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

doi:10.1023/a:1010782600380

Cited by 24 publications

(1 citation statement)

References 22 publications

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“…The latter was confirmed by Nielsen et al (2005), who reported that APR caused a negative nitrogen balance and a decreased functional liver mass that attenuated the urea synthesis increase [44]. In this regard, LPS severely affects the body's nitrogen metabolism at the intestinal level [45]. Indeed, several studies have reported that endotoxemia is characterized by decreased amino acid intestinal absorption [42,43].…”

Section: Discussionmentioning

confidence: 83%

Metabolic Fingerprinting of Feces from Calves, Subjected to Gram-Negative Bacterial Endotoxin

et al. 2021

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Gram-negative bacteria have a well-known impact on the disease state of neonatal calves and their mortality. This study was the first to implement untargeted metabolomics on calves’ fecal samples to unravel the effect of Gram-negative bacterial endotoxin lipopolysaccharide (LPS). In this context, calves were challenged with LPS and administered with fish oil, nanocurcumin, or dexamethasone to evaluate treatment effects. Ultra-high-performance liquid-chromatography high-resolution mass spectrometry (UHPLC-HRMS) was employed to map fecal metabolic fingerprints from the various groups before and after LPS challenge. Based on the generated fingerprints, including 9650 unique feature ions, significant separation according to LPS group was achieved through orthogonal partial least squares discriminant analysis (Q2 of 0.57 and p-value of 0.022), which allowed the selection of 37 metabolites as bacterial endotoxin markers. Tentative identification of these markers suggested that the majority belonged to the subclass of the carboxylic acid derivatives—amino acids, peptides, and analogs—and fatty amides, with these subclasses playing a role in the metabolism of steroids, histidine, glutamate, and folate. Biological interpretations supported the revealed markers’ potential to aid in disease diagnosis, whereas beneficial effects were observed following dexamethasone, fish oil, and nanocurcumin treatment.

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Section: Discussionmentioning

confidence: 83%

Metabolic Fingerprinting of Feces from Calves, Subjected to Gram-Negative Bacterial Endotoxin

et al. 2021

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

García-Barrios

Guillén

Gascón

et al. 2010

J of Cellular Biochemistry

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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.

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Cited by 24 publications

References 22 publications

Metabolic Fingerprinting of Feces from Calves, Subjected to Gram-Negative Bacterial Endotoxin

Metabolic Fingerprinting of Feces from Calves, Subjected to Gram-Negative Bacterial Endotoxin

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

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

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