Insulin downregulates diabetic-enhanced intestinal glucose transport rapidly in ileum and slowly in jejunum

Madsen, Karen L.; Ariano, D.; Fedorak, Richard N.

doi:10.1139/y96-141

Cited by 7 publications

(4 citation statements)

References 45 publications

(74 reference statements)

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“…For example, insulin has been shown to stimulate the function of oligopeptide transporter, Pept-1 (36), to decrease the transepithelial resistance (28), and to abrogate calcium-dependent chloride secretion in T84 intestinal epithelial cells (8). Additionally, previous studies have shown that insulin acutely decreased glucose flux across rat jejunum and ileum (27). Indeed, our data showed that insulin directly downregulated ASBT expression in an in vitro model using intestinal Caco-2 cells.…”

Section: G903 High Bile Acid Absorption In Stz-induced Diabetes Mellitussupporting

confidence: 57%

Ileal apical Na⁺-dependent bile acid transporter ASBT is upregulated in rats with diabetes mellitus induced by low doses of streptozotocin

Annaba

Kumar

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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bile acid transporter ASBT is upregulated in rats with diabetes mellitus induced by low doses of streptozotocin. Am J Physiol Gastrointest Liver Physiol 299: G898 -G906, 2010. First published July 22, 2010; doi:10.1152/ajpgi.00139.2010.-Increased intestinal bile acid absorption and expansion of the bile acid pool has been implicated in the hypercholesterolemia associated with diabetes mellitus. However, the molecular basis of the increase in bile acid absorption in diabetes mellitus is not fully understood. The ileal apical Na ϩ -dependent bile acid transporter (ASBT) is primarily responsible for active reabsorption of the majority of bile acids. Current studies were designed to investigate the modulation of ASBT function and expression in streptozotocin (STZ)-induced diabetes mellitus in rats and to examine the effect of insulin on rat ASBT promoter by insulin. Diabetes mellitus was induced in Sprague-Dawley rats by intraperitoneal injection of low doses of STZ (20 mg/kg body wt) on five consecutive days. Human insulin (10 U/day) was given to a group of diabetic rats for 3 days before euthanasia. RNA and protein were extracted from mucosa isolated from the small intestine and ASBT expression was assessed by real-time quantitative RT-PCR and Western blotting. Our data showed that ASBT mRNA and protein expression were significantly elevated in diabetic rats. Insulin treatment of diabetic rats reversed the increase in ASBT protein expression to control levels. Consistently, ileal Na ϩ -dependent [ 3 H]taurocholic uptake in isolated intestinal epithelial cells was significantly increased in diabetic rats. In vitro studies utilizing intestinal epithelial Caco-2 cells demonstrated that ASBT expression and promoter activity were significantly decreased by insulin. These studies demonstrated that insulin directly influences ASBT expression and promoter activity and that ASBT function and expression are increased in rats with STZinduced diabetes mellitus. The increase in ASBT expression may contribute to disturbances in cholesterol homeostasis associated with diabetes mellitus. hypercholesterolemia; insulinopenia; enterohepatic circulation DIABETES MELLITUS IS A COMPLEX disorder resulting from insulin imbalance and characterized by dyslipidemia and hypercholesterolemia (18,34

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Section: G903 High Bile Acid Absorption In Stz-induced Diabetes Mellitussupporting

confidence: 57%

Ileal apical Na⁺-dependent bile acid transporter ASBT is upregulated in rats with diabetes mellitus induced by low doses of streptozotocin

Annaba

Kumar

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Either in control or test intestinal segments, the transepithelial potential difference, which is expression of the ion transport function of the intestine, was constantly monitored as tissutal viability index by the two calomel electrodes. All through the experiments, the transepithelial voltage showed the constant value of 1.5 ± 0.2 mV, which is typical for this tract of rat intestine 29…”

Section: Methodsmentioning

confidence: 62%

A cellulose‐based hydrogel as a potential bulking agent for hypocaloric diets: An in vitro biocompatibility study on rat intestine

Sannino

Madaghiele

Lionetto

et al. 2006

J of Applied Polymer Sci

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A number of over-the-counter slimming products are currently available on the market. However, there is no scientific consensus over their effectiveness in promoting and sustaining weight loss. The need to develop an alternative dietary supplement for the treatment of obesity and overweight makes attractive a polyelectrolyte cellulose-based hydrogel, crosslinked through a water soluble carbodiimide, as a potential bulking agent or stomach filler for hypocaloric diets. The hydrogel is envisaged to be administered orally to absorb water in the stomach, thus swelling and giving a sense of fullness, and to be finally expelled by fecal way. To this purpose, a preliminary assessment of hydrogel swelling capacity in distilled water has been performed, and the biocompatibility of the material with respect to intestinal tissues has been evaluated in vitro. The direct contact with the intestinal mucosa in vivo has been simulated by contacting the hydrogel with the jejunum tract of rat intestine, and the capacity of the material to maintain the epithelial barrier integrity has been monitored by means of transepithelial electric resistance measurements and lactate dehydrogenase release assay. The reported results evidence that the hydrogel is well tolerated by the intestinal tissue during the expected time of contact in vivo.

