Invest Med ISSN: 0147-958X Impact factor: 0.825