Dimethyl sulfoxide enhances GLUT4 translocation through a reduction in GLUT4 endocytosis in insulin-stimulated 3T3-L1 adipocytes

Berenguer, Marie; Zhang, Jinzhong; Bruce, M. Christine; Martinez, Laurène; González, Teresa María Perandones; Gurtovenko, Andrey A.; Xu, Tao; Marchand-Brustel, Y. Le; Govers, Roland

doi:10.1016/j.biochi.2010.12.013

Cited by 19 publications

(15 citation statements)

References 59 publications

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“…The gradient is maintained by abundant hexokinase enzymes, which phosphorylate glucose as it enters the cardiomyocytes, leaving the transport into cells as the rate-limiting step [22]. In a study by Berenguer et al [23] on 3T3-L1 adipocytes and L6 myotubes, they found that low concentrations of DMSO were able to induce GLUT1 and GLUT4 recruitment to the cell surface and simultaneously inhibit the activity of the glucose transporters. The half-life for reversing these effects were t 1/21 2 min in 3T3-L1 adipocytes, and could possibly be longer in cardiomyocytes.…”

Section: Resultsmentioning

confidence: 99%

Myocardial Glucose Clearance by Aspalathin Treatment in Young, Mature, and Obese Insulin-Resistant Rats

et al. 2017

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Rooibos, an indigenous South African plant ingested as herbal tea, is well known for its antioxidant effects. This study investigated aspalathin (CHO), a dihydrochalcone unique to rooibos, for hypoglycemic effects in the context of age- and obesity-induced insulin resistance and the mechanisms involved. Male Wistar rats were allocated into three groups: 16 - 30 weeks feeding with either standard rat chow or a high-caloric diet, or 6 - 10 weeks feeding with standard rat chow. Ventricular cardiomyocytes were isolated by collagenase perfusion digestion, and glucose uptake was determined by 2-[H]-deoxyglucose accumulation. Viability was tested by trypan blue exclusion or propidium iodide staining. The high-caloric diet significantly increased body weight gain (508.5 ± 50.0 vs. 417.3 ± 40.0 g), visceral adiposity (42.30 ± 10.1 vs. 21.75 ± 7.0 g), and fasting blood glucose (5.7 ± 0.4 vs. 4.7 ± 0.1 mM). Aspalathin (10 µM for 90 min) induced 2-[H]-deoxyglucose uptake in young cardiomyocytes (37.2 ± 13.9 vs. 25.7 ± 2.5 pmol 2-[H]-deoxyglucose/mg protein) and enhanced insulin-mediated 2-[H]-deoxyglucose uptake in control cells (32.4 ± 6.4 vs. 23.5 ± 10.0 pmol 2-[H]-deoxyglucose/mg protein), but failed to induce 2-[H]-deoxyglucose uptake in high-caloric diet cells. Aspalathin induced glucose uptake in insulin-sensitive cardiomyocytes from young and aged rats, but not in high-caloric diet animals and enhanced the actions of insulin through a PI3K-dependent mechanism, resulting in an additive response.

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Section: Resultsmentioning

confidence: 99%

Myocardial Glucose Clearance by Aspalathin Treatment in Young, Mature, and Obese Insulin-Resistant Rats

et al. 2017

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“…Data on specifi c DMSO interaction with glucose metabolism is scarce, except for a recent study that demonstrates that translocation of glucose transporter 4 (GLUT4) in adipocytes was enhanced by a concentration higher than 7.5 % of DMSO. The process was specifi c to 3T3-L1 adipocytes, reversible and did not improve insulin-resistance [ 41 ] . The antioxidant and antiinfl ammatory properties of DMSO could explain our results, since in PCOS increased levels of C-reactive protein, cytokines and chemokines, white blood cells, oxidative stress and markers of endothelial infl ammation [ 42 ] are encountered.…”

Section: Glycaemiamentioning

confidence: 95%

Spironolactone and Dimethylsulfoxide Effect on Glucose Metabolism and Oxidative Stress Markers in Polycystic Ovarian Syndrome Rat Model

