Participation of β-adrenergic activity in modulation of GLUT4 expression during fasting and refeeding in rats

Zanquetta, Melissa Moreira; Nascimento, Monalisa Edi Cabral; Mori, Rosana Cristina Tieko; Schaan, Beatriz D.; Young, Martin E.; Machado, Ubiratan Fabres

doi:10.1016/j.metabol.2006.06.026

Cited by 28 publications

(35 citation statements)

References 41 publications

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“…Downregulation and upregulation of GLUT-4 mRNA have been described in response to fasting and refeeding, respectively (30,37). In the present study, the fasting condition was chosen to guarantee that transcriptional activity would not be at its maximal level, which could mask the enhancer effect of contraction.…”

Section: Discussionmentioning

confidence: 99%

“…Total cellular membrane fraction was obtained (6) and immunoblotting was carried out as previously described (37). Equal amounts of total membrane protein (30 g) were resolved by electrophoresis, electrotransferred to nitrocellulose membrane, incubated with anti-GLUT-4 antiserum (polyclonal rabbit raised anti-GLUT-4; AB1346; Chemicon International, Temecula, CA), and submitted to enhanced chemiluminescent detection (ECL Western blotting detection; RPN2106; Amersham Pharmacia Biotech, Amersham, UK).…”

Section: Animalsmentioning

confidence: 99%

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Contractile activity per se induces transcriptional activation of SLC2A4 gene in soleus muscle: involvement of MEF2D, HIF-1a, and TRα transcriptional factors

Lima¹,

Anhê²,

Giannocco³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Section: Discussionmentioning

confidence: 99%

Section: Animalsmentioning

confidence: 99%

Contractile activity per se induces transcriptional activation of SLC2A4 gene in soleus muscle: involvement of MEF2D, HIF-1a, and TRα transcriptional factors

Lima¹,

Anhê²,

Giannocco³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…Studies including the use of dominant negative SREBP and chromatin immunoprecipitation assay further support the hypothesis that SREBP-1c activates GLUT4 transcription in adipocytes (40,41). It was thus proposed that feeding behavior influences GLUT4 gene expression pattern through changes in sympathetic activity, especially during long-term starvation periods (112).…”

Section: Metabolic States That Modulate Glut4 Gene Expressionmentioning

confidence: 91%

“…Prolonged fasting resembles insulin resistance in that it leads to reduced cellular glucose transport rates (46). Prolonged fasting repressed GLUT4 gene expression and protein function in brown and white adipose tissues and soleus muscle, with no effect on the gastrocnemius muscle, whereas refeeding induced a rapid overexpression of GLUT4 mRNA in the various tissues (112). Refeeding was shown to increase GLUT4 mRNA levels concomitantly with enhanced levels of sterol regulatory element binding protein (SREBP)-1c (40).…”

Section: Metabolic States That Modulate Glut4 Gene Expressionmentioning

confidence: 99%

Transcriptional regulation of the insulin-responsive glucose transporter GLUT4 gene: from physiology to pathology

