Effect of dehydration on apical Na + -H + exchange activity and Na + -dependent sugar transport in brush-border membrane vesicles isolated from chick intestine

Horra, Maria Carmen De La; Calonge, M. L.; Ilundáin, A.

doi:10.1007/s004240050611

Cited by 13 publications

(9 citation statements)

References 18 publications

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“…In our previous study (6) we also suggested that AVT regulates jejunal NHE activity because it was not affected by Na ϩ depletion, but it was increased by dehydration. However, the current results show that neither aldosterone nor AVT significantly affected jejunal NHE activity.…”

Section: Discussionmentioning

confidence: 89%

“…As a result, the epithelia of the lower intestine process the ileal and ureteral outflow. We previously reported that dietary Na ϩ depletion decreased Na ϩ -sugar cotransport (SGLT-1) activity and increased that of apical sodium/hydrogen exchange (NHE) in the chick ileum and colon (6,7). We also showed (6) that 4 days of water deprivation increased the activities of both apical NHE and SGLT-1 in jejunum, ileum, and colon of the chicken.…”

mentioning

confidence: 94%

“…Therefore, Na ϩ depletion decreased intestinal SGLT-1 activity, whereas it was increased by dehydration. Because both treatments increased plasma aldosterone levels, it was concluded that aldosterone does not regulate intestinal SGLT-1 (6).…”

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confidence: 99%

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Hormonal regulation of chicken intestinal NHE and SGLT-1 activities

Horra

Cano

Peral

et al. 2001

American Journal of Physiology-Regulatory, Integrative and Comp

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-sugar cotransport (SGLT-1) activities have been investigated using brush-border membrane vesicles isolated from Hubbard chicken small and large intestines, and they were compared with those induced by either Na ϩ depletion or dehydration. Na ϩ depletion was induced by feeding the chickens with either a low-or a high-Na ϩ diet for either 0.5, 1, 2, 4, or 8 days. Ileal and colonic NHE2 activity increased with the duration of the Na ϩ depletion, whereas that of intestinal SGLT-1 decreased, reaching a plateau after 2 days of treatment. Three-hour incubation of the intestine with aldosterone produced the same effects on NHE activity as does Na ϩ depletion, without altering SGLT-1 activity. However, 3-h incubation of the intestine with AVT increased intestinal SGLT-1 activity, without affecting intestinal NHE activity. It is concluded that aldosterone regulates apical ileal and colonic NHE2 activity, whereas that of SGLT-1 is regulated by AVT.low-Na ϩ diet; aldosterone; arginine vasotocin; brush-border membrane vesicle; sodium/hydrogen exchange IN MAMMALS, THE KIDNEY and the large intestine are the major regulators of body electrolyte and water homeostasis. As birds do not have a urinary bladder, the urine is emptied into the cloaca, and retrograde flow carries urine into the coprodeum, the colon (rectum), and cecum. As a result, the epithelia of the lower intestine process the ileal and ureteral outflow. We previously reported that dietary Na ϩ depletion decreased Na ϩ -sugar cotransport (SGLT-1) activity and increased that of apical sodium/hydrogen exchange (NHE) in the chick ileum and colon (6, 7). We also showed (6) that 4 days of water deprivation increased the activities of both apical NHE and SGLT-1 in jejunum, ileum, and colon of the chicken. Therefore, Na ϩ depletion decreased intestinal SGLT-1 activity, whereas it was increased by dehydration. Because both treatments increased plasma aldosterone levels, it was concluded that aldosterone does not regulate intestinal SGLT-1 (6).The purpose of the current work was to investigate in brush-border membrane vesicles (BBMV) isolated from chicken small and large intestine the time course of the effects of Na ϩ depletion on intestinal NHE and SGLT-1 activities and the effects of aldosterone and arginine vasotocin (AVT) on those Na ϩ -linked transport systems activities.

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Section: Discussionmentioning

confidence: 89%

mentioning

confidence: 94%

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Hormonal regulation of chicken intestinal NHE and SGLT-1 activities

Horra

Cano

Peral

et al. 2001

American Journal of Physiology-Regulatory, Integrative and Comp

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“…For example, dehydration results in an increase in sodium-hydrogen exchange, albeit with segmental differences; NHE2 activity increases in the ileum and the colon, while in the jejunum, the activity of both NHE2 and NHE3 increases. Dehydration also leads to an increase in serum aldosterone levels and sodium glucose co-transport in all intestinal segments (De la Horra et al , 1998). Another example of intestinal adaptation is an increase in the intestinal uptake of Ca 2+ and calcium binding protein after restricted feeding during moulting in hens (Berry and Brake, 1991, al-Batshan et al , 1994).…”

Section: Adaptation Of Avian Intestinal Ion Transport To Nutritional mentioning

confidence: 99%

Pathophysiology of avian intestinal ion transport

Nighot

2018

World's Poultry Science Journal

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Summary The gut has great importance for the commercial success of poultry production. Numerous ion transporters, exchangers, and channels are present on both the apical and the basolateral membrane of intestinal epithelial cells, and their differential expression along the crypt-villus axis within the various intestinal segments ensures efficient intestinal absorption and effective barrier function. Recent studies have shown that intensive production systems, microbial exposure, and nutritional management significantly affect intestinal physiology and intestinal ion transport. Dysregulation of normal intestinal ion transport is manifested as diarrhoea, malabsorption, and intestinal inflammation resulting into poor production efficiency. This review discusses the basic mechanisms involved in avian intestinal ion transport and the impact of development during growth, nutritional and environmental alterations, and intestinal microbial infections on it. The effect of intestinal microbial infections on avian intestinal ion transport depends on factors such as host immunity, pathogen virulence, and the mucosal organisation of the particular intestinal segment.

