The administration of lipopolysaccharide, in vivo, induces alteration in L-leucine intestinal absorption

Abad, B.; Mesonero, José E.; Salvador, María Luisa Esteban; Herrera, Jennifer; Rodríguez-Yoldi, Ma. Jesus

doi:10.1016/s0024-3205(01)01440-0

Cited by 16 publications

(10 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results agree with our previous study on L-leucine intestinal absorption [17]. Other studies have shown that LPS decreases the uptake of glutamine, alanine, leucine and glucose by brush border vesicles [10,16] but in these cases the endotoxin was not applied directly to the incubation medium, suggesting that it alters intestinal nutrient transport as a function of the administration route.…”

Section: Discussionsupporting

confidence: 92%

Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

García-Herrera

Abad

Rodríguez-Yoldi

2003

Inflammation Research

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 92%

Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

García-Herrera

Abad

Rodríguez-Yoldi

2003

Inflammation Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…Salloum et al 10 used a systemic administration. Moreover, our group have found that intravenous administration of LPS decreases L-leucine uptake in brush border vesicles, 26 suggesting that endotoxin alters intestinal sodium-dependent amino acid transport as a function of the administration route. These results also suggest that, during sepsis, nutrients could be absorbed differently depending on whether the infection occurs directly in the GI tract or is a result of a systemic infection.…”

Section: Discussionmentioning

confidence: 98%

Cellular mechanism underlying LPS-induced inhibition of in vitro L-leucine transport across rabbit jejunum

Abad

Mesonero

Salvador

et al. 2002

Journal of Endotoxin Research

Self Cite

View full text Add to dashboard Cite

Lipopolysaccharide (LPS) is a known causative agent of sepsis. In previous studies, we have shown that it reduces L-leucine mediated transport across the rabbit jejunum by about 30%. In this study, the mechanism(s) of LPS inhibition on amino acid transport were analysed in detail. LPS did not inhibit L-leucine transport across brush border membrane vesicles, suggesting the need for an intracellular step. The inhibitory effect of LPS was not altered by the addition of protein kinase A (PKA) inhibitor (IP(20), 10(-7) M) or an analog of cAMP (DB-cAMP, 3 x 10(-4) M), indicating that the PKA signal transduction pathway was not involved in the LPS effect. However, the inhibitory effect of LPS was suppressed by trifluoroperazine (10(-7) M), a Ca(2+)/calmodulin inhibitor and staurosporine (10(-7) M), an protein kinase C (PKC) inhibitor. Likewise, LPS inhibition disappeared in media without calcium. These results suggest that LPS could inhibit the intestinal uptake of L-leucine across the small intestine in vitro by intracellular processes related to calcium, involving PKC and calmodulin protein.

show abstract

“…Moreover, after intravenous administration of the endotoxin, the intestinal absorption of these nutrients was inhibited. This LPS effect could be produced by the secretagogue action of TNF‐α on the gut, also implying protein kinases and other mediators such as NO and prostaglandins [Abad et al, 2001b, 2002b; García‐Herrera et al, 2004, 2007; Amador et al, 2007a,b].…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide involved in the IL‐1β‐induced inhibition of fructose intestinal transport

García-Barrios

Guillén

Gascón

et al. 2010

J of Cellular Biochemistry

View full text Add to dashboard Cite

Interleukin-1β (IL-1β) is a pleiotropic cytokine produced by cells of the immune system and a large variety of other cell types including endothelial cells. It is released during inflammatory and infectious diseases, and possesses a wide spectrum of autocrine, paracrine and endocrine activities. The aim of this work was to examine the IL-1β effect on D-fructose transport across rabbit jejunum and try to identify the mediators implicated in this process. A sepsis condition was induced for 90 min after intravenous (iv) administration of IL-1β and body temperature was recorded. Studies on cellular intestinal integrity have not shown modifications of the epithelium and the basement membrane. D-fructose intestinal transport was studied in rabbit jejunum from control and treated animals and it was reduced in the latter ones. This cytokine decreased both the mucosal to serosal transepithelial flux and the transport across brush-border membrane vesicles of D-fructose. The inhibition was reversed by L-NAME (nitric oxide [NO] synthase inhibitor), but not by indomethacin (cyclooxygenase 1 and 2 inhibitor). Both inhibitors were administered iv 15 min before the IL-1β. The protein levels of GLUT5 were not changed in all animal groups and those of mRNA were even increased. In summary, these findings indicate that IL-1β, at the time assayed, induced a significant reduction in the relative intrinsic activity of GLUT5 and in this decrease are involved NO signalling pathways. In this way, blockage of D-fructose intestinal uptake by IL-1β may be playing an essential role in the pathophysiology of septic shock.

show abstract

The administration of lipopolysaccharide, in vivo, induces alteration in L-leucine intestinal absorption

Cited by 16 publications

References 0 publications

Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

Cellular mechanism underlying LPS-induced inhibition of in vitro L-leucine transport across rabbit jejunum

Nitric oxide involved in the IL‐1β‐induced inhibition of fructose intestinal transport

Contact Info

Product

Resources

About