Regulation of muscle GLUT-4 transcription by AMP-activated protein kinase

Zheng, Donghai; MacLean, Paul S.; Pohnert, Steven C.; Knight, John; Olson, Ann Louise; Winder, W. W.; Dohm, G. Lynis

doi:10.1152/jappl.2001.91.3.1073

Cited by 261 publications

(208 citation statements)

References 51 publications

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“…Since regulation of glucose uptake is critical for treatment of the metabolic syndrome as well as diabetes, upregulation of GLUT4 at the protein and gene level is an important mechanism in the enhancement of glucose uptake in animal cells. It has been reported that AMPK controlled the capacity of skeletal muscle carbohydrate metabolism by regulating the abundance of GLUT4, which increased the maximal rate of glucose transport into skeletal muscle [36,37]. Eid et al have shown that quercetin and quercetin glycosides stimulated AMPK and enhanced basal glucose uptake in C2C12 cells Fig.…”

Section: Discussionmentioning

confidence: 99%

Pentamethylquercetin generates beneficial effects in monosodium glutamate-induced obese mice and C2C12 myotubes by activating AMP-activated protein kinase

Shen

Han

et al. 2012

Diabetologia

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Aims/hypothesis Pentamethylquercetin (PMQ) has recently been shown to have glucose-lowering properties. Here, we aimed to characterise the effectiveness and underlying mechanisms of PMQ for ameliorating metabolic disorders in vivo and vitro. Methods We generated a mouse model of obesity by neonatal administration of monosodium glutamate (MSG) and used it to assess the properties of PMQ as a treatment for metabolic disorders. We also investigated the possible underlying mechanisms of PMQ in the prevention of metabolic disorders. Results Compared with normal mice, MSG mice had metabolic disorders, including central obesity, hyperinsulinaemia, insulin resistance, hyperglycaemia, hyperlipidaemia, decreased phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC), and downregulated levels of GLUT4 in gastrocnemius muscles. In MSG mice, PMQ treatment (5, 10, 20 mg/kg daily) reduced body weight gain, waist circumference, adipose tissue mass, serum glucose, triacylglycerol and total cholesterol, while improving insulin resistance, activating AMPK and increasing ACC phosphorylation and GLUT4 abundance. In C2C12 myotubes, PMQ (10 μmol/l) increased glucose consumption by ∼65%. PMQ treatment (1-10 μmol/l) also activated AMPK, increased ACC phosphorylation and GLUT4 abundance, and upregulated the expression of some key genes involved in fatty acid oxidation. Conclusions/interpretation These findings suggest that PMQ can ameliorate metabolic disorders at least in part via stimulation of AMPK activity.

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Section: Discussionmentioning

confidence: 99%

Pentamethylquercetin generates beneficial effects in monosodium glutamate-induced obese mice and C2C12 myotubes by activating AMP-activated protein kinase

Shen

Han

et al. 2012

Diabetologia

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“…Several groups have reported that AICAR treatment increased muscle GLUT4 mRNA and protein in a fiber type-specific manner (Buhl et al, 2001;Zheng et al, 2001). First, we confirmed the effect of AICAR on GLUT4 mRNA level as a positive control.…”

Section: Effects Of Aicar Injection On Mct4 Expression In Rat Skeletamentioning

confidence: 99%

“…Several studies have shown that 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR), an AMPK activator, activates glucose transport and increases the expression of glucose transporter 4 (GLUT4) and several metabolic enzymes in skeletal muscle (Buhl et al, 2001;Holmes et al, 1999Holmes et al, , 2005Ojuka et al, 2002;Stoppani et al, 2002;Winder et al, 2000;Zheng et al, 2001). It has been reported that an increase in glucose uptake induced by AICAR results in increased lactic acid production in isolated rat skeletal muscle (Miyamoto et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

AMP-activated protein kinase regulates the expression of monocarboxylate transporter 4 in skeletal muscle

et al. 2011

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AimsThe aim of this study was to determine the effect of 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, on monocarboxylate transporter 4 (MCT4) expression in rat skeletal muscle and a prototypic embryonal rhabdomyosarcoma cell line (RD cells). Main methodsWe examined the alteration in Glucose transporter 4 (GLUT4) and MCT4 mRNA levels by quantitative real-time PCR. Alteration in GLUT4 and MCT4 protein levels were examined by Western blotting. Key findingsIn an in vivo study, AICAR increased MCT4 mRNA and protein levels in a fiber-type specific manner. In an in vitro study, AICAR increased MCT4 mRNA and protein levels. Moreover, AICAR-induced MCT4 expression was blocked by Compound C, an AMPK inhibitor. SignificanceIn this study, we found that AMPK activation induced expression of MCT4 in RD cells and rat skeletal muscle in a fiber-type specific manner. These results indicate the possible involvement of an AMPK-mediated pathway associated with MCT4 expression in skeletal muscle.

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“…Coimmunoprecipitation and transient transfection assays demonstrated that GEF and MEF2A exert synergistic activation of the GLUT4 gene promoter by interacting with each other. Moreover, activation through these two regulatory cis-elements was affected by AMPK (56). Regulation of GEF by AMPK may be stimulated both by upregulation and accompanying phosphorylation.…”

Section: Muscle-specific Glut4 Enhancer Factor (Gef)mentioning

confidence: 99%

Regulation of glucose transporter type 4 isoform gene expression in muscle and adipocytes

Kwon

Kim

et al. 2007

IUBMB Life

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SummaryThe gene expression of glucose transporter type 4 isoform (GLUT4) is known to be controlled by metabolic, nutritional, or hormonal status. Understanding the molecular mechanisms governing GLUT4 gene expression is critical, because glucose disposal in the body depends on the activities of GLUT4 in the muscle and adipocytes. The GLUT4 activities are regulated by a variety of mechanisms. One of them is transcriptional regulation. GLUT4 gene expression is regulated by a variety of transcriptional factors in muscle and adipose tissue. These data are accumulating regarding the transcriptional factors regulating GLUT4 gene expression. These include MyoD, MEF2A, GEF, TNF-a, TR-1a, KLF15, SREBP-1c, C/EBP-a, O/E-1, free fatty acids, PAPRg, LXRa, NF-1, etc. These factors are involved in the positive or negative regulation of GLUT4 gene expression. In addition, there is a complex interplay between these factors in transactivating GLUT4 promoter activity. Understanding the mechanisms controlling GLUT4 gene transcription in these tissues will greatly promote the potential therapeutic drug development for obesity and T2DM.

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Regulation of muscle GLUT-4 transcription by AMP-activated protein kinase

Cited by 261 publications

References 51 publications

Pentamethylquercetin generates beneficial effects in monosodium glutamate-induced obese mice and C2C12 myotubes by activating AMP-activated protein kinase

Pentamethylquercetin generates beneficial effects in monosodium glutamate-induced obese mice and C2C12 myotubes by activating AMP-activated protein kinase

AMP-activated protein kinase regulates the expression of monocarboxylate transporter 4 in skeletal muscle

Regulation of glucose transporter type 4 isoform gene expression in muscle and adipocytes

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