Avian and Mammalian Facilitative Glucose Transporters

Byers, Mary Shannon; Howard, Christianna; Wang, Xiaofei

doi:10.3390/microarrays6020007

Cited by 33 publications

(37 citation statements)

References 82 publications

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“…While the 537 presence of transcript does not necessarily mean that the final protein form is being fully 538 transcribed (Vogel and Marcotte, 2012), it is clear that hepatic GLUT1 is not translocated to the 539 plasma membrane. Our findings are similar to others that have failed to detect GLUT1 in the 540 avian liver (Byers et al, 2017;Carver et al, 2001), raising the possibility that the role of hepatic 541 GLUT1 protein may be much more reduced among birds than previously appreciated. 542…”

supporting

confidence: 89%

Glucose Transporter Expression and Regulation Following a Fast in the Ruby-throated Hummingbird,Archilochus colubris

Ali

Dick

Muhammad

et al. 2020

Preprint

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statement: Hummingbird ingest nectar rich in glucose and fructose. When fasted, 14 tissue capacity for circulating glucose import declines while remaining elevated for fructose. 15This may underlie maintenance of high blood glucose and rapid depletion of blood fructose. 16Abstract 17 Hummingbirds subsist almost exclusively on nectar sugar and face extreme challenges 18 blood sugar regulation. Transmembrane sugar transport is mediated by facilitative glucose 19 transporters (GLUTs) and the capacity for sugar transport is dependent on both the activity of 20GLUTs and their localisation to the plasma membrane (PM). In this study, we determined the 21 relative protein abundance in whole-tissue (WT) homogenates and PM fractions via immunoblot 22 List of Abbreviations39 AIC Akaike Information Criterion 40 AICc Akaike Information Criterion for small sample sizes 41 ANOVA Analysis of Variance 42 APS Ammonium Persulfate 43 cDNA Complementary Deoxyribonucleic Acid 44 CO 2 Carbon Dioxide 45 DTT Dithiothreitol 46 f exo Proportion of expired CO 2 fuelled by oxidation of exogenous sugar 47 GAPDH Glyceraldehyde-3-Phosphate Dehydrogenase 48 GLUT Glucose Transporter 49 HEK293T Homo sapiens Embryonic Kidney cell line with Mutant SV40 large T antigen 50 HRP Horseradish Peroxidase 51 LC MRM/MS Liquid Chromatography Multiple Reaction Monitoring Mass 52 Spectrometry 53 LMM Linear Mixed-effects Model 54 mM Millimolar 55 mRNA Messenger Ribonucleic Acid 56 MW Molecular Weight 57

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supporting

confidence: 89%

Glucose Transporter Expression and Regulation Following a Fast in the Ruby-throated Hummingbird,Archilochus colubris

Ali

Dick

Muhammad

et al. 2020

Preprint

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“…Studies have reported that during diabetes, the insulin-stimulated glucose uptake by GLUT-4 is largely hampered in muscle and adipose tissue leading to the development of insulin resistance. Studies have also reported that over expression of GLUT-4 in the adipose tissue of GLUT-4 knockout mice ameliorate insulin resistance, diabetes and enhance insulin sensitivity [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Herbal Anti-Hyperglycemic Compound Increases Expression of Glucose Transporter Molecules in Diabetic Rats

