Effects of semistarvation on transintestinald-glucose transport andd-glucose uptake in brush border and basolateral membranes of rat enterocytes

Marciani, P.; Lindi, C.; Faelli, A.; Esposito, Giovanni

doi:10.1007/bf02181462

Cited by 14 publications

(7 citation statements)

References 23 publications

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“…The continuous lines show the theoretical total uptake curves calculated by applying Eq. 1 and the kinetic parameters estimated from these data on female guinea pigs listed in Table 1. confirming work done by others with intact-tissue preparations (4)(5)(6)(7)21). Extending the older work, however, nonlinear regression analysis of our data reveals the transport increase induced by semistarvation to be highly specific: semistarvation affects only S-2.…”

Section: Resultssupporting

confidence: 76%

“…To establish whether the effects seen were due, in whole or in part, to changes in the unspecific permeability of the membrane (see refs. 7 and 26), diffusion was monitored either by using L-glucose as a marker or by estimating by nonlinear regression analysis the Pr6c. Natl.…”

Section: Discussionmentioning

confidence: 99%

“…No satisfactory explanation of these discrepancies thus far exists, but many variables that have escaped appropriate control may be involved. Furthermore, the procedures of analysis and data expression differ widely and complicate the situation (3)(4)(5)(6)(7).…”

mentioning

confidence: 99%

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Independent modulation by food supply of two distinct sodium-activated D-glucose transport systems in the guinea pig jejunal brush-border membrane.

Brot-Laroche¹,

Dao²,

Alcalde³

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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D-glucose transport across the intestinal brush-border membrane involves two transport systems designated here as systems 1 and 2. Kinetic properties for both D-glucose and methyl a-D-glucopyranoside transport were measured at 350C by using brush-border membrane vesicles prepared from either control, fasted (48 hr), or semistarved (10 days) animals. The results show the following: (i) The sugar influx rate by simple diffusion was identical under either altered condition. (ii) Semistarvation stimulated D-glucose uptake by system 2 (both its V__ and Km increased), whereas system 1 was untouched. (iii) Fasting increased the capacity of system 1 without affecting either Km of system 1 or V..: and Km of system 2. The effect of fasting on Vx,,,, of system 1 cannot be attributed to indirect effects from changes in ionic permeability because the kinetic difference between control and fasted animals persisted when the membrane potential was short-circuited with equilibrated K+ and valinomycin. This work provides further evidence for the existence of two distinct sodium-activated D-glucose transport systems in the intestinal brush-border membrane, which adapt independently to either semistarvation or fasting.D-glucose transport in the small intestine responds to a variety of pathophysiological conditions that include qualitative and quantitative modifications of the diet, small-bowel resection, and diabetes. Often, however, published results are contradictory. For instance, under apparently similar conditions total sugar absorption has been described as either increasing, decreasing, or exhibiting no change (for reviews, see refs. 1-3). No satisfactory explanation of these discrepancies thus far exists, but many variables that have escaped appropriate control may be involved. Furthermore, the procedures of analysis and data expression differ widely and complicate the situation (3-7).An additional source of confusion is the heterogeneity in intestinal transport. Although the suggestion that two Dglucose transport systems occur in the apical border of the intestine has existed since the work of Honegger and Semenza (for review, see ref. 8), D-glucose absorption is usually treated as involving a single homogeneous transport system, the D-glucose/Na+ cotransporter identified in the sixties (for reviews, see refs. 8-11). Consequently, work on intestinal adaptation has been concerned with overall transport function of the intestine, providing no answers to whether individual transport systems were being selectively affected. In this paper we describe experiments permitting such a diagnosis.We demonstrated recently that D-glucose transport across the intestinal brush-border membrane involves at least two distinct, sodium-activated transport agencies (12-14). Although we identified the first, system 1 (S-1), as being identical with the classical D-glucose/Na' cotransporter (12), the exact nature of system 2 (S-2) remains to be established.[In this paper we use our own classification (12-14); although two distinct D-glucos...

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Section: Resultssupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

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Independent modulation by food supply of two distinct sodium-activated D-glucose transport systems in the guinea pig jejunal brush-border membrane.

Brot-Laroche¹,

Dao²,

Alcalde³

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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“…Similar findings were observed in the jejunum of undernourished piglets (19). Recent studies in adult rats subjected to semistarvation, indicate that this nutritional adaptation may be due to increased sodium and glucose uptake by brush border membrane vesicles (20). The mechanisms triggering the alterations in mucosal structure and function observed in the intestine of malnourished animals are unknown.…”

supporting

confidence: 61%

Effects of Chronic Protein-Calorie Malnutrition on Small Intestinal Repair after an Acute Bacterial Enteritis: A Study in Infant Rabbits

