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

Amador, P.; García-Herrera, J.; Marca, M.C.; Osada, Jesús; Acı́n, Sergio; Navarro, M.A.; Salvador, María Luisa Esteban; Lostao, M. P.; Rodríguez-Yoldi, Ma. Jesus

doi:10.1002/jcb.21168

Cited by 28 publications

(18 citation statements)

References 92 publications

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“…When the LPS is intravenously administered it can release cytokines and other mediators that help to increase the effect. In fact, we have found that TNF-α effect on D-galactose intestinal absorption is similar to that induced by LPS and could be a mediator of the endotoxin [25].…”

Section: Discussionmentioning

confidence: 66%

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: Discussionmentioning

confidence: 66%

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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“…Also, 12-h maternal and food deprivation in P8 mouse pups does not alter plasma leptin (1). This reduction in plasma leptin could therefore reflect a reduction in the contribution coming from the pups themselves via an as yet unknown mechanism or an alteration in the absorption of leptin from the gastric tract (2). Whatever the mechanism of this significant reduction in circulating leptin, especially in the females, there appears to be no resulting alterations in related adult physiology, suggesting that the change in leptin we see here is either too short-lived or too small to result in long-term alterations.…”

Section: Discussionmentioning

confidence: 87%

Neonatal immune challenge does not affect body weight regulation in rats

Spencer¹,

Mouihate²,

Galic³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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The perinatal environment plays a crucial role in programming many aspects of adult physiology. Myriad stressors during pregnancy, from maternal immune challenge to nutritional deficiency, can alter longterm body weight set points of the offspring. In light of the increasing concern over body weight issues, such as obesity and anorexia, in modern societies and accumulating evidence that developmental stressors have long-lasting effects on other aspects of physiology (e.g., fever, pain), we explored the role of immune system activation during neonatal development and its impact on body weight regulation in adulthood. Here we present a thorough evaluation of the effects of immune system activation (LPS, 100 g/kg ip) at postnatal days 3, 7, or 14 on long-term body weight, adiposity, and body weight regulation after a further LPS injection (50 g/kg ip) or fasting and basal and LPS-induced circulating levels of the appetite-regulating proinflammatory cytokine leptin. We show that neonatal exposure to LPS at various times during the neonatal period has no long-term effects on growth, body weight, or adiposity. We also observed no effects on body weight regulation in response to a short fasting period or a further exposure to LPS. Despite reductions in circulating leptin levels in response to LPS during the neonatal period, no long-term effects on leptin were seen. These results convincingly demonstrate that adult body weight and weight regulation are, unlike many other aspects of adult physiology, resistant to programming by a febrile-dose neonatal immune challenge.gender; leptin; lipopolysaccharide; obesity THE PERINATAL ENVIRONMENT is known to play a crucial role in programming body weight. In humans, low birth weight and malnutrition during gestation have been linked with abdominal obesity in adulthood (31,45,46). Similarly, a variety of behavioral, physiological (including dietary manipulations), and immune stressors given to pregnant experimental animals have been reported to alter the body weight of adult offspring (4,15,27,36,40,63). It appears, however, that the timing of perinatal stress is critical in programming many aspects of adult physiology (35) and relatively little is known regarding the influence of postnatal stress on adult body weight regulation.The long-term physiological consequences of a neonatal immune challenge with LPS have been extensively described by our laboratory and others. For example, we have shown attenuated febrile and associated host defense responses in adulthood to an immune challenge of the same type as that experienced at postnatal day (P) 14 (9,17,18). Changes have also been demonstrated in memory processing (7), hypothalamic-pituitary-adrenal axis activation (51, 52), and susceptibility to pathological insults in adulthood (10, 55, 56). However, the long-term effects of a neonatal immune challenge on body weight regulation are less clear, and given the concern over the current obesity epidemic in modern society [e.g., (29)], demand further investigation. For instance, Walker ...

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“…The most likely candidates are the elevated plasma concentrations of inflammatory cytokines and bacterial endotoxins that are associated with NEC. Exemplary is the decreased sugar absorption by intestinal tissue exposed to TNF-␣ (32,33). It is unknown if therapeutic regimens that reduce inflammatory cytokines and the associated mucosal responses of infants with NEC (34 -37) will improve nutrient absorption.…”

Section: Discussionmentioning

confidence: 99%

Aldohexose Malabsorption in Preterm Pigs Is Directly Related to the Severity of Necrotizing Enterocolitis

et al. 2008

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Necrotizing enterocolitis (NEC) causes morbidity and mortality among preterm infants and is associated with nutrient malabsorption. Therefore, a preterm pig model that spontaneously develops NEC was used to investigate the relationship between severity of NEC lesions and galactose absorption in vivo and carriermediated glucose absorption by intact mid small intestine. Preterm pigs collected by caesarian section at 92% of gestation received parenteral nutrition with and without minimal enteral nutrition for 48 h before conversion to enteral nutrition with colostrum or an enteral formula. Pigs were killed when symptoms of NEC were observed or after 36 -40 h of enteral nutrition. NEC lesions decreased in vivo absorption of galactose and mannitol by more than 50% and abolished carrier-mediated glucose uptake by tissues with lesions. Moreover, when NEC lesions were restricted to the colon, small intestinal tissues that seemed clinically healthy had decreased in vitro glucose absorption due to reduced uptake via the sodiumdependent glucose transporter with little or no involvement of the apical facilitative glucose carrier. The present findings reveal a direct relationship between the severity of NEC lesions and the magnitude of sugar malabsorption that is detectable before clinical symptoms are evident. (Pediatr Res 63: 382-387, 2008)

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

Cited by 28 publications

References 92 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>

Neonatal immune challenge does not affect body weight regulation in rats

Aldohexose Malabsorption in Preterm Pigs Is Directly Related to the Severity of Necrotizing Enterocolitis

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