Interaction of glucose transporters SGLT1 and GLUT2 with cytoskeleton in enterocytes and Caco2 cells during hexose absorption

Grefner, N. M.; Громова, Л. В.; Груздков, А. А.; Komissarchik, Ya. Yu.

doi:10.1134/s1990519x15010034

Cited by 14 publications

(8 citation statements)

References 25 publications

(36 reference statements)

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“…It is quite possible that the failure to determine the presence of the GLUT2 transporter in the brush border membrane of enterocytes in the case of a high concentration of glucose in the lumen of the small intestine in mice in the above study is associated with the authors’ use of experimental conditions to which the GLUT2 transporter is sensitive [ 54 ]. Immunohistochemical studies confirmed the incorporation of the GLUT2 transporter into the apical membrane of enterocytes during perfusion of an isolated segment of the jejunum of rats in chronic experiments (in the absence of anesthesia) with a high (75 mM) glucose solution [ 38 , 55 ]. In addition, in a mouse study, increased absorption of α-methyl-D-glucoside (AMG) and the content of the SGLT1 and GLUT2 proteins in the vesicles of the brush border of enterocytes were found in the small intestine 30 min after the glucose gavage.…”

Section: Adaptive Reactions Of Transporters Sglt1 and Glut2 In Physiological Conditionsmentioning

confidence: 92%

Mechanisms of Glucose Absorption in the Small Intestine in Health and Metabolic Diseases and Their Role in Appetite Regulation

2021

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The worldwide prevalence of metabolic diseases such as obesity, metabolic syndrome and type 2 diabetes shows an upward trend in recent decades. A characteristic feature of these diseases is hyperglycemia which can be associated with hyperphagia. Absorption of glucose in the small intestine physiologically contributes to the regulation of blood glucose levels, and hence, appears as a putative target for treatment of hyperglycemia. In fact, recent progress in understanding the molecular and cellular mechanisms of glucose absorption in the gut and its reabsorption in the kidney helped to develop a new strategy of diabetes treatment. Changes in blood glucose levels are also involved in regulation of appetite, suggesting that glucose absorption may be relevant to hyperphagia in metabolic diseases. In this review we discuss the mechanisms of glucose absorption in the small intestine in physiological conditions and their alterations in metabolic diseases as well as their relevance to the regulation of appetite. The key role of SGLT1 transporter in intestinal glucose absorption in both physiological conditions and in diabetes was clearly established. We conclude that although inhibition of small intestinal glucose absorption represents a valuable target for the treatment of hyperglycemia, it is not always suitable for the treatment of hyperphagia. In fact, independent regulation of glucose absorption and appetite requires a more complex approach for the treatment of metabolic diseases.

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Section: Adaptive Reactions Of Transporters Sglt1 and Glut2 In Physiological Conditionsmentioning

confidence: 92%

Mechanisms of Glucose Absorption in the Small Intestine in Health and Metabolic Diseases and Their Role in Appetite Regulation

2021

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“…The absorption of glucose may be adjusted by other transporters, such as GLUT2 [ 16 , 17 , 18 ]. Translocation of GLUT2 from cytoplasmic vesicles into the apical membrane markedly increases the capacity of glucose uptake by the enterocyte [ 19 , 20 , 21 ]. Thus, any factor that influences the activities of SGLT1 and GLUT2 will also alter the absorption and metabolism of glucose.…”

Section: Mechanisms Of Glucose Absorption In the Intestinementioning

confidence: 99%

Regulation of Intestinal Glucose Absorption by Ion Channels and Transporters

2016

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The absorption of glucose is electrogenic in the small intestinal epithelium. The major route for the transport of dietary glucose from intestinal lumen into enterocytes is the Na+/glucose cotransporter (SGLT1), although glucose transporter type 2 (GLUT2) may also play a role. The membrane potential of small intestinal epithelial cells (IEC) is important to regulate the activity of SGLT1. The maintenance of membrane potential mainly depends on the activities of cation channels and transporters. While the importance of SGLT1 in glucose absorption has been systemically studied in detail, little is currently known about the regulation of SGLT1 activity by cation channels and transporters. A growing line of evidence suggests that cytosolic calcium ([Ca2+]cyt) can regulate the absorption of glucose by adjusting GLUT2 and SGLT1. Moreover, the absorption of glucose and homeostasis of Ca2+ in IEC are regulated by cation channels and transporters, such as Ca2+ channels, K+ channels, Na+/Ca2+ exchangers, and Na+/H+ exchangers. In this review, we consider the involvement of these cation channels and transporters in the regulation of glucose uptake in the small intestine. Modulation of them may be a potential strategy for the management of obesity and diabetes.

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“…A recent study identified that the cytoskeletal components α-tubulin and actin participate in the redistribution of SGLT1 [26 ▪ ,27]. In addition, when caveolin-1, a plasma membrane protein known to regulate the insertion and retrieval of transport proteins, and SGLT1 are coexpressed in oocytes, SGLT1 protein abundance and glucose transport increase [28].…”

Section: Regulation Of Sodium-glucose Cotransportermentioning

confidence: 99%

Sodium-glucose cotransport

Poulsen

Fenton

Rieg

2015

Current Opinion in Nephrology and Hypertension

129

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Purpose of review Sodium-glucose cotransporters (SGLTs) are important mediators of glucose uptake across apical cell membranes. SGLT1 mediates almost all sodium-dependent glucose uptake in the small intestine, while in the kidney SGLT2, and to a lesser extent SGLT1, account for more than 90% and nearly 3%, respectively, of glucose reabsorption from the glomerular ultrafiltrate. Although the recent availability of SGLT2 inhibitors for the treatment of diabetes mellitus has increased the number of clinical studies, this review has a focus on mechanisms contributing to the cellular regulation of SGLTs. Recent findings Studies have focused on the regulation of SGLT expression under different physiological/pathophysiological conditions, for example diet, age or diabetes mellitus. Several studies provide evidence of SGLT regulation via cyclic adenosine monophosphate/protein kinase A, protein kinase C, glucagon-like peptide 2, insulin, leptin, signal transducer and activator of transcription-3 (STAT3), phosphoinositide-3 kinase (PI3K)/Akt, mitogen-activated protein kinases (MAPKs), nuclear factor-kappaB (NF-kappaB), with-no-K[Lys] kinases/STE20/SPS1-related proline/alanine-rich kinase (Wnk/SPAK) and regulatory solute carrier protein 1 (RS1) pathways. Summary SGLT inhibitors are important drugs for glycemic control in diabetes mellitus. Although the contribution of SGLT1 for absorption of glucose from the intestine as well as SGLT2/SGLT1 for renal glucose reabsorption has been comprehensively defined, this review provides an up-to-date outline for the mechanistic regulation of SGLT1/SGLT2.

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Interaction of glucose transporters SGLT1 and GLUT2 with cytoskeleton in enterocytes and Caco2 cells during hexose absorption

Cited by 14 publications

References 25 publications

Mechanisms of Glucose Absorption in the Small Intestine in Health and Metabolic Diseases and Their Role in Appetite Regulation

Mechanisms of Glucose Absorption in the Small Intestine in Health and Metabolic Diseases and Their Role in Appetite Regulation

Regulation of Intestinal Glucose Absorption by Ion Channels and Transporters

Sodium-glucose cotransport

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