Genetic regulation of enterocyte differentiation

Smith, Michael W.

doi:10.1079/pns19930065

Cited by 10 publications

(5 citation statements)

References 34 publications

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“…AMG-feeding does not sustain SGLT1 expression, indicating that T3 effects are mediated by glucose metabolism. The regulation of SGLT1 in Caco-2\TC7 cells thus differs from that observed in animal models in i o, showing that non-metabolizable glucose analogues induce the expression of SGLT1 in crypt cells and that a functional cotransporter is found, inasmuch as cells migrate and mature along the villus [13,48,49].…”

Section: Discussionmentioning

confidence: 71%

“…Identical cDNA sequences were found for SGLT1 cDNA from normal human and Caco-2 enterocytes [12]. In normal small intestine the expression of SGLT1 mRNA is undetectable in the crypts where enterocytes are mainly undifferentiated, and it appears as soon as the cells migrate and mature along the villus axis [13][14][15]. The mechanisms underlying the control of SGLT1 expression are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

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Thyroid hormone regulation of the Na+/glucose cotransporter SGLT1 in Caco-2 cells

Matosin-Matekalo

Mesonero

Delézay³

et al. 1998

Biochemical Journal

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The expression of the Na+/glucose cotransporter (SGLT1) in response to thyroid hormone [3,5,3'-tri-iodo-l-thyronine (T3)] was investigated in the enterocytic model cell line Caco-2/TC7. In differentiated cells, T3 treatment induces an average 10-fold increase in glucose consumption as well as a T3 dose-dependent increase in SGLT1 mRNA abundance. Only cells grown on glucose-containing media, but not on the non-metabolizable glucose analogue alpha-methylglucose (AMG), could respond to T3-treatment. The Vmax parameter of AMG transport was enhanced 6-fold by T3 treatment, whereas the protein abundance of SGLT1 was unchanged. The role of Na+ recycling in the T3-related activation of SGLT1 activity was suggested by both the large increase in Na+/K+ATPase protein abundance and the inhibition, down to control levels, of AMG uptake in ouabain-treated cells. Further investigations aimed at identifying the presence of a second cotransporter that could be expressed erroneously in the colon cancer cell line were unsuccessful: T3-treatment did not modify the sugar-specificity profile of AMG transport and did not induce the expression of SGLT2 as assessed by reverse transcription-PCR. Our results show that T3 can stimulate the SGLT1 cotransport activity in Caco-2 cells. Both transcriptional and translational levels of regulation are involved. Finally, glucose metabolism is required for SGLT1 expression, a result that contrasts with the in vivo situation and may be related to the fetal phenotype of the cells.

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Section: Discussionmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Thyroid hormone regulation of the Na+/glucose cotransporter SGLT1 in Caco-2 cells

Matosin-Matekalo

Mesonero

Delézay³

et al. 1998

Biochemical Journal

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“…The ensemble of these modifications could be responsible for the previously hypothesised modification of luminal nutrient abundance and the consequent variation of amino acid transport rates because of competition or inhibition phenomena, as suggested by Rosas et al, (2008). Likewise, histopathological modifications previously described in salmonids (Baeverfjord and Krogdahl, 1996;Krogdahl et al, 2003) and sea bream (Sitjà-Bobadilla et al, 2005;Santigosa et al, 2008) fed plant protein-based meals could be partially responsible for this transport modulation since transporters are immersed in the lipid bilayer and diffusion and absorption efficiency are affected by bilayer characteristics (Houpe et al:, 1997;Spektor and Yorek, 1985) and enterocyte development (Smith, 1993).…”

