Acute increase, stimulated by prostaglandin E<sub>2</sub>, in glucose absorption via the sodium dependent glucose transporter-1 in rat intestine

Scholtka, Bettina; Stümpel, Frank; Jungermann, Kurt

doi:10.1136/gut.44.4.490

Cited by 25 publications

(17 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous work has reported changes in intestinal glucose transport over a similar time course to that observed following AII reported here. For example, leptin inhibits glucose uptake by rat jejunal mucosa within 2–3 min (Ducroc et al 2005), whilst cAMP (Stumpel et al 1998), AMP (Kimura et al 2005), PGE2 (Scholtka et al 1999) and enteric‐derived glucagon (Stumpel et al 1998) all stimulate phlorizin‐sensitive glucose transport within 5 min of exposure to these agents. These very rapid changes in glucose transport are likely to be the result of alterations in membrane insertion of SGLT1 from a submembrane storage compartment.…”

Section: Discussionmentioning

confidence: 99%

Involvement of an enterocyte renin–angiotensin system in the local control of SGLT1‐dependent glucose uptake across the rat small intestinal brush border membrane

Wong

Debnam

Leung

2007

The Journal of Physiology

View full text Add to dashboard Cite

There is increasing evidence that locally produced angiotensin AII (AII) regulates the function of many tissues, but the involvement of enterocyte-derived AII in the control of intestinal transport is unknown. This study examined whether there is a local renin-angiotensin system (RAS) in rat villus enterocytes and assessed the effects of AII on SGLT1-dependent glucose transport across the brush border membrane (BBM). Gene and protein expression of angiotensinogen, ACE, and AT 1 and AT 2 receptors were studied in jejunal and ileal enterocytes using immunocytochemistry, Western blotting and RT-PCR. Mucosal uptake of D-[ 14 C]glucose by everted intestinal sleeves before and after addition of AII (0-100 nM) to the mucosal buffer was measured in the presence or absence of the AT 1 receptor antagonist losartan (1 μM). Immunocytochemistry revealed the expression of angiotensinogen, ACE, and AT 1 and AT 2 receptors in enterocytes; immunoreactivity of AT 1 receptor and angiotensinogen proteins was especially pronounced at the BBM. Expression of angiotensinogen and AT 1 and AT 2 receptors, but not ACE, was greater in the ileum than the jejunum. Addition of AII to mucosal buffer inhibited phlorizin-sensitive (SGLT1-dependent) jejunal glucose uptake in a rapid and dose-dependent manner and reduced the expression of SGLT1 at the BBM. Losartan attenuated the inhibitory action of AII on glucose uptake. AII did not affect jejunal uptake of L-leucine.

show abstract

Section: Discussionmentioning

confidence: 99%

Involvement of an enterocyte renin–angiotensin system in the local control of SGLT1‐dependent glucose uptake across the rat small intestinal brush border membrane

Wong

Debnam

Leung

2007

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…gov/BLAST/) were: (forward) 5Ј-ATG GCT CTG GGA GAC AGA GA-3Ј and (reverse) 5Ј-GGA GAA ATG GAC TGG GTG TG-3Ј. SGLT-1 mRNA primers were based on a report by Scholtka et al (26). PCR mixtures for amplification of cDNA were performed in a 50-l total volume containing 0.2 mM dNTPs, 1ϫ PCR buffer without MgCl2, 1.5 mM MgCl2, template cDNA, forward and reverse primers, 2.5 U Taq polymerase (GIBCO-BRL), and primers and competimers for 18S (4:6 ratio; Ambion).…”

Section: Animalsmentioning

confidence: 99%

Hypoxia differentially regulates nutrient transport in rat jejunum regardless of luminal nutrient present

