1984
DOI: 10.1113/expphysiol.1984.sp002772
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MONOSACCHARIDE TRANSPORT BY THE SMALL INTESTINE OF LEAN AND GENETICALLY OBESE (ob/ob) MICE

Abstract: SUMMARYThe effect of the obese (ob/ob) genotype on monosaccharide transport in mouse small intestine has been examined, using several different methodologies, at various stages in the development of the syndrome. Evidence for an elevation of the total capacity of the small intestine for monosaccharide transport was found at 10, 20 and 40 weeks of age in obese mice by comparison with lean controls, the difference being most prominent at 20 weeks of age after the hyperphagic phase of the syndrome had ceased. No … Show more

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Cited by 18 publications
(14 citation statements)
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“…In order to confirm this hypothesis, it will be interesting to further study and compare GLUT4 subcellular localization in the OB of the two genotypes of Zucker rats. Concerning SGLT1, the up-regulation observed in the OB of fa/fa rats is consistent with previous studies performed on peripheral tissues in obese, hyperinsulinemic and diabetic rodent models as well in human (Morton and Hanson, 1984; Ferraris and Vinnakota, 1995; Dyer et al, 2002; Osswald et al, 2005; Tabatabai et al, 2009). In central nervous system, during pathological conditions such as ischemia or epileptic seizure which induce an over-consumption of glucose (Poppe et al, 1997; Elfeber et al, 2004) SGLT1 was up-regulated (Yu et al, 2010, 2013).…”
Section: Discussionsupporting
confidence: 90%
“…In order to confirm this hypothesis, it will be interesting to further study and compare GLUT4 subcellular localization in the OB of the two genotypes of Zucker rats. Concerning SGLT1, the up-regulation observed in the OB of fa/fa rats is consistent with previous studies performed on peripheral tissues in obese, hyperinsulinemic and diabetic rodent models as well in human (Morton and Hanson, 1984; Ferraris and Vinnakota, 1995; Dyer et al, 2002; Osswald et al, 2005; Tabatabai et al, 2009). In central nervous system, during pathological conditions such as ischemia or epileptic seizure which induce an over-consumption of glucose (Poppe et al, 1997; Elfeber et al, 2004) SGLT1 was up-regulated (Yu et al, 2010, 2013).…”
Section: Discussionsupporting
confidence: 90%
“…Ear ly experiment s by Morton and Hans on [22] examining intestinal transport in leptin-deficient (Lep ob ) obese mice showed an increased total capacity of obese mice to transport glucose compared with lean mice. The influx of glucose per centimeter in both jejunum and ileum was greater in obese mice compared with lean controls.…”
Section: Discussionmentioning
confidence: 98%
“…We propose that BSA, a constituent protein within WPI, provides some of the bioactivity to WPI because our previous work showed that BSA reduced adiposity and plasma leptin and increased cumulative energy intake in obese mice (29), and the data presented here from that study extended the link to include the growth of the intestine. The signaling mechanism may involve leptin given that leptin-deficient (ob/ob) mice show increased intestinal weight (31).…”
Section: Discussionmentioning
confidence: 99%