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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-31913

Nasir, O; Artunc, F; Wang, K; Rexhepaj, R; Föller, M; Ebrahim, A; Kempe, D S; Biswas, R; Bhandaru, M; Walter, M; Mohebbi, N; Wagner, C A; Saeed, A M; Lang, F (2010). Downregulation of mouse intestinal Na(+)-coupled glucose transporter SGLT1 by gum arabic (Acacia Senegal). Cellular Physiology and Biochemistry, 25(2-3):203-210.

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Abstract

Intestinal Na(+)-coupled glucose transporter SGLT1 determines the rate of glucose transport, which in turn influences glucose-induced insulin release and development of obesity. The present study explored effects of Gum Arabic (GA), a dietary polysaccharide from dried exudates of Acacia Senegal, on intestinal glucose transport and body weight in wild-type C57Bl/6 mice. Treatment with GA (100 g/l) in drinking water for four weeks did not affect intestinal SGLT1 transcript levels but decreased SGLT1 protein abundance in jejunal brush border membrane vesicles. Glucose-induced jejunal short-circuit currents revealed that GA treatment decreased electrogenic glucose transport. Drinking a 20% glucose solution for four weeks significantly increased body weight and fasting plasma glucose concentrations, effects significantly blunted by simultaneous treatment with GA. GA further significantly blunted the increase in body weight, fasting plasma glucose and fasting insulin concentrations during high fat diet. In conclusion, the present observations disclose a completely novel effect of gum arabic, i.e. its ability to decrease intestinal SGLT1 expression and activity and thus to counteract glucose-induced obesity.

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7 citations in Web of Science®
7 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology
DDC:570 Life sciences; biology
Language:English
Date:2010
Deposited On:10 Mar 2010 07:43
Last Modified:27 Nov 2013 16:45
Publisher:Karger
ISSN:1015-8987
Additional Information:© 2010 S. Karger AG
Publisher DOI:10.1159/000276554
PubMed ID:20110681

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