Kles¹,

Tappenden

2002

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

nutrition and poor intestinal perfusion are hypothesized to play an important pathogenic role in nonocclusive small bowel necrosis. This study tests the hypothesis that glucose and glutamine transport are differentially regulated during hypoxia regardless of the luminal nutrient present. Sprague-Dawley rats (247 Ϯ 3 g; n ϭ 16) were randomized to receive 1 h of intestinal hypoxia or serve as normoxic controls. During this hour, jejunal loops were randomized to receive in situ perfusions of mannitol, glucose, or glutamine. When compared with normoxic groups, glucose but not glutamine transport was impaired (P Ͻ 0.001) during hypoxia. Messenger RNA abundance of the sodium glucose cotransporter sodium-dependent glucose cotransporter-1 (SGLT-1) and neutral basic amino acid transporter B o did not differ with hypoxia or nutrient perfused. Jejunal brush-border SGLT-1 abundance was decreased (P ϭ 0.039) with hypoxia; however, total cellular SGLT-1 protein abundance did not differ among treatment groups. These data indicate that SGLT-1 activity is regulated during hypoxia at the posttranslational level. Additional information regarding the mechanisms regulating nutrient transport in the hypoperfused intestine is critical for optimizing the composition of enteral nutrient formulas.sodium-dependent glucose cotransporter-1; nutrient absorption; small intestine THE INCIDENCE OF NONOCCLUSIVE small bowel necrosis is significant in traumatically injured patients, despite adequate systemic resuscitation. Currently, the causative mechanism remains unknown; however, enteral nutrition has been provided in ϳ90% of cases (21), suggesting that the inappropriate administration of specific nutrients into a poorly perfused small bowel may play a pathogenic role (12,21,23,25). During states of low blood flow to the intestine, enteral nutrients may increase oxygen demand beyond that available, potentially increasing intestinal hypoxia and impairing intestinal function. Gastrointestinal function has been shown to be impaired during hypoperfusion or decreased oxygenation of the intestine (28). Previous in vivo rat studies from our lab indicate that, during hypoperfusion, impaired barrier function, increased lactate concentration, decreased ATP concentration, and altered nutrient transport are characteristic (15). The detrimental effects of hypoperfusion may be minimized with an enteral formula composed of nutrients easily processed by the hypoperfused intestine.The purpose of the current study was to determine how nutrient perfusion alters sodium-dependent glucose and glutamine transport activity and their regulation at the cellular level during hypoperfusion. Glutamine transport occurs via system B o , which is part of a family of transporters for neutral amino acids (14). Glucose transport occurs via the sodium-glucose cotransporter [sodium-dependent glucose cotransporter-1 (SGLT-1)]. We previously reported that, during hypoxia, brush-border glucose transport is impaired, but glutamine transport remains unaltered following luminal perfusio...

show abstract

“…Adenosine is not unique in modulating glucose uptake, as a diversity of hostderived regulatory signals are known to rapidly alter intestinal absorption of nutrients and the secretion of ions, and several of these have been considered for therapeutic purposes. Notable examples include glucagon-like peptide 2 (1), epidermal growth factor (7), insulin (41), glucagon (10), vasoactive intestinal peptide (32), and prostaglandin E 2 (36). Additional signaling molecules that influence nutrient uptake include epinephrine and adrenergic agonists (21) and polyamines (45).…”

Section: Discussionmentioning

confidence: 98%

Lumenal adenosine and AMP rapidly increase glucose transport by intact small intestine

Kimura¹,

Turner²,

Braasch³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Adenosine modulates the intestinal functions of secretion, motility, and immunity, yet little is known about the regulation of nutrient absorption. Therefore, we measured the carrier-mediated uptake of tracer D-[(14)C]glucose (2 microM) by everted sleeves of the mouse intestine after a lumenal exposure to adenosine and a disodium salt of AMP. Rates of glucose uptake by intact tissues increased almost twofold after a 7-min exposure to 5 mM adenosine (a physiological dose). The response was slightly more pronounced for AMP and could be induced by forskolin. The response to adenosine was blocked by theophylline and the A(2) receptor antagonist 3,7-dimethyl-1-proparglyxanthine but not by the A(1) receptor antagonist 8-phenyltheophylline. Glucose uptake by control and AMP-stimulated tissues was inhibited by phloridzin, implying that sodium-dependent glucose transporter 1 (SGLT1) is the responsive transporter, but the involvement of glucose transporter 2 (GLUT2) cannot be excluded. Of clinical relevance, AMP accelerated the systemic availability of 3-O-methylglucose after an oral administration to mice. Our results indicate that adenosine causes a rapid increase in carrier-mediated glucose uptake that is of clinical relevance and acts via receptors linked to a signaling pathway that involves intracellular cAMP production.

show abstract

Acute increase, stimulated by prostaglandin E₂, in glucose absorption via the sodium dependent glucose transporter-1 in rat intestine

Cited by 25 publications

References 41 publications

Involvement of an enterocyte renin–angiotensin system in the local control of SGLT1‐dependent glucose uptake across the rat small intestinal brush border membrane

Involvement of an enterocyte renin–angiotensin system in the local control of SGLT1‐dependent glucose uptake across the rat small intestinal brush border membrane

Hypoxia differentially regulates nutrient transport in rat jejunum regardless of luminal nutrient present

Lumenal adenosine and AMP rapidly increase glucose transport by intact small intestine

Contact Info

Product

Resources

About

Acute increase, stimulated by prostaglandin E2, in glucose absorption via the sodium dependent glucose transporter-1 in rat intestine

Cited by 25 publications

References 41 publications

Involvement of an enterocyte renin–angiotensin system in the local control of SGLT1‐dependent glucose uptake across the rat small intestinal brush border membrane

Involvement of an enterocyte renin–angiotensin system in the local control of SGLT1‐dependent glucose uptake across the rat small intestinal brush border membrane

Hypoxia differentially regulates nutrient transport in rat jejunum regardless of luminal nutrient present

Lumenal adenosine and AMP rapidly increase glucose transport by intact small intestine

Contact Info

Product

Resources

About

Acute increase, stimulated by prostaglandin E₂, in glucose absorption via the sodium dependent glucose transporter-1 in rat intestine