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“…ϩ -Glucose Cotransportinduced NHE3 Translocation-Initiation of Na ϩ -glucose cotransport triggers NHE3 translocation to the plasma membrane, thereby activating Na ϩ -H ϩ exchange and resulting in net intestinal Na ϩ absorption (6,7,27,28). Moreover, the net cytosolic alkalinization that results from this NHE3 activation (1) provides the driving force for intestinal H ϩ -dipeptide transport (29).…”

Section: Mapkapk-2 Is Required For Namentioning

confidence: 99%

MAPKAPK-2 Is a Critical Signaling Intermediate in NHE3 Activation Following Na+-Glucose Cotransport

Wang

Graham

et al. 2006

Journal of Biological Chemistry

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Villus enterocyte nutrient absorption occurs via precisely orchestrated interactions among multiple transporters. For example, transport by the apical Na ؉ -glucose cotransporter, SGLT1, triggers translocation of NHE3, Na ؉ -H ؉ antiporter isoform 3, to the plasma membrane. This translocation requires activation of p38 mitogen-activated protein kinase (MAPK), Akt2, and ezrin. Akt2 directly phosphorylates ezrin, but the precise role of p38 MAPK in this process remains to be defined. Sequence analysis suggested that p38 MAPK could not directly phosphorylate Akt2. We hypothesized that MAPKAPK-2 might link p38 MAPK and Akt2 activation. MAPKAPK-2 was phosphorylated after initiation of Na ؉ -glucose cotransport with kinetics that paralleled activation of p38 MAPK, Akt2, and ezrin. MAPKAPK-2, Akt2, and ezrin phosphorylation were all attenuated by p38 MAPK inhibition but were unaffected by dominant negative ezrin expression. Akt2 inhibition blocked ezrin but not p38 MAPK or MAPKAPK-2 phosphorylation, suggesting that MAPKAPK-2 could be an intermediate in p38 MAPK-dependent Akt2 activation. Consistent with this, MAP-KAPK-2 could phosphorylate an Akt2-derived peptide in vitro. siRNA-mediated MAPKAPK-2 knockdown inhibited phosphorylation of Akt2 and ezrin but not p38 MAPK. MAPKAPK-2 knockdown also blocked NHE3 translocation. Thus, MAP-KAPK-2 controls Akt2 phosphorylation. In so doing, MAP-KAPK-2 links p38 MAPK to Akt2, ezrin, and NHE3 activation after SGLT1-mediated transport.Intestinal nutrient absorption occurs via precisely orchestrated regulation of multiple transporters. One critical example involves coordinated Na ϩ and glucose absorption by villus enterocytes (1, 2). This process may, in part, explain why inclusion of Na ϩ and glucose in oral rehydration solutions used to treat life-threatening diarrheal disease augments therapeutic efficacy (3, 4). In mechanistic terms, Na ϩ -glucose cotransport mediated by SGLT1 leads to activation of the apical Na ϩ -H ϩ antiporter NHE3. This generates a favorable osmotic gradient that drives transepithelial water absorption (5, 6). Coordination of SGLT1 and NHE3 involves a complex signal transduction pathway where activation of p38 mitogen-activated protein kinase (MAPK) 2 leads to Akt2 activation, ezrin phosphorylation, and NHE3 translocation to the brush border (1,7,8).Although it is clear that p38 MAPK is critical to this process (1), the mechanisms by which p38 MAPK activates Akt2 are unknown. Available data suggest that p38 MAPK cannot activate Akt2 directly. We therefore considered p38 MAPK effectors as potential signaling intermediates in this process.A large number of kinases have been reported to be p38 MAPK effectors, including Mnk1, Mnk2, PRAK, MEF2, ATF-2, Stat1, and MAPK-activated protein kinase-2 (MAPKAPK-2) (9, 10). These, in turn, act on additional substrates, including CREB and HSP27 (11-17). Among these effectors, two recent reports suggest that MAPKAPK-2, a serine/threonine protein kinase, may link p38 MAPK and Akt. These studies showed that recombinant MAPKAPK...

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Effect of dehydration on apical Na + -H + exchange activity and Na + -dependent sugar transport in brush-border membrane vesicles isolated from chick intestine

Cited by 13 publications

References 18 publications

Hormonal regulation of chicken intestinal NHE and SGLT-1 activities

Hormonal regulation of chicken intestinal NHE and SGLT-1 activities

Pathophysiology of avian intestinal ion transport

MAPKAPK-2 Is a Critical Signaling Intermediate in NHE3 Activation Following Na+-Glucose Cotransport

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