Glucose transporters (GLUT and SGLT): expanded families of sugar transport proteins

Wood, I. Stuart; Trayhurn, Paul

doi:10.1079/bjn2002763

Cited by 722 publications

(510 citation statements)

References 53 publications

(48 reference statements)

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“…Thus, disruption of GLUT4 function is associated with obesity and diabetes (Thorens and Mueckler, 2009). GLUT4 vesicles are intracellularly translocated to the plasma membrane through an insulin signaling-mediated pathway Dupont et al, 2009;Seki et al, 2003;Wood and Trayhurn, 2003). In short, the binding of insulin to the insulin receptor activates insulin receptor substrate (IRS)-1 and phosphoinositide-3 kinase (PI3K), leading to translocation of GLUT4 Dupont et al, 2009).…”

Section: Mechanisms Of Carrier-mediated Glucose Uptakementioning

confidence: 99%

“…The GLUT proteins mediate transport through facilitated diffusion, while SGLTs rely on sodium gradients (Wood and Trayhurn, 2003). At least 14 GLUT isoforms have been identified in mammals Thorens and Mueckler, 2009;Wood and Trayhurn, 2003).…”

Section: Mechanisms Of Carrier-mediated Glucose Uptakementioning

confidence: 99%

“…GLUT2 is expressed in pancreatic β-cells, intestinal and kidney epithelial cells, and hepatocytes. In β-cells, GLUT2 plays a critical role in glucose sensing, where oxidation of glucose leads to insulin secretion (Thorens and Mueckler, 2009;Wood and Trayhurn, 2003). GLUT4 is predominantly expressed in skeletal muscle and adipose tissue, where it functions as the primary insulin-dependent glucose transporter in mammals (Seki et al, 2003;Thorens and Mueckler, 2009;Wood and Trayhurn, 2003).…”

Section: Mechanisms Of Carrier-mediated Glucose Uptakementioning

confidence: 99%

“…In mammals, GLUT4 functions as the primary insulin-dependent glucose transporter in mammals (Seki et al, 2003;Thorens and Mueckler, 2009;Wood and Trayhurn, 2003), while an avian orthologue for GLUT4 has not been reported. Although several avian GLUTs have been identified, with expression varying among tissues, there appears to be very low expression of all isoforms in skeletal muscle (Kono et al, 2005), raising the question of how chicken skeletal muscle clears glucose from the bloodstream.…”

Section: Introductionmentioning

confidence: 99%

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Chickens from lines artificially selected for juvenile low and high body weight differ in glucose homeostasis and pancreas physiology

Sumners

Zhang

Zhao

et al. 2014

Comparative Biochemistry and Physiology Part A: Molecular &

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Early pancreatectomy experiments performed in ducks and pigeons at the end of the 19 th century revealed that avians, unlike mammals, do not display signs of diabetes. Relative to mammals, birds are considered hyperglycemic, displaying fasting blood glucose concentrations twice that of a normal human. While circulating levels of insulin are similar in avians and mammals, and structure and function of the insulin receptor are also conserved among vertebrate species, birds do not experience deleterious effects of chronic hyperglycemia as observed in mammals. Understanding avian glucose homeostasis, particularly in chickens, has both agricultural and biomedical implications.Improvement of feed efficiency and accelerated growth in poultry may come from a greater understanding of the physiological processes associated with glucose utilization in muscle and fat. The chicken has also recently been recognized as an attractive model for human diabetes, where there is a great need for preventative and therapeutic strategies.The link between type 2 diabetes and obesity, coupled with the inherent hyperglycemic nature of chickens, make chickens artificially selected for juvenile low (LWS) and high (HWS) body weight a favorable model for investigating glucose regulation and pancreas physiology. Oral glucose tolerance and insulin sensitivity tests revealed differences in threshold sensitivity to insulin and glucose clearance rate between the lines. Results from real-time PCR showed greater pancreatic mRNA expression of four glucose regulatory genes (preproinsulin, PPI; preproglucagon, PPG; glucose transporter 2, GLUT2; and iii pancreatic duodenal homeobox 1, Pdx1) in LWS, than HWS chickens. Histological analysis of pancreas revealed that HWS chickens have larger pancreatic islets, less pancreatic islet mass, and more pancreatic inflammation than LWS chickens, all of which presumably contribute to impaired glucose metabolism. In summary, results suggest that at selection age, there are differences in pancreas physiology that may explain the differences in glucose regulation between LWS and HWS. These data pave the way for future studies aimed at understanding the developmental regulation of endocrine pancreas function in chickens, as well as how aging affects homeostatic control of blood glucose in chickens.

