Current understanding of glucose transporter 4 expression and functional mechanisms

Table 5 Recent studies of glucose transporter 4 expression and translocation in the heart

Methods	Materials	Comparisons	Conclusions	Ref.
Western blot.	Cytosol and membrane fractions of left ventricular, heart, and blood from male Sprague-Dawley rats. Anti-GLUT4 from Santa Cruz Biotechnology (1:200).	Groups without or with the indicated treatments. Na+/K+-ATPase and β-actin were loading controls of the membrane and cytosol fractions, respectively. Losartan was used as a positive control.	Ginsenoside Rb1 treatment can increase GLUT4 expression via inhibition of the TGF-β1/Smad and ERK pathways, and activation of the Akt pathway.	[134]
Real-time PCR,Western blot.	Isolated ventricular cells from heart of male adult (aged 6-8 wk) and neonatal (1-3 d old) Wistar rats.Anti GLUT4 from Abcam (unknown dilution).	Groups with or without the ethanol feeding. Gapdh and β-actin were included as loading controls for real-time PCR and Western blot, respectively.	Long-term (22 wk) ethanol consumption increases AMPK and MEF2 expressions, and reduces GLUT4 mRNA and protein expression in rat myocardium	[135]
Western Blot.	Isolated ventricular cells from heart of adult male Wistar rats. Polyclonal rabbit anti-human GLUT4 from AbD Serotec (4670–1704 1:750)	Groups with or without the indicated treatments.	Heart failure and MI reduce glucose uptake and utilization. GGF2 partially rescues GLUT4 translocation during MI.	[136]
Western blot, Immunofluorescence.	Isolated ventricular cells from heart of adult rats. Polyclonal anti-GLUT4 from Thermo Fisher Scientific (1:100).	Treatment groups were compared with that of 100 nM insulin.	Catestatin can induce AKT phosphorylation, stimulate glucose uptake, and increase GLUT4 translocation.	[137]
Western blot, Flow cytometric analysis.	Isolated ventricular cells from heart of adult male Wistar rats. Anti-GLUT4 (H-61) from unknow source (1:1000 for Western) and conjugated to Alexa Fluor 488.	Treatment groups with or without AMPK agonists.	AMPK activation does not affect GLUT4 translocation and glucose uptake in isolated cardiomyocytes.	[138]
Real-time PCRUsing TaqMan® Gene Expression assays.	Blood, heart, frontal cortex cerebellum from male Wistar rats.	Tissues from control and diabetic rats.	Slc2a4’s expression is downregulated in STZ-treated rat’s heart, but unaffected in tissue protected by blood-brain barrier like frontal cortex.	[139]
Western blot, Immunohistochemistry.	Heart from male Sprague-Dawley rats, anti-GLUT4 from Cell Signaling Technology (2213, 1:1000), anti GLUT4 from Abcam (ab654, 1:200 for ICC/IF)	Treatment groups without or with the indicated treatments.	PEDF can increase glucose uptake and GLUT4 translocation in ischemic myocardium.	[140]
Real-time PCR,Western blot.	Heart from male wild type rats and SHRs. Rabbit polyclonal antibody GLUT4 from Millipore	Wild type rats and SHRs without or with the indicated treatments.	Sitagliptin upregulates levels of GLUT4 protein and Slc2a4 mRNA, and its translocation in cardiac muscles of SHRs.	[141]
Real-time PCR,Western blot.	Left ventricles muscle from male Wistar rats. Anti-GLUT4 from Chemicon (1:1000)	Saline as untreated control and reagent treated groups.	Growth hormone stimulates the translocation of GLUT4 to the cell membrane of cardiomyocytes in adult rats.	[142]

GLUT4: Glucose transporter 4; AMPK: Adenosine monophosphate-activated protein kinase; ERK: Extracellular signal-regulated kinase; GGF2: Glial growth factor 2; GAPDH: Glyceraldehyde-3-Phosphate Dehydrogenase; MEF2: Myocyte enhancer factor-2; MI: Myocardial infarction; PEDF: Pigment epithelium-derived factor; SHR: Spontaneously hypertensive rats; STZ: Streptozotocin; TGF: Transforming growth factors.