Daneasa

Cucolas

Furcea

et al. 2014

Exp Clin Endocrinol Diabetes

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Because polycystic ovarian syndrome (PCOS) is a risk factor for type 2 diabetes, the affected women can present frequently prediabetic states such as impaired fasting glycaemia and/or impaired glucose tolerance. The purpose of our study is to explore the effect of antiandrogenic spironolactone on glucose metabolism and oxidative stress (OS) parameters in oestradiol valerate (OV) induced PCOS rat model.72 female Wistar rats were distributed either to PCOS group (n=65, OV dissolved in sesame oil, 5 mg/0.4 ml), or to non-PCOS control group (n=7, sesame oil, 0.4 ml). After a month, ultrasound was performed to assess the ovarian morphology, and the results of an initial oral glucose tolerance test (OGTT) were used to identify the animals with altered glucose metabolism (AGM). Glucose transporter 4 (GLUT4) was evaluated from muscle biopsies, OS parameters were assessed from blood and muscle samples, and ovaries of 3 rats were removed for histopathological examination. Afterwards, the AGM group was divided in a treated PCOS group denoted as Sp+D (per os spironolactone dissolved in DMSO, 2 mg/0.2 ml), and a PCOS control treated with DMSO (0.2 ml). After one month of daily treatment, a final OGTT was performed. GLUT4 and OS parameters were again evaluated and ovaries were removed for histopathological examination.As compared to the values prior to the treatment, Sp+D reversed fasting hyperglycaemia (p<0.001), increased GLUT4 immunoreactivity in the perinuclear compartment (p<0.05) and translocation to plasmalemma (p<0.001) and improved superoxide dismutase (0.001

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“…GLUT4 internalization was measured essentially as described by Williams et al [20] and Berenguer et al [27]. HA-GLUT4expressing adipocytes were treated for 30 min with 100 nM insulin, cooled down on ice, washed extensively with PBS and KRM [120 mM NaCl, 6 mM KCl, 1.2 mM MgSO 4 , 20 mM Mes (pH 5.5), 1 mM CaCl 2 and 0.2 % BSA] to remove insulin from its receptor, washed with DMEM containing 20 mM Hepes and 0.2 % BSA (pH 7.4) and incubated on ice for 30 min with an anti-HA antibody in DMEM/Hepes/BSA.…”

Section: Fluorescence-based Techniquesmentioning

confidence: 99%

Deciphering the role of GLUT4 N-glycosylation in adipocyte and muscle cell models

Zaarour

Berenguer

Marchand-Brustel

et al. 2012

Biochemical Journal

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GLUT4 (glucose transporter 4) is responsible for the insulin-induced uptake of glucose by muscle and fat cells. In non-stimulated (basal) cells, GLUT4 is retained intracellularly, whereas insulin stimulation leads to its translocation from storage compartments towards the cell surface. How GLUT4 is retained intracellularly is largely unknown. Previously, aberrant GLUT4 N-glycosylation has been linked to increased basal cell-surface levels, while N-glycosylation-deficient GLUT4 was found to be quickly degraded. As recycling and degradation of GLUT4 are positively correlated, we hypothesized that incorrect N-glycosylation of GLUT4 might reduce its intracellular retention, resulting in an increased cell-surface recycling, in increased basal cell-surface levels, and in enhanced GLUT4 degradation. In the present study, we have investigated N-glycosylation-deficient GLUT4 in detail in 3T3-L1 preadipocytes, 3T3-L1 adipocytes and L6 myoblasts. We have found no alterations in retention, insulin response, internalization or glucose transport activity. Degradation of the mutant molecule was increased, although once present at the cell surface, its degradation was identical with that of wild-type GLUT4. Our findings indicate that N-glycosylation is important for efficient trafficking of GLUT4 to its proper compartments, but once the transporter has arrived there, N-glycosylation plays no further major role in its intracellular trafficking, nor in its functional activity.

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Dimethyl sulfoxide enhances GLUT4 translocation through a reduction in GLUT4 endocytosis in insulin-stimulated 3T3-L1 adipocytes

Cited by 19 publications

References 59 publications

Myocardial Glucose Clearance by Aspalathin Treatment in Young, Mature, and Obese Insulin-Resistant Rats

Myocardial Glucose Clearance by Aspalathin Treatment in Young, Mature, and Obese Insulin-Resistant Rats

Spironolactone and Dimethylsulfoxide Effect on Glucose Metabolism and Oxidative Stress Markers in Polycystic Ovarian Syndrome Rat Model

Deciphering the role of GLUT4 N-glycosylation in adipocyte and muscle cell models

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