Karnieli¹,

Armoni²

2008

American Journal of Physiology-Endocrinology and Metabolism

110

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Karnieli E, Armoni M. Transcriptional regulation of the insulinresponsive glucose transporter GLUT4 gene: from physiology to pathology. Am J Physiol Endocrinol Metab 295: E38 -E45, 2008. First published May 20, 2008 doi:10.1152/ajpendo.90306.2008The insulin-responsive glucose transporter 4 (GLUT4) plays a key role in glucose uptake and metabolism in insulin target tissues. Being a rate-limiting step in glucose metabolism, the expression and function of the GLUT4 isoform has been extensively studied and found to be tightly regulated at both mRNA and protein levels. Adaptation to states of enhanced metabolic demand is associated with increased glucose metabolism and GLUT4 gene expression, whereas states of insulin resistance such as type 2 diabetes mellitus (DM2), obesity, and aging are associated with impaired regulation of GLUT4 gene expression and function. The present review focuses on the interplay among hormonal, nutritional, and transcription factors in the regulation of GLUT4 transcription in health and sickness. adipose; diabetes; gene expression; muscle; obesity; peroxisome proliferator-activated receptor-␥; forkhead box O1 GLUCOSE UPTAKE IN EUKARYOTIC CELLS is mediated by a family of highly related facilitative glucose transporters (GLUT), and to date, 13 GLUT isoforms have already been identified and cloned, with their tissue specificity extensively studied (39, 44). The insulin-regulated glucose transporter GLUT4 is mainly expressed in insulin-responsive tissues, i.e., white and brown adipose (41,99,101), and in heart and skeletal muscles (1,95,115), where it mediates glucose uptake in response to acute insulin stimulation. We also have found expression of GLUT4 in bone and cancer tissues, where it is predominantly regulated through the insulin-like growth factor 1 receptor (8,61,87).Because glucose uptake is a rate-limiting step in glucose metabolism, the expression and function of the GLUT4 isoform have been studied extensively and found to be tightly regulated at both mRNA and protein levels (6, 77). Unlike most other GLUT isoforms, in resting muscle and adipose cells, GLUT4 is sequestered in specialized intracellular membrane compartments, in GLUT4-containing vesicles. According to the translocation hypothesis (24, 48), following insulin stimulation, these vesicles translocate to the plasma membrane and fuse with it via a multistep process that involves numerous docking and fusion proteins (see reviews, Refs. 13,39,42,55). Because glucose transport via GLUT4 is a key component in insulin action, the study of the structure, function, and regulation of GLUT4 has been a major focus of research in the field of diabetes and obesity. The present review focuses on the interplay between factors that govern GLUT4 gene expression in health and sickness. This information will hopefully assist in understanding the molecular processes regulating glucose homeostasis and shed light on potential targets for therapy that are associated with the GLUT4 transcriptional machinery, aiming at improving insulin sensitiv...

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“…4 (10 mmol/l Tris-HCl, 1 mmol/l EDTA and 250 mmol/l sucrose) and subjected to differential centrifugations to obtain PM, microsomalenriched (M), and total membrane (TM) fractions of adipose tissue (Machado et al 1994) and skeletal muscle (Mori et al 2008). Protein (40 mg) from each sample was subjected to electrophoresis and immunodetection as described (Zanquetta et al 2006). The blots were quantified by densitometry (ImageQuant TL, Amersham Biosciences UK Limited), and normalized for loading control by densitometry of the lane from the Coomassie stained gel (Ferguson et al 2005).…”

Section: Glut4 Protein Analysis By Western Blottingmentioning

confidence: 99%

Intensive insulin treatment induces insulin resistance in diabetic rats by impairing glucose metabolism-related mechanisms in muscle and liver

Okamoto

Anhê²,

Sabino-Silva³

et al. 2011

Journal of Endocrinology

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Insulin replacement is the only effective therapy to manage hyperglycemia in type 1 diabetes mellitus (T1DM). Nevertheless, intensive insulin therapy has inadvertently led to insulin resistance. This study investigates mechanisms involved in the insulin resistance induced by hyperinsulinization. Wistar rats were rendered diabetic by alloxan injection, and 2 weeks later received saline or different doses of neutral protamine Hagedorn insulin (1 . 5, 3, 6, and 9 U/day) over 7 days.Insulinopenic-untreated rats and 6U-and 9U-treated rats developed insulin resistance, whereas 3U-treated rats revealed the highest grade of insulin sensitivity, but did not achieve good glycemic control as 6U-and 9U-treated rats did. This insulin sensitivity profile was in agreement with glucose transporter 4 expression and translocation in skeletal muscle, and insulin signaling, phosphoenolpyruvate carboxykinase/ glucose-6-phosphatase expression and glycogen storage in the liver. Under the expectation that insulin resistance develops in hyperinsulinized diabetic patients, we believe insulin sensitizer approaches should be considered in treating T1DM.

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Participation of β-adrenergic activity in modulation of GLUT4 expression during fasting and refeeding in rats

Cited by 28 publications

References 41 publications

Contractile activity per se induces transcriptional activation of SLC2A4 gene in soleus muscle: involvement of MEF2D, HIF-1a, and TRα transcriptional factors

Contractile activity per se induces transcriptional activation of SLC2A4 gene in soleus muscle: involvement of MEF2D, HIF-1a, and TRα transcriptional factors

Transcriptional regulation of the insulin-responsive glucose transporter GLUT4 gene: from physiology to pathology

Intensive insulin treatment induces insulin resistance in diabetic rats by impairing glucose metabolism-related mechanisms in muscle and liver

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