Glucose and thyroid hormone co-regulate the expression of the intestinal fructose transporter GLUT5

Matosin-Matekalo, Miriam; Mesonero, José E.; Laroche, Thibaut J.; Lacasa, Michel; Brot-Laroche, Édith

doi:10.1042/bj3390233

Cited by 44 publications

(15 citation statements)

References 42 publications

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“…In Caco-2 cells transfected with reporter gene constructs containing the human GLUT5, promoter expression was stimulated by adenylate cyclase [255]. Using the same experimental setup, transcriptional regulation by thyroid hormone was observed [260]. It was shown that binding of thyroid hormone receptor/retinoid X receptor heteromers to the promotor was blunted by thyroid hormone.…”

Section: Regulation Of Glut5mentioning

confidence: 95%

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Glucose transporters in the small intestine in health and disease

Koepsell

2020

Pflugers Arch - Eur J Physiol

172

146

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Absorption of monosaccharides is mainly mediated by Na +-D-glucose cotransporter SGLT1 and the facititative transporters GLUT2 and GLUT5. SGLT1 and GLUT2 are relevant for absorption of D-glucose and D-galactose while GLUT5 is relevant for D-fructose absorption. SGLT1 and GLUT5 are constantly localized in the brush border membrane (BBM) of enterocytes, whereas GLUT2 is localized in the basolateral membrane (BLM) or the BBM plus BLM at low and high luminal D-glucose concentrations, respectively. At high luminal D-glucose, the abundance SGLT1 in the BBM is increased. Hence, D-glucose absorption at low luminal glucose is mediated via SGLT1 in the BBM and GLUT2 in the BLM whereas high-capacity D-glucose absorption at high luminal glucose is mediated by SGLT1 plus GLUT2 in the BBM and GLUT2 in the BLM. The review describes functions and regulations of SGLT1, GLUT2, and GLUT5 in the small intestine including diurnal variations and carbohydrate-dependent regulations. Also, the roles of SGLT1 and GLUT2 for secretion of enterohormones are discussed. Furthermore, diseases are described that are caused by malfunctions of small intestinal monosaccharide transporters, such as glucose-galactose malabsorption, Fanconi syndrome, and fructose intolerance. Moreover, it is reported how diabetes, small intestinal inflammation, parental nutrition, bariatric surgery, and metformin treatment affect expression of monosaccharide transporters in the small intestine. Finally, food components that decrease D-glucose absorption and drugs in development that inhibit or downregulate SGLT1 in the small intestine are compiled. Models for regulations and combined functions of glucose transporters, and for interplay between D-fructose transport and metabolism, are discussed.

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Section: Regulation Of Glut5mentioning

confidence: 95%

“…The promoter regions of human, rat, and/or mouse GLUT5/ Glut5 contain response elements for cAMP (CRE), glucocorticoid receptor (GR), liver X receptor (LXR), carbohydrateresponsive element-binding protein (ChREBP), and thyroid hormone receptor/retinoid X receptor heteromer [255,260,283,385,441].…”

Section: Regulation Of Glut5mentioning

confidence: 99%

Glucose transporters in the small intestine in health and disease

Koepsell

2020

Pflugers Arch - Eur J Physiol

172

146

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“…In this review, I exclude most studies on regulation of sugar transport in oocytes and cell cultures, not only because regulation sometimes differs among and within cell lines themselves [17], but also because regulation in cell culture sometimes differs from that observed in i o and in isolated intestinal tissues. For example, in fully differentiated Caco-2\TC7 cells, thyroxine and glucose clearly increase GLUT5 mRNA abundance in a dose-dependent manner [18]. In rat intestine, however, changes in dietary glucose [19,20] and plasma thyroxine [21] concentrations have no effect on either GLUT5 mRNA and protein abundance or fructose transport.…”

Section: Figure 1 Intestinal Absorptive Cells or Enterocytes Are Founmentioning

confidence: 99%

“…Moreover, an intact mucosa is necessary for rapid upregulation of glucose transporters by luminal glucose [22]. Nonetheless, important experiments, such as identification of critical sequences in the promoter region of transporter genes, can only be performed using these cells [18,23,24].…”

