Overexpression of GLUT5 in Diabetic Muscle Is Reversed by Pioglitazone

Stuart, Charles Alexander; Howell, Mary E. A.; Yin, Deling

doi:10.2337/dc06-1788

Cited by 38 publications

(30 citation statements)

References 34 publications

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“…These differences may arise from species differences or from the different composition of diets consumed by control and diabetic patients in the human study. Interestingly, treating the diabetic rats with troglitazone (another drug enhancing insulin action) specifically downregulates GLUT5 protein levels, consistent with previous observations (143).…”

Section: Pathology and Glut5supporting

confidence: 78%

“…Patients with type 2 diabetes exhibited dramatic increases in GLUT5 mRNA and protein abundance in skeletal muscle (143). These increases were specific, because expression of GLUT1, GLUT3, GLUT4, GLUT8, GLUT11, and GLUT12 did not change with diabetes and could be reversed if diabetic patients were treated for 8 wk with pioglitazone, a drug enhancing insulin action.…”

Section: Pathology and Glut5mentioning

confidence: 91%

“…GLUT5 is expressed in skeletal muscle of human (14,40,41,66,71,81,125,137,143,144), rat (40), and mouse (131). In fact, GLUT5 is, along with GLUT4 and GLUT12, one of the more significantly expressed GLUTs in human skeletal muscle compared with the other members of the GLUT family (144).…”

Section: Physiology and Functionmentioning

confidence: 97%

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Regulation of the fructose transporter GLUT5 in health and disease

Douard¹,

Ferraris²

2008

American Journal of Physiology-Endocrinology and Metabolism

400

366

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Fructose is now such an important component of human diets that increasing attention is being focused on the fructose transporter GLUT5. In this review, we describe the regulation of GLUT5 not only in the intestine and testis, where it was first discovered, but also in the kidney, skeletal muscle, fat tissue, and brain where increasing numbers of cell types have been found to have GLUT5. GLUT5 expression levels and fructose uptake rates are also significantly affected by diabetes, hypertension, obesity, and inflammation and seem to be induced during carcinogenesis, particularly in the mammary glands. We end by highlighting research areas that should yield information needed to better understand the role of GLUT5 during normal development, metabolic disturbances, and cancer.

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Section: Pathology and Glut5supporting

confidence: 78%

Section: Pathology and Glut5mentioning

confidence: 91%

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Regulation of the fructose transporter GLUT5 in health and disease

Douard¹,

Ferraris²

2008

American Journal of Physiology-Endocrinology and Metabolism

400

366

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“…6A). GLUT5 mRNA encodes the 'fructose-specific' glucose transporter, and its expression is elevated in the muscle from diabetic patients (Stuart et al 2007) and normalized after pioglitazone treatment.…”

Section: Stable Ectopic Vp16-rorg Expression Modulates Myogenin Mrna mentioning

confidence: 99%

Retinoid-related orphan receptor regulates several genes that control metabolism in skeletal muscle cells: links to modulation of reactive oxygen species production

Raichur¹,

Lau²,

Staels³

et al. 2007

Journal of Molecular Endocrinology

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Retinoid-related orphan receptor g (RORg) is an orphan nuclear hormone receptor (NR) that is preferentially expressed in skeletal muscle and several other tissues, including pancreas, thymus, prostate, liver and testis. Surprisingly, the specific role of RORg in skeletal muscle, a peripheral tissue, has not been examined. Muscle is one of the most energy demanding tissues which accounts for w40% of the total body mass and energy expenditure, O75% of glucose disposal and relies heavily on b-oxidation of fatty acids. We hypothesize that RORg regulates metabolism in this major mass lean tissue. This hypothesis was examined by gain and loss of function studies in an in vitro mouse skeletal muscle cell culture model. We show that RORg mRNA and protein are dramatically induced during skeletal muscle cell differentiation. We utilize stable ectopic over-expression of VP16-RORg (gain of function), native RORg and RORgDH12 (loss of function) vectors to modulate RORg mRNA expression and function. Ectopic VP16 (herpes simplex virus transcriptional activator)-RORg and native RORg expression increases RORa mRNA expression. Candidate-driven expression profiling of lines that ectopically express the native and variant forms of RORg suggested that this orphan NR has a function in regulating the expression of genes that control lipid homeostasis (fatty acid-binding protein 4, CD36 (fatty acid translocase), lipoprotein lipase and uncoupling protein 3), carbohydrate metabolism (GLUT5 (fructose transporter), adiponectin receptor 2 and interleukin 15 (IL-15)) and muscle mass . Surprisingly, the investigation revealed a function for RORg in the pathway that regulates production of reactive oxygen species.

