ARAP2 promotes GLUT1-mediated basal glucose uptake through regulation of sphingolipid metabolism

2016 ◽  
Vol 1861 (11) ◽  
pp. 1643-1651 ◽  
Author(s):  
Aditi Chaudhari ◽  
Liliana Håversen ◽  
Reza Mobini ◽  
Linda Andersson ◽  
Marcus Ståhlman ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Sphingolipid Metabolism ◽  
Basal Glucose Uptake

Does impaired mitochondrial function affect insulin signaling and action in cultured human skeletal muscle cells?

2008 ◽  
Vol 294 (1) ◽  
pp. E97-E102 ◽  
Author(s):  
Audrey E. Brown ◽  
Matthias Elstner ◽  
Stephen J. Yeaman ◽  
Douglass M. Turnbull ◽  
Mark Walker
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
Mitochondrial Respiration ◽  
Respiratory Function ◽  
Insulin Action ◽  
Human Skeletal Muscle ◽  
Human Skeletal Muscle Cells ◽  
Basal Glucose Uptake

Insulin-resistant type 2 diabetic patients have been reported to have impaired skeletal muscle mitochondrial respiratory function. A key question is whether decreased mitochondrial respiration contributes directly to the decreased insulin action. To address this, a model of impaired cellular respiratory function was established by incubating human skeletal muscle cell cultures with the mitochondrial inhibitor sodium azide and examining the effects on insulin action. Incubation of human skeletal muscle cells with 50 and 75 μM azide resulted in 48 ± 3% and 56 ± 1% decreases, respectively, in respiration compared with untreated cells mimicking the level of impairment seen in type 2 diabetes. Under conditions of decreased respiratory chain function, insulin-independent (basal) glucose uptake was significantly increased. Basal glucose uptake was 325 ± 39 pmol/min/mg (mean ± SE) in untreated cells. This increased to 669 ± 69 and 823 ± 83 pmol/min/mg in cells treated with 50 and 75 μM azide, respectively (vs. untreated, both P < 0.0001). Azide treatment was also accompanied by an increase in basal glycogen synthesis and phosphorylation of AMP-activated protein kinase. However, there was no decrease in glucose uptake following insulin exposure, and insulin-stimulated phosphorylation of Akt was normal under these conditions. GLUT1 mRNA expression remained unchanged, whereas GLUT4 mRNA expression increased following azide treatment. In conclusion, under conditions of impaired mitochondrial respiration there was no evidence of impaired insulin signaling or glucose uptake following insulin exposure in this model system.

Role of glycogen concentration and epinephrine on glucose uptake in rat epitrochlearis muscle

1997 ◽  
Vol 272 (4) ◽  
pp. E649-E655 ◽  
Author(s):  
J. Jensen ◽  
R. Aslesen ◽  
J. L. Ivy ◽  
O. Brors
Keyword(s):  
Glucose Uptake ◽  
Muscle Glycogen ◽  
Similar Treatment ◽  
Glycogen Concentration ◽  
Spearman's Rho ◽  
Spearman’S Rho ◽  
Tracer Amount ◽  
Muscle Glycogen Concentration ◽  
Basal Glucose Uptake

The effects of diet-manipulated variations in muscle glycogen concentration and epinephrine on glucose uptake were studied in epitrochlearis muscles from Wistar rats. Both basal and insulin-stimulated glucose uptake [measured with a tracer amount of 2-[1,2-3H(N)]deoxy-D-glucose] inversely correlated with initial glycogen concentration (glycogen concentration vs. basal glucose uptake: Spearman's rho = -0.76, n = 84, P < 0.000001; glycogen concentration vs. insulin-stimulated glucose uptake: Spearman's rho = -0.67, n = 44, P < 0.00001). Two fasting-refeeding procedures were used that resulted in differences in muscle glycogen concentrations, although with similar treatment for the last 48 h before the experiment. In the rats with the lower glycogen concentration, basal as well as insulin-stimulated glucose uptake was elevated. The muscle glycogen concentration had no effect on epinephrine-stimulated glycogenolysis. Epinephrine, however, was found to reduce basal glucose uptake in all groups. These results suggest that 1) the glycogen concentration participates in the regulation of both basal and insulin-stimulated glucose uptake in skeletal muscle, 2) the magnitude of epinephrine-stimulated glycogen breakdown is independent of the glycogen concentration, and 3) epinephrine inhibits basal glucose uptake at all glycogen concentrations.