Section: Figure 1 Intestinal Absorptive Cells or Enterocytes Are Founmentioning

confidence: 99%

Dietary and developmental regulation of intestinal sugar transport

Ferraris

2001

Biochemical Journal

216

124

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The Na+-dependent glucose transporter SGLT1 and the facilitated fructose transporter GLUT5 absorb sugars from the intestinal lumen across the brush-border membrane into the cells. The activity of these transport systems is known to be regulated primarily by diet and development. The cloning of these transporters has led to a surge of studies on cellular mechanisms regulating intestinal sugar transport. However, the small intestine can be a difficult organ to study, because its cells are continuously differentiating along the villus, and because the function of absorptive cells depends on both their state of maturity and their location along the villus axis. In this review, I describe the typical patterns of regulation of transport activity by dietary carbohydrate, Na+ and fibre, how these patterns are influenced by circadian rhythms, and how they vary in different species and during development. I then describe the molecular mechanisms underlying these regulatory patterns. The expression of these transporters is tightly linked to the villus architecture; hence, I also review the regulatory processes occurring along the crypt-villus axis. Regulation of glucose transport by diet may involve increased transcription of SGLT1 mainly in crypt cells. As cells migrate to the villus, the mRNA is degraded, and transporter proteins are then inserted into the membrane, leading to increases in glucose transport about a day after an increase in carbohydrate levels. In the SGLT1 model, transport activity in villus cells cannot be modulated by diet. In contrast, GLUT5 regulation by the diet seems to involve de novo synthesis of GLUT5 mRNA synthesis and protein in cells lining the villus, leading to increases in fructose transport a few hours after consumption of diets containing fructose. In the GLUT5 model, transport activity can be reprogrammed in mature enterocytes lining the villus column. Innovative experimental approaches are needed to increase our understanding of sugar transport regulation in the small intestine. I close by suggesting specific areas of research that may yield important information about this interesting, but difficult, topic.

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“…The 5 -deletion constructs were generated from the − 2500/+ 41 region of the GLUT5 promoter inserted into the episomal replicative p205-GTI plasmid. Caco-2/TC7 and Caco-2/PD7 cells were stably transfected with these constructs [28]. Studies on the UTRs of the GLUT5 mRNA were performed with the full-length GLUT5 cDNA.…”

Section: Vectorsmentioning

confidence: 99%

Fructose modulates GLUT5 mRNA stability in differentiated Caco-2 cells: role of cAMP-signalling pathway and PABP (polyadenylated-binding protein)-interacting protein (Paip) 2

Gouyon

Onesto

Dalet

et al. 2003

Biochemical Journal

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In intestinal cells, levels of the fructose transporter GLUT5 are increased by glucose and to a greater extent by fructose. We investigated the mechanism by which fructose increases GLUT5 expression. In Caco-2 cells, fructose and glucose increased activity of the -2500/+41 GLUT5 promoter to the same extent. cAMP also activated the GLUT5 promoter. However, if a protein kinase A inhibitor was used to block cAMP signalling, extensive GLUT5 mRNA degradation was observed, with no change in basal transcription levels demonstrating the involvement of cAMP in GLUT5 mRNA stability. Indeed, the half-life of GLUT5 mRNA was correlated ( R2=0.9913) with cellular cAMP levels. Fructose increased cAMP concentration more than glucose, accounting for the stronger effect of fructose when compared with that of glucose on GLUT5 production. We identified several complexes between GLUT5 3'-UTR RNA (where UTR stands for untranslated region) and cytosolic proteins that might participate in mRNA processing. Strong binding of a 140 kDa complex I was observed in sugar-deprived cells, with levels of binding lower in the presence of fructose and glucose by factors of 12 and 6 respectively. This may account for differences in the effects of fructose and glucose. In contrast, the amounts of two complexes of 96 and 48 kDa increased equally after stimulation with either glucose or fructose. Finally, PABP (polyadenylated-binding protein)-interacting protein 2, a destabilizing partner of PABP, was identified as a component of GLUT5 3'-UTR RNA-protein complexes. We conclude that the post-transcriptional regulation of GLUT5 by fructose involves increases in mRNA stability mediated by the cAMP pathway and Paip2 (PABP-interacting protein 2) binding.

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Glucose and thyroid hormone co-regulate the expression of the intestinal fructose transporter GLUT5

Cited by 44 publications

References 42 publications

Glucose transporters in the small intestine in health and disease

Glucose transporters in the small intestine in health and disease

Dietary and developmental regulation of intestinal sugar transport

Fructose modulates GLUT5 mRNA stability in differentiated Caco-2 cells: role of cAMP-signalling pathway and PABP (polyadenylated-binding protein)-interacting protein (Paip) 2

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