Regulation of rat intestinal GLUT2 mRNA abundance by luminal and systemic factors

Cui, Xuelin; Jiang, Lan; Ferraris, Ronaldo P.

doi:10.1016/s0005-2736(03)00129-9

Cited by 46 publications

(34 citation statements)

References 30 publications

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“…The overall mean uptake per milligram was 7.45 Ϯ 0. 44,6.54 Ϯ 0.92, and 7.37 Ϯ 0.81 nmol · mg Ϫ1 · min Ϫ1 at 15, 20, and 26 d of age, respectively. These uptake measurements are similar to those of recent previous experiments in same-age pups, indicating that glucose transporter activity in these intestines was normal (16,29).…”

Section: Corticosterone Studymentioning

confidence: 93%

“…In rat pups, ASBT mRNA, protein, and activity are expressed in fetal tissue, disappear completely in early neonatal life, and reappear abruptly at 17 d of age during early weaning (4). In contrast, the mRNA, protein, and activity of various transporters such as the rat sodium-dependent glucose transporter (SGLT1) and the facilitated glucose transporter GLUT2 are already significantly expressed during early gestation (5,6).…”

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confidence: 99%

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Ontogenetic Development of Rat Intestinal Bile Acid Transport Requires Thyroxine But Not Corticosterone

2004

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Absorption of bile acids by the distal ileum is an essential component of the enterohepatic circulation. In neonatal rats, the appearance of the apical sodium-dependent bile acid transporter (ASBT) at 17 d of age coincides with increases in serum corticosterone and thyroxine. We tested the hypothesis that these hormones modulate ASBT expression during ileal development. Taurocholate uptake into the isolated ileum of normal 20-d-old pups exhibited saturable (K m ϭ 0.52 mM, J max ϭ 0.34 pmol mg/min) and nonsaturable (K diff ϭ 0.015 min Ϫ1 ) components and was two to five times greater than uptake in the proximal intestine. Hypothyroid or euthyroid pups received daily thyroxine injections starting at 6 d of age. At 12 d of age, serum concentrations of thyroxine, ileal abundance of ASBT mRNA, and ileal rates of taurocholate uptake were low in hypothyroid pups that received an injection of vehicle (HTϪ) or thyroxine (HTϩ) and in euthyroid pups that received an injection of vehicle (ETϪ) or thyroxine (ETϩ). At 20 and 26 d, ileal ASBT mRNA abundance and taurocholate uptake rate remained low in HTϪ pups but increased dramatically in ETϪ and ETϩ pups, paralleling the increase in serum thyroxine. Restoration of normal plasma thyroxine in HTϪ pups by thyroxine injections (HTϩ) restored normal ASBT development. Sodium-glucose co-transporter activity and mRNA expression were independent of serum thyroxine levels. Corticosterone levels were significantly lower in pups that were adrenalectomized at 10 d of age. ASBT mRNA abundance and taurocholate uptake rate increased markedly with age but were the same in adrenalectomized, sham-operated, and nonoperated pups. Hence, endogenous thyroxine but not corticosterone regulates the developmentally timed appearance of ASBT. Bile acids expelled from the gallbladder into the intestinal lumen emulsify dietary lipids to aid digestion, then form micelles with the products of lipid digestion to facilitate absorption. Synthesis of bile acids by the liver is insufficient to meet physiologic needs, and bile acids are recycled in a process that involves their absorption from the intestinal lumen back into the circulation and eventual resecretion from the liver. Bile acids are absorbed passively and in modest amounts in the jejunum (1) but are absorbed actively and in greater amounts in the distal ileum by the apical sodium-dependent transporter (ASBT) located at the brush border membrane of the enterocyte (2). It is not clear when active bile acid absorption begins during ontogenetic development of the small intestine. Sodium-dependent uptake of the bile acid taurocholate has been observed in the small intestine of an 8-mo-old child but not in that of a fetus or a neonate (3). Because reabsorption in the distal small intestine of neonates is inefficient or absent,~10 -20% of fat intake in the formula-fed newborn is thought to be malabsorbed, even though the rate of bile acid synthesis in the neonatal liver is markedly higher than that of older age groups. In rat pups, ASBT mRNA, protein, and ac...

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Section: Corticosterone Studymentioning

confidence: 93%

mentioning

confidence: 99%

Ontogenetic Development of Rat Intestinal Bile Acid Transport Requires Thyroxine But Not Corticosterone

2004

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“…After the RNA was UV cross-linked on the membrane and dried for 2 h, cDNA probes of rat GLUT5 and 18S were labeled with [ 32 P]dCTP using a random primer labeling kit (RTS RadPrime DNA labeling system; GIBCO-BRL). Hybridization and quantification followed methods previously described (7,27) The ratio of GLUT5 mRNA to 18S rRNA (loading and transfer control) abundance was calculated to represent relative GLUT5 gene expression in the intestine.…”

Section: Methodsmentioning

confidence: 99%

Fructose-induced increases in neonatal rat intestinal fructose transport involve the PI3-kinase/Akt signaling pathway