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Section: Mechanisms Of Carrier-mediated Glucose Uptakementioning

confidence: 99%

Section: Mechanisms Of Carrier-mediated Glucose Uptakementioning

confidence: 99%

Section: Mechanisms Of Carrier-mediated Glucose Uptakementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Chickens from lines artificially selected for juvenile low and high body weight differ in glucose homeostasis and pancreas physiology

Sumners

Zhang

Zhao

et al. 2014

Comparative Biochemistry and Physiology Part A: Molecular &

View full text Add to dashboard Cite

show abstract

“…L LUNDHOLM, G BRYZGALOVA and others . Improvement of glucose tolerance by PPT Interestingly, these genes are known to affect hepatic glucose production and insulin sensitivity (Wang et al 2000, Croniger et al 2001, Wood & Trayhurn 2003, Gray et al 2007). …”

Section: Decreased By Ppt and Ementioning

confidence: 99%

The estrogen receptor α-selective agonist propyl pyrazole triol improves glucose tolerance in ob/ob mice; potential molecular mechanisms

Lundholm

Bryzgalova

Gao

et al. 2008

Journal of Endocrinology

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The aim of this study was to validate the role of estrogen receptor a (ERa) signaling in the regulation of glucose metabolism, and to compare the molecular events upon treatment with the ERa-selective agonist propyl pyrazole triol (PPT) or 17b-estradiol (E 2 ) in ob/ob mice. Female ob/ob mice were treated with PPT, E 2 or vehicle for 7 or 30 days. Intraperitoneal glucose and insulin tolerance tests were performed, and insulin secretion was determined from isolated islets. Glucose uptake was assayed in isolated skeletal muscle and adipocytes. Gene expression profiling in the liver was performed using Affymetrix microarrays, and the expression of selected genes was studied by real-time PCR analysis. PPTand E 2 treatment improved glucose tolerance and insulin sensitivity. Fasting blood glucose levels decreased after 30 days of PPT and E 2 treatment. However, PPT and E 2 had no effect on insulin secretion from isolated islets. Basal and insulin-stimulated glucose uptake in skeletal muscle and adipose tissue were similar in PPT and vehicle-treated ob/ob mice. Hepatic lipid content was decreased after E 2 treatment. In the liver, treatment with E 2 and PPT increased and decreased the respective expression levels of the transcription factor signal transducer and activator of transcription 3, and of glucose-6-phosphatase. In summary, our data demonstrate that PPTexerts anti-diabetic effects, and these effects are mediated via ERa.

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Tumor Metabolism: Focused on Tumor Glycolysis, Progress, and Prospects in Cancer Therapy

Kumar

Singh

Sharma

et al. 2021

Burger's Medicinal Chemistry and Drug Discovery

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The metabolic reprogramming of cell is a well‐established clinical hallmark of cancer and accordingly has attracted significant attention from researchers in the field of drug discovery. The dependency of cancer cells toward altered “cancer metabolism” (CM) encouraged scientists to work to better understand their metabolic alteration and tumor microenvironment. In fact, the cellular energetics of cancer cells is significantly different from normal cells due to the high demand of energy and metabolites that are required for cancer cell growth and proliferation. A combination of identification of metabolic processes and detailed study of how oncogenic signaling pathways can modulate the metabolic processes might be useful to achieve the selective killing of cancer cells. Recently, several studies have confirmed that cancer metabolism plays a fundamental role in cancer progression and metastasis. Carbohydrate metabolism, particularly glucose metabolism in tumor cells, has received significant attention because rapidly growing cancer cells preferentially rely on the enhanced rate of tumor glycolytic process uncoupled with oxidative phosphorylation. Small molecules targeting tumor glycolysis hold promise for drug discovery and drug development in cancer therapeutics. In addition, it offers the development of new treatment options by synergizing potential glycolytic inhibitors with existing drugs. Therefore, this article includes recent updates on tumor glycolysis and small molecules that counteract tumor glycolysis.

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Glucose transporters (GLUT and SGLT): expanded families of sugar transport proteins

Cited by 722 publications

References 53 publications

Chickens from lines artificially selected for juvenile low and high body weight differ in glucose homeostasis and pancreas physiology

Chickens from lines artificially selected for juvenile low and high body weight differ in glucose homeostasis and pancreas physiology

The estrogen receptor α-selective agonist propyl pyrazole triol improves glucose tolerance in ob/ob mice; potential molecular mechanisms

Tumor Metabolism: Focused on Tumor Glycolysis, Progress, and Prospects in Cancer Therapy

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