Glucose transport by rat small intestine after extensive small-bowel resection

Urban, Ernest; Haley, Diane P.

doi:10.1007/bf01072697

Cited by 13 publications

(8 citation statements)

References 28 publications

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“…A chow diet fails to stimulate ileal transport because most glucose has already been absorbed before the ileum. Yet the ileum is perfectly capable of responding to glucose loads with induced glucose transport: for instance, if ileal tissue experiences a glucose load because it is transplanted to the duodenum (Dowling, 1973), or because the jejunum is excised (Dowling & Booth, 1967;Urban & Haley, 1978), or because a high-glucose diet sufficient to saturate the transport capacity of duodenum and jejunum is presented (Nunn & Ellert, 1967;Bode et al 1981). …”

Section: Dietary Control Of Intestinal Sugar Transportmentioning

confidence: 99%

Effect of dietary carbohydrate on monosaccharide uptake by mouse small intestine in vitro.

Diamond¹,

Karasov²,

Cary³

et al. 1984

The Journal of Physiology

156

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SUMMARY1. Using intestinal sleeves in vitro, we studied the effect of dietary carbohydrate on active monosaccharide uptake in mice.2. Dietary carbohydrate did not affect numerous parameters ofintestinal structure, such as length, circumference, weight, protein content, villus dimensions and density, and area at the villus level.3. Mice on a carbohydrate-free diet had active D-glucose uptake relatively independent of position along the small intestine. A carbohydrate-containing diet reversibly and within 1 day stimulated uptake except in the ileum, restoring the proximal-to-distal gradient in glucose uptake normally observed.4. This stimulation involved a 81-116 % increase in the Michaelis-Menton constant Vmax, and also an apparent increase in the Michaelis-Menton constant Km, that may however be an artifact arising from unstirred-layer effects.5. Active uptake of 3-0-methyl-D-glucose also increased, permeability to glucose remained unchanged, and proline uptake reversibly decreased (probably due to the lower protein content of the carbohydrate-containing diets).6. The effect of fasting on active monosaccharide uptake seemed largely due to withdrawal of dietary carbohydrate, rather than of calories per se.7. It is concluded that dietary carbohydrate causes induction of monosaccharide carriers in the intestine, along with its more familiar induction of pancreatic amylase and intestinal disaccharidases. Substrate-dependent carrier induction may be physiologically significant in maintaining the proximal-to-distal gradient of glucose transport.8. An appendix presents measurements of villus area as a function ofposition along the intestine.

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Section: Dietary Control Of Intestinal Sugar Transportmentioning

confidence: 99%

Effect of dietary carbohydrate on monosaccharide uptake by mouse small intestine in vitro.

Diamond¹,

Karasov²,

Cary³

et al. 1984

The Journal of Physiology

156

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show abstract

“…1). By a kinetic analysis, we have shown elsewhere (9) (16), because the jejunum is excised (17,18), or because a high-glucose diet sufficient to saturate the transport capacity of the duodenum and jejunum is presented (8,19 …”

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confidence: 99%

Regulation of proline and glucose transport in mouse intestine by dietary substrate levels.

Karasov¹,

Pond²,

Solberg³

et al. 1983

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

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Active uptake of D-glucose and L-proline at 50 mM was measured in everted intestinal sleeves of mice whose dietary carbohydrate and protein levels were being varied experimentally. Compared to a nearly carbohydrate-free meat diet, a 50% carbohydrate laboratory chow diet stimulated active glucose uptake in the proximal intestine without affecting proline uptake, passive glucose permeability, or several measures of mucosal mass. Switching from a low-protein high-carbohydrate to a high-protein no-carbohydrate diet reversibly stimulated proline uptake while inhibiting glucose uptake. For each solute and diet switch, the stimulation of transport was complete within 1 day, while the inhibition required several days. The results imply induction and repression of intestinal glucose and proline transport by dietary substrate levels. This mechanism, in conjunction with the normal gradient of nutrient concentrations along the intestine, is probably largely responsible for the gradient in nutrient transport along the intestine.The mechanisms by which mammalian small intestine absorbs amino acids and sugars have been studied extensively in recent decades. Both of these classes of solutes are taken up against a concentration gradient at the lumen-facing (brush-border) membrane of the intestinal cell, with the energy for uptake coming mainly or exclusively from the Na' gradient (1, 2). Our detailed knowledge of the mechanisms themselves contrasts with our limited understanding of their regulation. While uptake of sugars and of at least some amino acids is stimulated by dietary carbohydrate and protein levels, respectively, the molecular mechanisms and signals involved in this regulation remain unknown (refs. 3-9; see ref. 10 for review).One complicating factor in understanding the regulation of intestinal nutrient transport is that both solute-specific and solute-nonspecific regulatory processes exist (10). On the one hand, pregnancy, lactation, diabetes, and intestinal resection are accompanied by parallel nonspecific increases in both sugar and amino acid uptake. These increases are mediated at least in part by growth of the intestinal mucosa, which tends to yield increased uptake of any solute. A steeper Na' gradient would similarly tend to stimulate the uptake of any solute cotransported with Na'. On the other hand, a nutrient transport mechanism may also be regulated specifically by dietary levels or body stores of its substrate as is well established for intestinal uptake of the minerals calcium and iron.In the present investigation, we tested for the existence of specific regulatory processes by measuring glucose and proline uptake simultaneously as a function of time while varying dietary carbohydrate and protein levels oppositely. We found that glucose uptake and proline uptake responded in opposite directions and with different time courses, thereby proving that under these conditions they are not coregulated.MATERIALS AND METHODS Animals. We used adult male white Swiss Webster mice (body weight, 30-40 g) w...

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“…Malnutri tion itself might affect the absorption of amino acids, sugars and macromolecules. However, increased absorptive capacity of the small intestine was found in semi-starved animals [10] including the enhanced trans port of macromolecules [20], However, a combined effect of malnutrition and Giardia infection on transport of amino acids and glucose has not been reported.…”

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confidence: 99%

Intestinal Uptake of Nutrients in Normal and Malnourished Animals Infected with <i>Giardia lambli</i><i>a</i>

Upadhyay¹,

Ganguly²,

Mahajan³

et al. 1985

Digestion

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The effect of malnutrition on the uptake of nutrients was studied in Swiss albino mice infected with Giardia lamblia. The moderate deficiency (8 % protein-deficient diet) was observed to enhance the uptake of nutrients like glucose and alanine, whereas in severely malnourished (3% protein-deficient diet) animals the uptake was significantly decreased (p < 0.001). G. lamblia infection in mice decreased the uptake of nutrients and this recovered slightly with the recovery of infection. The combined effect of moderate protein deficiency and infection lowered the enhanced uptake observed in moderately malnourished animals to a significant level (p < 0.001). In severely malnourished animals, infection with G. lamblia showed further deleterious effects on the uptake of nutrients.

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Glucose transport by rat small intestine after extensive small-bowel resection

Cited by 13 publications

References 28 publications

Effect of dietary carbohydrate on monosaccharide uptake by mouse small intestine in vitro.

Effect of dietary carbohydrate on monosaccharide uptake by mouse small intestine in vitro.

Regulation of proline and glucose transport in mouse intestine by dietary substrate levels.

Intestinal Uptake of Nutrients in Normal and Malnourished Animals Infected with <i>Giardia lambli</i><i>a</i>

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