Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

García-Herrera, J.; Abad, B.; Rodríguez-Yoldi, María Jesús

doi:10.1007/s000110300069

Cited by 21 publications

(15 citation statements)

References 57 publications

(42 reference statements)

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“…Thus, we can suggest that the intracellular mediators could be related to the action of endotoxin on galactose absorption modulating the intrinsic activities of SGLT1 and Na + , K + -ATPase. This hypothesis is also supported by studies in our laboratory that show that LPS additioned to the tissue in vitro also inhibits D-fructose intestinal uptake which occurs through the Na + independent transporter GLUT5 [12]. Findings to date indicate that all these intracellular mediators are well-known regulators and/or modulators of intestinal ion [8,9], sugar transport [22,31,37,38] and nitric oxide (NO) production [39].…”

Section: Discussionsupporting

confidence: 61%

“…In this way, we reported an inhibitory effect of LPS on D-fructose uptake across the small intestine of rabbit in vitro and in vivo [12,13] and on D-galactose intestinal absorption in vivo [14].…”

Section: Introductionmentioning

confidence: 96%

“…We examined the effects of 10 -6 M GF 109203X, a selective inhibitor of protein kinase C (PKC) [12], on LPS effect using intestinal rings. When this inhibitor was added to the medium, the inhibitory effect of LPS on D-galactose intestinal absorption is practically abolished (Fig.…”

Section: Intracellular Mediators In Lps Actionmentioning

confidence: 99%

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Lipopolysaccharide Induces Inhibition of Galactose Intestinal Transport in Rabbits <i>in vitro</i>

Amador¹,

Marca

García-Herrera³

et al. 2008

Cell Physiol Biochem

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Background/Aims: Previous studies from our laboratory have revealed impaired intestinal absorption of D-galactose in lipopolysaccharide-treated rabbits. The aim of the present work was to examine the effect of LPS on D-galactose intestinal absorption in vitro. Methods: D-galactose intestinal transport was assessed employing three techniques: sugar uptake in rings of everted jejunum, transepithelial flux in Ussing-type chambers and transport assays in brush border membrane vesicles. The level of expression of the Na⁺/D-galactose cotransporter (SGLT1) was analyzed by Western blot. Results: LPS decreased the mucosal D-galactose transport in rabbit jejunum but a preexposition to the endotoxin was required. LPS affected the Na⁺-dependent transport system by increasing the apparent Km value without affecting the Vmax. It also decreased the Na⁺, K⁺-ATPase activity. However, it did not inhibit neither the uptake of D-galactose by brush border membrane vesicles nor modified the SGLT1 protein levels in the brush border, suggesting an indirect endotoxin effect. This inhibitory effect, was reduced by selective inhibitors of Ca²⁺-calmodulin (W13), protein kinase C (GF 109203X), p38 mitogen-activated protein kinase (SB 203580), c-Jun N-terminal kinase (SP 600125) and mitogen extracellular kinase (U 0126). Conclusion: LPS inhibits the mucosal Na⁺-dependent D-galactose intestinal absorption and the Na⁺, K⁺-ATPase activity when it is added to the tissue. Intracellular processes related to protein kinases seem to be implicated in the endotoxin effect.

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Section: Discussionsupporting

confidence: 61%

Section: Introductionmentioning

confidence: 96%

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Lipopolysaccharide Induces Inhibition of Galactose Intestinal Transport in Rabbits <i>in vitro</i>

Amador¹,

Marca

García-Herrera³

et al. 2008

Cell Physiol Biochem

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“…In rats, 2-8 days after iodoacetamide-induced colitis, GLUT5 protein and mRNA levels decreased in noninflamed small intestine, thereby paralleling the time course of inflammation manifested in the large intestine and suggesting that GLUT5 in noninflamed tissues may be sensitive to inflammation inducers or to inflammatory signals in the blood (77). In the case of sepsis induced by lipopolysaccharide (LPS) or tumor necrosis factor-␣ (TNF-␣) in rabbit, fructose absorption also decreased in the jejunum (57,59). When injected intravenously, LPS, which is a component of the membrane of gram-negative bacteria, stimulates cytokine (including TNF-␣) and glucocorticoid production.…”

Section: Pathology and Glut5mentioning

confidence: 99%

Regulation of the fructose transporter GLUT5 in health and disease

Douard¹,

Ferraris²

2008

American Journal of Physiology-Endocrinology and Metabolism

395

366

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Fructose is now such an important component of human diets that increasing attention is being focused on the fructose transporter GLUT5. In this review, we describe the regulation of GLUT5 not only in the intestine and testis, where it was first discovered, but also in the kidney, skeletal muscle, fat tissue, and brain where increasing numbers of cell types have been found to have GLUT5. GLUT5 expression levels and fructose uptake rates are also significantly affected by diabetes, hypertension, obesity, and inflammation and seem to be induced during carcinogenesis, particularly in the mammary glands. We end by highlighting research areas that should yield information needed to better understand the role of GLUT5 during normal development, metabolic disturbances, and cancer.

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“…Among the toxins produced by these agents, LPS stimulates the synthesis of inflammatory mediators such as cytokines [Damas et al, 1997]. In previous studies, we reported that LPS inhibits the intestinal transport of L-leucine and D-fructose both when the toxin is directly added to the intestinal tissue [Abad et al, 2001b[Abad et al, , 2002aGarcía-Herrera et al, 2003] or i.v. administered [Abad et al, 2001a].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of TNF‐α on the intestinal absorption of galactose

Amador¹,

García-Herrera²,

Marca³

et al. 2006

J of Cellular Biochemistry

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Sepsis is a systemic response to infection in which toxins, such as bacterial lipopolysaccharide (LPS), stimulate the production of inflammatory mediators like the cytokine tumor necrosis factor alpha (TNF-alpha). Previous studies from our laboratory have revealed that LPS inhibits the intestinal absorption of L-leucine and D-fructose in rabbit when it was intravenously administered, and that TNF-alpha seems to mediate this effect on amino acid absorption. To extend this work, the present study was designed to evaluate the possible effect of TNF-alpha on D-galactose intestinal absorption, identify the intracellular mechanisms involved and establish whether this cytokine mediates possible LPS effects. Our findings indicate that TNF-alpha decreases D-galactose absorption both in rabbit intestinal tissue preparations and brush-border membrane vesicles. Western blot analysis revealed reduced amounts of the Na+/glucose cotransporter (SGLT1) protein in the plasma membrane attributable to the cytokine. On the contrary, TNF-alpha increased SGLT1 mRNA levels. Specific inhibitors of the secondary messengers PKC, PKA, the MAP kinases p38 MAP, JNK, MEK1/2 as well as the proteasome, diminished the TNF-alpha-evoked inhibitory effect. LPS inhibition of the uptake of the sugar was blocked by a TNF-alpha antagonist. In conclusion, TNF-alpha inhibits D-galactose intestinal absorption by decreasing the number of SGLT1 molecules at the enterocyte plasma membrane through a mechanism in which several protein-like kinases are involved.

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Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

Abstract: LPS can inhibit the intestinal uptake of D-fructose across the rabbit jejunum in vitro by intracellular processes related to PKC and calmodulin protein.

Cited by 21 publications

References 57 publications

Lipopolysaccharide Induces Inhibition of Galactose Intestinal Transport in Rabbits <i>in vitro</i>

Lipopolysaccharide Induces Inhibition of Galactose Intestinal Transport in Rabbits <i>in vitro</i>

Regulation of the fructose transporter GLUT5 in health and disease

Inhibitory effect of TNF‐α on the intestinal absorption of galactose

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