Section: Discussionmentioning

confidence: 78%

Modifications of intestinal nutrient absorption in response to dietary fish meal replacement by plant protein sources in sea bream (Sparus aurata) and rainbow trout (Onchorynchus mykiss)

et al. 2011

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Modifications of intestinal nutrient absorption in response toTwo experimental diets in which fish meal was partially (75%; diet PP75) or totally 24 (diet PP100) replaced by plant protein sources were fed to gilthead sea bream and 25 rainbow trout. We studied the effects of these diets on intestinal nutrient absorption in 26 comparison to fish fed the fish meal diet (FM). A mixture of vegetal ingredients (corn 27 gluten meal, wheat gluten, extruded peas and rapeseed meal) was used to meet the 28 amino acid requirements of the fish. Over a 12-week trial, 3 groups of the two 29 species were fed one experimental diet twice a day until visual satiation. 30After the experimental growth trial, we measured amino acid (L-leucine, L-lysine, L-31 phenylalanine, L-alanine and L-proline) and D-glucose absorption at 6 h and long-32 term (48 h for sea bream and 36 h for rainbow trout) post-feeding in pyloric caeca, 33 proximal intestine and distal intestine segments using brush border membrane 34 vesicles. The absorption pattern 6 h post-feeding was modified in both species in 35 response to fish meal replacement: total absorption capacities were generally 36 maintained in PP75 trout because absorption was delayed from pyloric caeca to 37 proximal and/or distal intestinal segments, while absorption uptake was significantly 38 decreased in both sea bream groups and trout fed the 100% vegetable diet. Glucose 39 transport capacities were increased in both experimental sea bream groups and in 40 trout fed the PP75 diet. Long-term transport capacities showed an up-regulation for 41 both studied species. 42Results obtained in this work show that intestinal nutrient absorption is modified in 43 response to fish meal replacement by plant protein sources and that changes are 44 species-specific and not dose-dependent. 45 46

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“…A similar pattern of the calbindin response to calcitriol in chickens has been explained by changes in the calbindin synthesis control mechanisms during enterocyte differentiation because calbindin mRNA is expressed maximally in the basal villus enterocytes (60) . In contrast, rat studies show that TRPV6 is only expressed in villi tips (27) , which further supports the hypothesis that the delay in positive or negative adaptation is a result of enterocyte differentiation (Fig.…”

Section: Adaptive Mechanisms Of Calcium Homeostasismentioning

confidence: 79%

A novel model to explain dietary factors affecting hypocalcaemia in dairy cattle

Martín-Tereso

Verstegen

2011

Nutr. Res. Rev.

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Most dairy cows exhibit different degrees of hypocalcaemia around calving because the gestational Ca requirements shift to the disproportionately high Ca requirements of lactation. Ca homeostasis is a robust system that effectively adapts to changes in Ca demand or supply. However, these adaptations often are not rapid enough to avoid hypocalcaemia. A delay in the reconfiguration of intestinal Ca absorption and bone resorption is probably the underlying cause of this transient hypocalcaemia. Several dietary factors that affect different aspects of Ca metabolism are known to reduce the incidence of milk fever. The present review describes the interactions between nutrition and Ca homeostasis using observations from cattle and extrapolations from other species and aims to quantitatively model the effects of the nutritional approaches that are used to induce dry cows into an early adaptation of Ca metabolism. The present model suggests that reducing dietary cation -anion difference (DCAD) increases Ca clearance from the blood by dietary induction of systemic acidosis, which results in hypercalciuria due to the loss of function of the renal Ca transient receptor potential vanilloid channel TRPV5. Alternatively, reducing the gastrointestinal availability of Ca by reducing dietary Ca or its nutritional availability will also induce the activation of Ca metabolism to compensate for basal blood Ca clearance. Our model of gastrointestinal Ca availability as well as blood Ca clearance in the transition dairy cow allowed us to conclude that the most common dietary strategies for milk fever prevention may have analogous modes of action that are based on the principle of metabolic adaptation before calving.

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Genetic regulation of enterocyte differentiation

Cited by 10 publications

References 34 publications

Thyroid hormone regulation of the Na+/glucose cotransporter SGLT1 in Caco-2 cells

Thyroid hormone regulation of the Na+/glucose cotransporter SGLT1 in Caco-2 cells

Modifications of intestinal nutrient absorption in response to dietary fish meal replacement by plant protein sources in sea bream (Sparus aurata) and rainbow trout (Onchorynchus mykiss)

A novel model to explain dietary factors affecting hypocalcaemia in dairy cattle

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