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“…Key elements of insulin action have been quantified in the muscle of persons with type 2 diabetes. Insulin receptors and the insulin-responsive glucose transporter 4 (GLUT4) have been normal or nearly normal in muscle homogenates (6,7), suggesting that their levels of expression could not explain the severe insulin resistance seen in type 2 diabetes.…”

mentioning

confidence: 99%

Slow-Twitch Fiber Proportion in Skeletal Muscle Correlates With Insulin Responsiveness

Stuart¹,

McCurry²,

Marino³

et al. 2013

The Journal of Clinical Endocrinology &Amp; Metabolism

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186

146

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Context:The metabolic syndrome, characterized by central obesity with dyslipidemia, hypertension, and hyperglycemia, identifies people at high risk for type 2 diabetes.Objective: Our objective was to determine how the insulin resistance of the metabolic syndrome is related to muscle fiber composition.Design: Thirty-nine sedentary men and women (including 22 with the metabolic syndrome) had insulin responsiveness quantified using euglycemic clamps and underwent biopsies of the vastus lateralis muscle. Expression of insulin receptors, insulin receptor substrate-1, glucose transporter 4, and ATP synthase were quantified with immunoblots and immunohistochemistry.Participants and Setting: Participants were nondiabetic, metabolic syndrome volunteers and sedentary control subjects studied at an outpatient clinic. Main Outcome Measures:Insulin responsiveness during an insulin clamp and the fiber composition of a muscle biopsy specimen were evaluated.Results: There were fewer type I fibers and more mixed (type IIa) fibers in metabolic syndrome subjects. Insulin responsiveness and maximal oxygen uptake correlated with the proportion of type I fibers. Insulin receptor, insulin receptor substrate-1, and glucose transporter 4 expression were not different in whole muscle but all were significantly less in the type I fibers of metabolic syndrome subjects when adjusted for fiber proportion and fiber size. Fat oxidation and muscle mitochondrial expression were not different in the metabolic syndrome subjects. Conclusion:Lower proportion of type I fibers in metabolic syndrome muscle correlated with the severity of insulin resistance. Even though whole muscle content was normal, key elements of insulin action were consistently less in type I muscle fibers, suggesting their distribution was important in mediating insulin effects. ) has more than doubled since 1980 (1). Because of obesity-related illness, the average life expectancy in the United States may soon decline for the first time (2). The metabolic syndrome is a precursor to the development of overt diabetes (3). Insulin resistance and hyperinsulinemia are key elements of the metabolic syndrome that is characterized by visceral obesity, hypertension, hyperlipidemia, hyperglycemia, coronary heart disease, and increased mortality (4). The severity of insulin re- Abbreviations: BMI, body mass index; GIR, glucose infusion rate; GLUT4, glucose transporter 4; IRS-1, insulin receptor substrate-1; SSGIR, steady-state glucose infusion rate; VO 2 max, maximal oxygen consumption.

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Overexpression of GLUT5 in Diabetic Muscle Is Reversed by Pioglitazone

Cited by 38 publications

References 34 publications

Regulation of the fructose transporter GLUT5 in health and disease

Regulation of the fructose transporter GLUT5 in health and disease

Retinoid-related orphan receptor regulates several genes that control metabolism in skeletal muscle cells: links to modulation of reactive oxygen species production

Slow-Twitch Fiber Proportion in Skeletal Muscle Correlates With Insulin Responsiveness

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