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      The Na+/glucose cotransporters: from genes to therapy

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          Abstract

          Glucose enters eukaryotic cells via two types of membrane-associated carrier proteins, the Na+/glucose cotransporters (SGLT) and the facilitative glucose transporters (GLUT). The SGLT family consists of six members. Among them, the SGLT1 and SGLT2 proteins, encoded by the solute carrier genes SLC5A1 and SLC5A2, respectively, are believed to be the most important ones and have been extensively explored in studies focusing on glucose fluxes under both physiological and pathological conditions. This review considers the regulation of the expression of the SGLT promoted by protein kinases and transcription factors, as well as the alterations determined by diets of different compositions and by pathologies such as diabetes. It also considers congenital defects of sugar metabolism caused by aberrant expression of the SGLT1 in glucose-galactose malabsorption and the SGLT2 in familial renal glycosuria. Finally, it covers some pharmacological compounds that are being currently studied focusing on the interest of controlling glycemia by antagonizing SGLT in renal and intestinal tissues.

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          T1R3 and gustducin in gut sense sugars to regulate expression of Na+-glucose cotransporter 1.

          Robert Margolskee, Jane Dyer, Zaza Kokrashvili … (2007)
          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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            Tubulointerstitial changes as a major determinant in the progression of renal damage.

            Karl A. Nath (1992)
            Tubulointerstitial injury is an invariant finding in the chronically diseased kidney, irrespective of the type of disease or the compartment in which the disease originates. Such histologic changes are functionally significant in that scores for such damage, rather than glomerular injury, correlate with decline of renal function. This review summarizes (1) clinical evidence attesting to tubulointerstitial changes as an index of functional impairment, (2) mechanisms by which tubulointerstitial injury impairs renal function, and (3) interactions of pathologic processes in the vascular, glomerular, tubular, and interstitial compartments that culminate in tubulointerstitial injury. This report concludes with a review of interstitial fibrosis, a pathologic process regarded as an irreversible outcome from tubulointerstitial injury.
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              Glucose transporters (GLUT and SGLT): expanded families of sugar transport proteins.

              I. Wood, Paul Trayhurn (2003)
              The number of known glucose transporters has expanded considerably over the past 2 years. At least three, and up to six, Na+-dependent glucose transporters (SGLT1-SGLT6; gene name SLC5A) have been identified. Similarly, thirteen members of the family of facilitative sugar transporters (GLUT1-GLUT12 and HMIT; gene name SLC2A) are now recognised. These various transporters exhibit different substrate specificities, kinetic properties and tissue expression profiles. The number of distinct gene products, together with the presence of several different transporters in certain tissues and cells (for example, GLUT1, GLUT4, GLUT5, GLUT8, GLUT12 and HMIT in white adipose tissue), indicates that glucose delivery into cells is a process of considerable complexity.
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                Author and article information

                Journal
                Journal ID (publisher-id): bjmbr
                Title: Brazilian Journal of Medical and Biological Research
                Abbreviated Title: Braz J Med Biol Res
                Publisher: Associação Brasileira de Divulgação Científica (Ribeirão Preto, SP, Brazil )
                ISSN (Print): 0100-879X
                ISSN (Electronic): 1414-431X
                Publication date (Print and electronic): November 2010
                Volume: 43
                Issue: 11
                Pages: 1019-1026
                Affiliations
                [01] São Paulo SP orgnameUniversidade de São Paulo orgdiv1Instituto de Ciências Biomédicas orgdiv2Departamento de Fisiologia e Biofísica Brasil
                Article
                Publisher ID: S0100-879X2010001100002 Publisher ID: S0100-879X(10)04301102
                DOI: 10.1590/S0100-879X2010007500115
                SO-VID: 3ff3204c-d7f8-4ed4-9fe4-050e2f0607e6
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                Date received : 22 April 2010
                Date accepted : 18 October 2010
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 60, Pages: 8
                Product

                SciELO Brazil

                Categories
                Subject: Review

                Keywords: SGLT1,HNF-1,SLC5A2,SLC5A1,SGLT2,Diabetes
                Data availability:
                Keywords: SGLT1, HNF-1, SLC5A2, SLC5A1, SGLT2, Diabetes

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