Jafri¹,

Sharma²,

Khurana³

et al. 2019

J Diabetes Metab

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Background:In previous studies, Sharma et al. has already isolated an anti-hyperglycemic compound from the fruit pulp of Eugenia jambolana using HPLC and other chromatographic techniques. However, the effect of antihyperglycemic compound (FIIc) on the expression of Glucose transporters and Kv 1.3 potassium channel in Streptozotocin-Nicotinamide induced diabetic rats has not been studied so far. Objective:To study the effect of HPLC purified herbal anti-hyperglycemic compound (FIIc) on the expression of GLUT-4, GLUT-8 and Kv 1.3 potassium channel in Streptozotocin-Nicotinamide induced diabetic rats.Methods: 24 Male Wistar rats were taken and diabetes was induced in group B, C and D rats (n=6 each) by injecting Streptozotocin at a dose of 45 mg/kg of body weight 15 minutes after the administration of Nicotinamide at a dose of 230 mg/kg of body weight, intraperitoneally to overnight fasted rats. Active compound (FIIc) was orally administered to group C and Pioglitazone to group D at a dose of 20 mg/kg of body weight for 6 weeks respectively. Serum was separated for the estimation of Adiponectin and TNF alpha at week 0 and week 6 of the study. Real time mRNA expression of GLUT-4, GLUT-8 and Kv 1.3 potassium channel was measured and compared between healthy and diabetic control rats. Expression of GLUT-4, GLUT-8 and Kv 1.3 potassium channel was also measured at protein level through Immunohistochemistry and compared between healthy and diabetic controls.Results: After treatment with FIIc for 6 weeks there was a 1.28 folds increase in GLUT-4 mRNA expression in skeletal muscles and 2.67 folds increase in GLUT-8 mRNA expression in liver tissues of group C rats as compared to group B rats. However, Kv 1.3 potassium channel mRNA expression was found to be at par among the four study groups. TNF alpha levels were found to be significantly decreased in group C rats as compared to group B. A slight increase in serum Adiponectin level was observed in group C as compared to group B, which was found to be statistically insignificant. Conclusion:FIIc treatment for 6 weeks significantly increases the expression of GLUT-4, GLUT-8 mRNA expression in liver and skeletal muscles leading to increased peripheral insulin sensitivity.

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“…As stated above, glucose and lactose also serve as significant energy source for myocardial cells. Glucose transporters (GLUT) are a family of proteins which mediate entry of glucose into cells [ 27 , 28 ]. Of these, GLUT4 is the most abundant glucose transporter in heart [ 29 ].…”

Section: Resultsmentioning

confidence: 99%

PIMT/NCOA6IP Deletion in the Mouse Heart Causes Delayed Cardiomyopathy Attributable to Perturbation in Energy Metabolism

Jia

Liu

Viswakarma

et al. 2018

IJMS

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PIMT/NCOA6IP, a transcriptional coactivator PRIP/NCOA6 binding protein, enhances nuclear receptor transcriptional activity. Germline disruption of PIMT results in early embryonic lethality due to impairment of development around blastocyst and uterine implantation stages. We now generated mice with Cre-mediated cardiac-specific deletion of PIMT (csPIMT−/−) in adult mice. These mice manifest enlargement of heart, with nearly 100% mortality by 7.5 months of age due to dilated cardiomyopathy. Significant reductions in the expression of genes (i) pertaining to mitochondrial respiratory chain complexes I to IV; (ii) calcium cycling cardiac muscle contraction (Atp2a1, Atp2a2, Ryr2); and (iii) nuclear receptor PPAR- regulated genes involved in glucose and fatty acid energy metabolism were found in csPIMT−/− mouse heart. Elevated levels of Nppa and Nppb mRNAs were noted in csPIMT−/− heart indicative of myocardial damage. These hearts revealed increased reparative fibrosis associated with enhanced expression of Tgfβ2 and Ctgf. Furthermore, cardiac-specific deletion of PIMT in adult mice, using tamoxifen-inducible Cre-approach (TmcsPIMT−/−), results in the development of cardiomyopathy. Thus, cumulative evidence suggests that PIMT functions in cardiac energy metabolism by interacting with nuclear receptor coactivators and this property could be useful in the management of heart failure.

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Avian and Mammalian Facilitative Glucose Transporters

Cited by 33 publications

References 82 publications

Glucose Transporter Expression and Regulation Following a Fast in the Ruby-throated Hummingbird,Archilochus colubris

Glucose Transporter Expression and Regulation Following a Fast in the Ruby-throated Hummingbird,Archilochus colubris

Herbal Anti-Hyperglycemic Compound Increases Expression of Glucose Transporter Molecules in Diabetic Rats

PIMT/NCOA6IP Deletion in the Mouse Heart Causes Delayed Cardiomyopathy Attributable to Perturbation in Energy Metabolism

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