Cui¹,

Schlesier²,

Fisher³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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Cui, Xue-Lin, Anna M. Schlesier, Elda L. Fisher, Carla Cerqueira, and Ronaldo P. Ferraris. Fructose-induced increases in neonatal rat intestinal fructose transport involve the PI3-kinase/Akt signaling pathway. Am J Physiol Gastrointest Liver Physiol 288: G1310 -G1320, 2005. First published February 3, 2005 doi:10.1152/ajpgi.00550.2004.-Expression of rat glucose transporter-5 (GLUT5) is tightly regulated during development. Expression and activity are low throughout the suckling and weaning stages, but perfusion of the small intestinal lumen with fructose solutions during weaning precociously enhances GLUT5 activity and expression. Little is known, however, about the signal transduction pathways involved in the substrate-induced precocious GLUT5 development. We found that wortmannin and LY-294002, inhibitors of phosphatidylinositol 3-kinase (PI3-kinase) specifically inhibited the increase in fructose uptake rate and brushborder GLUT5 protein abundance but not GLUT5 mRNA abundance. Perfusion of EGF, an activator of PI3-kinase, also resulted in a marked wortmannin-inhibitable increase in fructose uptake. Perfusion of fructose for 4 h increased cytosolic immunostaining of phosphatidylinositol-3,4,5-triphosphate (PIP 3), the primary product of PI3-kinase, mainly in the mid-to upper-villus regions in which the brush-border membrane also stained strongly with GLUT5. Perfusion of glucose for 4 h had little effect on fructose or glucose uptake and PIP 3 or GLUT5 staining. SH-5, an Akt inhibitor, prevented the increase in fructose uptake and GLUT5 protein induced by fructose solutions, and had no effect on glucose uptake. The PI3-kinase/Akt signaling pathway may be involved in the synthesis and/or recruitment to the brush border of GLUT5 transporters by luminal fructose in the small intestine of weaning rats. Increases in fructose transport during the critical weaning period when rats are shifting to a new diet may be modulated by several signaling pathways whose cross talk during development still needs to be elucidated. development; glucose; intestine; epidermal growth factor; mucosa BECAUSE OF DRAMATIC INCREASES in consumption of soft drinks and fruit juices, per capita consumption of fructose in the United States has increased by 10 times in 30 yr to almost 60 g fructose per day (4, 39). Paralleling this remarkable increase in fructose consumption is an alarming increase in incidence of obesity and in prevalence of type II diabetes (4,14). What makes this correlation disturbing is that per capita fructose consumption in very young children has increased faster than that of the general population and in the 1980s was already ϳ30 -40 g fructose per day representing 10% of their energy intake (39). The top 10th percentile of subjects in all age groups typically consume approximately two times more fructose, exposing this particular age group (1-6 yr of age) to potential metabolic derangements caused by excessive fructose consumption. There are very few studies on physiological adaptations to excessive fructose consumpti...

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“…GLUT2 is a facilitative transporter for the hexose sugars glucose and fructose that also operates with low affinity and high capacity (38). GLUT2 mRNA expression has been shown to be upregulated by both glucose and fructose (13). However, there have been questions raised about the distribution of these GLUT transporters, with GLUT5 found to be localized to the basolateral membrane in human jejunum (5).…”

Section: Transport Of Fructosementioning

confidence: 99%

Intestinal fructose transport and malabsorption in humans

Jones

Butler

Brooks

2011

American Journal of Physiology-Gastrointestinal and Liver Physi

161

120

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Fructose is a hexose sugar that is being increasingly consumed in its monosaccharide form. Patients who exhibit fructose malabsorption can present with gastrointestinal symptoms that include chronic diarrhea and abdominal pain. However, with no clearly established gastrointestinal mechanism for fructose malabsorption, patient analysis by the proxy of a breath hydrogen test (BHT) is controversial. The major transporter for fructose in intestinal epithelial cells is thought to be the facilitative transporter GLUT5. Consistent with a facilitative transport system, we show here by analysis of past studies on healthy adults that there is a significant relationship between fructose malabsorption and fructose dose ( r = 0.86, P < 0.001). Thus there is a dose-dependent and limited absorption capacity even in healthy individuals. Changes in fructose malabsorption with age have been observed in human infants, and this may parallel the developmental regulation of GLUT5 expression. Moreover, a GLUT5 knockout mouse has displayed the hallmarks associated with profound fructose malabsorption. Fructose malabsorption appears to be partially modulated by the amount of glucose ingested. Although solvent drag and passive diffusion have been proposed to explain the effect of glucose on fructose malabsorption, this could possibly be a result of the facilitative transporter GLUT2. GLUT5 and GLUT2 mRNA have been shown to be rapidly upregulated by the presence of fructose and GLUT2 mRNA is also upregulated by glucose, but in humans the distribution and role of GLUT2 in the brush border membrane are yet to be definitively decided. Understanding the relative roles of these transporters in humans will be crucial for establishing a mechanistic basis for fructose malabsorption in gastrointestinal patients.

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Regulation of rat intestinal GLUT2 mRNA abundance by luminal and systemic factors

Cited by 46 publications

References 30 publications

Ontogenetic Development of Rat Intestinal Bile Acid Transport Requires Thyroxine But Not Corticosterone

Ontogenetic Development of Rat Intestinal Bile Acid Transport Requires Thyroxine But Not Corticosterone

Fructose-induced increases in neonatal rat intestinal fructose transport involve the PI3-kinase/Akt signaling pathway

Intestinal fructose transport and malabsorption in humans

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