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“…A high sugar intake is a physiological regulator of this process, increasing monosaccharide uptake threefold in vivo (6). The recruitment of GLUT2 in BBM was also observed in conditions of increased calorie demand and glucagon-like peptide 2 treatment (7)(8)(9)(10)(11).…”

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confidence: 97%

Insulin Internalizes GLUT2 in the Enterocytes of Healthy but Not Insulin-Resistant Mice

et al. 2008

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OBJECTIVES-A physiological adaptation to a sugar-rich meal is achieved by increased sugar uptake to match dietary load, resulting from a rapid transient translocation of the fructose/ glucose GLUT2 transporter to the brush border membrane (BBM) of enterocytes. The aim of this study was to define the contributors and physiological mechanisms controlling intestinal sugar absorption, focusing on the action of insulin and the contribution of GLUT2-mediated transport. RESEARCH DESIGN AND METHODS-The studies were performed in the human enterocytic colon carcinoma TC7 subclone (Caco-2/TC7) cells and in vivo during hyperinsulinemiceuglycemic clamp experiments in conscious mice. Chronic highfructose or high-fat diets were used to induce glucose intolerance and insulin resistance in mice. RESULTS AND CONCLUSIONS-InCaco-2/TC7 cells, insulin action diminished the transepithelial transfer of sugar and reduced BBM and basolateral membrane (BLM) GLUT2 levels, demonstrating that insulin can target sugar absorption by controlling the membrane localization of GLUT2 in enterocytes. Similarly, in hyperinsulinemic-euglycemic clamp experiments in sensitive mice, insulin abolished GLUT2 (i.e., the cytochalasin B-sensitive component of fructose absorption), decreased BBM GLUT2, and concomitantly increased intracellular GLUT2. Acute insulin treatment before sugar intake prevented the insertion of GLUT2 into the BBM. Insulin resistance in mice provoked a loss of GLUT2 trafficking, and GLUT2 levels remained permanently high in the BBM and low in the BLM. We propose that, in addition to its peripheral effects, insulin inhibits intestinal sugar absorption to prevent excessive blood glucose excursion after a sugar meal. This protective mechanism is lost in the insulin-resistant state induced by high-fat or high-fructose feeding. Diabetes 57: 555-562, 2008 I ntestinal sugar transport constantly adapts to the dietary environment. At low levels, the end products of carbohydrate digestion are absorbed by a twostep membrane-transport process involving the sodium-dependent glucose cotransporter (SGLT1) and the facilitative fructose transporter (GLUT5) in the brush border membrane (BBM) (1) lining the lumen. GLUT2 in the basolateral membrane (BLM) (2) ensures sugar exit into the blood stream (3). The level of sugar absorption is also regulated by a rapid and transient recruitment of GLUT2 into enterocyte BBM (4,5). A high sugar intake is a physiological regulator of this process, increasing monosaccharide uptake threefold in vivo (6). The recruitment of GLUT2 in BBM was also observed in conditions of increased calorie demand and glucagon-like peptide 2 treatment (7-11).The mechanisms by which GLUT2 leaves the BBM in the absence of luminal sugar (interprandial periods) are unknown. Of the possible physiological stimuli occurring during feeding, insulin was thought to be a candidate because it exerts systemic hypoglycemic effects by stimulating the translocation of GLUT4 into the plasma membrane of skeletal muscle and adipose cells (rev. in 12) and d...

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Insulin downregulates diabetic-enhanced intestinal glucose transport rapidly in ileum and slowly in jejunum

Cited by 7 publications

References 45 publications

Ileal apical Na⁺-dependent bile acid transporter ASBT is upregulated in rats with diabetes mellitus induced by low doses of streptozotocin

Ileal apical Na⁺-dependent bile acid transporter ASBT is upregulated in rats with diabetes mellitus induced by low doses of streptozotocin

A cellulose‐based hydrogel as a potential bulking agent for hypocaloric diets: An in vitro biocompatibility study on rat intestine

Insulin Internalizes GLUT2 in the Enterocytes of Healthy but Not Insulin-Resistant Mice

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Insulin downregulates diabetic-enhanced intestinal glucose transport rapidly in ileum and slowly in jejunum

Cited by 7 publications

References 45 publications

Ileal apical Na+-dependent bile acid transporter ASBT is upregulated in rats with diabetes mellitus induced by low doses of streptozotocin

Ileal apical Na+-dependent bile acid transporter ASBT is upregulated in rats with diabetes mellitus induced by low doses of streptozotocin

A cellulose‐based hydrogel as a potential bulking agent for hypocaloric diets: An in vitro biocompatibility study on rat intestine

Insulin Internalizes GLUT2 in the Enterocytes of Healthy but Not Insulin-Resistant Mice

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Ileal apical Na⁺-dependent bile acid transporter ASBT is upregulated in rats with diabetes mellitus induced by low doses of streptozotocin

Ileal apical Na⁺-dependent bile acid transporter ASBT is upregulated in rats with diabetes mellitus induced by low doses of streptozotocin