Butzner

Gall

1988

Pediatr Res

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ABSTRACT. The aim of this study was to determine if recovery of intestinal function in infant rabbits subjected to protein-calorie malnutrition was delayed as a result of inflammatory injury induced by an experimental bacterial enteritis. Rabbits were malnourished by expanding litter size at 7 days of age and infecting undernourished animals and dietary controls with Yersinia enterocolitica at either 17 or 21 days of age. Intestinal morphology and function were evaluated in infected and noninfected animals from both dietary groups at 27 days of age. Undernutrition alone significantly reduced animal weight, small intestinal weight, segmental jejunal and ileal mucosal weight, villus height, crypt depth, disaccharidase activities, mucosal protein and DNA contents, but increased ileal short-circuited glucose-stimulated Na+ absorption compared to controls. The jejunum of undernourished rabbits at 6 days postinfection exhibited an intestinal injury, as evidenced by a mild inflammatory infiltrate and further reductions in villus height, mucosal weight, lactase activity, protein and DNA content, not seen in infected dietary controls. Jejunal recovery was complete by 10 days postinfection. In the ileum of infected animals of both dietary groups at 6 days postinfection, a severe inflammatory response, decreased villus height, elongated crypts, and depressed stimulation of Na+ absorption by glucose was observed. By 10 days after infection, while recovery was nearly complete in dietary controls, intestinal damage persisted in the undernourished rabbits, as evidenced by absent glucose-stimulated Na+ absorption, continued severe inflammation and microabscess formation. We conclude that intestinal injury is more severe and chronic in the undernourished, compared to dietary control infant rabbits subjected to an acute bacterial enteritis. 4(The combination of malnutrition and diarrheal disease is the leading cause of death in children under the age of 5 yr (I). Most of these children suffer from primary protein-calorie malnutrition which is aggravated by severe diarrhea. Clinical studies have shown that acute enteric infections aggravate and potentiate nutrient deficiencies. In turn, the inability of the nutrient-deprived host to respond appropriately to an infectious insult leads to prolonged diarrheal illness (2). Little is known about the nature of the interactions between enteric infections and the intestinal epithelium in the chronically malnourished host. The aim herein was to examine the recovery of intestinal function after an acute infectious enteritis in an infant animal model of protein-calorie malnutrition. Our results indicate that intestinal damage is more severe and recovery delayed in the malnourished infant than in dietary controls after an experimental inflammatory insult. METHODSDoes and litters of New Zealand White rabbits were quarantined at 4 days after birth and observed over 3 days for signs of infection. Protein-calorie malnutrition was induced in the experimental group by combining two litters at 7 da...

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“…A study evidenced by diminished mucosal wt, protein, and DNA content on adult rats subjected to semistarvation indicates that this in both jejunal and ileal segments. On examination of morphol-adaptation may be due to increased sodium and glucose uptake ogy, villus ht, and/or crypt depth were decreased at most time by the brush border membrane (24). Although mechanisms periods.…”

Section: Clinicalmentioning

confidence: 99%

Impact of Refeeding on Intestinal Development and Function in Infant Rabbits Subjected to Protein-Energy Malnutrition

Butzner

Gall

1990

Pediatr Res

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ABSTRACT. The impact of early postnatal protein-energy malnutrition and of 4, 7, and 14 d of nutritional rehabilitation on small intestinal growth, development, structure and function was examined in 28-, 32-, 35-, and 42-d-old infant rabbits. Malnutrition was induced by litter expansion 7 d postpartum and, in randomly selected malnourished animals, refeeding was begun at weaning, 28 d. Results are compared to ad libitum fed dietary controls. Malnutrition altered the small intestine of the developing rabbit, as evidenced by: 1 ) reduced jejunal and ileal mass as shown by decreased mucosal wt, protein, and DNA content; 2) depressed epithelial proliferation and enterocyte migration along the crypt-villus axis; 3) delayed epithelial maturation as measured by mucosal enzyme activities; and 4) enhanced glucose-stimulated Na+ transport. Refeeding stimulated rapid and complete recovery, as evidenced by: l ) restoration of jejunal and ileal mucosal mass within 4 d; 2) enhancement of epithelial renewal and enterocyte migration by 7 d; and 3) complete return of the normal pattern of mucosal enzymes by 14 d. With 7 d of refeeding, glucose-stimulated Na+ transport was downregulated to the level of dietary controls. We conclude that early postnatal protein-energy malnutrition has a severe impact on small intestinal growth, development, structure, and function. Furthermore, a brief period refeeding induced a rapid and complete recovery of these parameters. In early infancy, the small intestine undergoes a period of rapid growth and development associated with multiple alterations of intestinal structure and function. Also in the immediate postnatal period when nutrient reserves are marginal, the infant is particularly susceptible to intestinal injury. With the refeeding July 17, 1989; accepted October 13, 1989. Correspondence and reprint requests J.

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Effects of semistarvation on transintestinald-glucose transport andd-glucose uptake in brush border and basolateral membranes of rat enterocytes

Cited by 14 publications

References 23 publications

Independent modulation by food supply of two distinct sodium-activated D-glucose transport systems in the guinea pig jejunal brush-border membrane.

Independent modulation by food supply of two distinct sodium-activated D-glucose transport systems in the guinea pig jejunal brush-border membrane.

Effects of Chronic Protein-Calorie Malnutrition on Small Intestinal Repair after an Acute Bacterial Enteritis: A Study in Infant Rabbits

Impact of Refeeding on Intestinal Development and Function in Infant Rabbits Subjected to Protein-Energy Malnutrition

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