1147-P: Pseudo Insulin Resistance: Palmitate Inactivates Insulin Signaling but Stimulates Basal Glucose Uptake in 3T3-L1 Adipocytes

Diabetes ◽  
2021 ◽  
Vol 70 (Supplement 1) ◽  
pp. 1147-P
Author(s):  
NIKITA PODKUYCHENKO ◽  
SVETLANA MICHURINA ◽  
IURII STAFEEV ◽  
ASKER Y. KHAPCHAEV ◽  
VLADIMIR P. SHIRINSKY ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
Basal Glucose Uptake

Effect of insulin and poisons on glucose uptake of sheep and goat placenta

1961 ◽  
Vol 200 (1) ◽  
pp. 64-66 ◽  
Author(s):  
Frederick C. Battaglia ◽  
Giacomo Meschia ◽  
Jack Blechner ◽  
Donald H. Barron
Keyword(s):  
Glucose Uptake ◽  
Glucose Utilization ◽  
Sheep And Goats ◽  
Uterine Mucosa ◽  
Basal Glucose Uptake

The basal glucose uptake of the cotyledons of sheep and goats was found to be 1.44 ± 0.09 mg/gm/hr.; that of the fetal chorion to be 2.22 ± 0.11; and that of the maternal uterine mucosa to be 2.05 ± 0.16 mg/gm of tissue/hr. The tissue was obtained from pregnant animals between 45 and 55 days gestation. Insulin, at a concentration of 100 mu/ml, has no effect on net glucose utilization of any of these tissues. Nitrogen and cyanide both increased the basal uptake of cotyledons by approximately 70%. Phlorizin was shown to inhibit both the basal uptake of glucose and the cyanide-accelerated uptake of glucose.

Reversal of Insulin Resistance by ATP in Hemorrhagic Shock

1975 ◽  
Vol 53 (5) ◽  
pp. 859-865 ◽  
Author(s):  
Irshad H. Chaudry ◽  
Mohammed M. Sayeed ◽  
Arthur E. Baue
Keyword(s):  
Insulin Resistance ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Glucose Uptake ◽  
Insulin Concentration ◽  
Insulin Effect ◽  
Intracellular Atp ◽  
Basal Glucose Uptake ◽  
Stimulation Of

Hemorrhagic shock was produced by bleeding rats to a mean arterial pressure of 40 mm Hg (1 mm Hg = 133 N/m2), which was maintained for 2 h. Muscles from these animals ('shock' muscles) showed resistance to the stimulation of glucose uptake by insulin. Addition of 1 mM ATP–MgCl2 to the medium had no effect on basal glucose uptake in either group of muscles, but it permitted insulin to exert its stimulatory effect in 'shock' muscles. An optimal insulin effect on glucose uptake in 'shock' muscles incubated without ATP was observed at an insulin concentration of 0.2 Unit/ml. When 1 mM ATP–MgCl2 was added to the medium, optimal insulin effect in 'shock' muscles was observed at an insulin concentration of 0.007 Unit/ml. Increasing the concentration of ATP–MgCl2 to 2.5 mM in the medium resulted in an optimal insulin effect at an insulin concentration of 0.001 Unit/ml in 'shock' muscles. Following 1 h incubation in Krebs–HCO3 medium, intracellular ATP contents of 'shock' muscles were approximately 50% lower than in control muscles. Addition of 1 mM ATP–MgCl2 to the incubation medium had no effect on the intracellular ATP contents of either group of muscles following incubation; however, 2.5 mM ATP–MgCl2 elevated intracellular ATP contents of 'shock' muscles but had no effect in control muscles. Possible mechanisms for this reversal of insulin resistance by ATP-MgCl2 in shock are discussed.

DAG accumulation from saturated fatty acids desensitizes insulin stimulation of glucose uptake in muscle cells

2001 ◽  
Vol 280 (2) ◽  
pp. E229-E237 ◽  
Author(s):  
Eulàlia Montell ◽  
Marco Turini ◽  
Mario Marotta ◽  
Matthew Roberts ◽  
Véronique Noé ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Insulin Response ◽  
Insulin Stimulation ◽  
Kinase C ◽  
Basal Glucose Uptake ◽  
Stimulation Of

The increased availability of saturated lipids has been correlated with development of insulin resistance, although the basis for this impairment is not defined. This work examined the interaction of saturated and unsaturated fatty acids (FA) with insulin stimulation of glucose uptake and its relation to the FA incorporation into different lipid pools in cultured human muscle. It is shown that basal or insulin-stimulated 2-deoxyglucose uptake was unaltered in cells preincubated with oleate, whereas basal glucose uptake was increased and insulin response was impaired in palmitate- and stearate-loaded cells. Analysis of the incorporation of FA into different lipid pools showed that palmitate, stearate, and oleate were similarly incorporated into phospholipids (PL) and did not modify the FA profile. In contrast, differences were observed in the total incorporation of FA into triacylglycerides (TAG): unsaturated FA were readily diverted toward TAG, whereas saturated FA could accumulate as diacylglycerol (DAG). Treatment with palmitate increased the activity of membrane-associated protein kinase C, whereas oleate had no effect. Mixture of palmitate with oleate diverted the saturated FA toward TAG and abolished its effect on glucose uptake. In conclusion, our data indicate that saturated FA-promoted changes in basal glucose uptake and insulin response were not correlated to a modification of the FA profile in PL or TAG accumulation. In contrast, these changes were related to saturated FA being accumulated as DAG and activating protein kinase C. Therefore, our results suggest that accumulation of DAG may be a molecular link between an increased availability of saturated FA and the induction of insulin resistance.

The Effect of Insulin on Glucose Uptake in Soleus Muscle during Hemorrhagic Shock

1975 ◽  
Vol 53 (1) ◽  
pp. 67-73 ◽  
Author(s):  
Irshad H. Chaudry ◽  
Mohammed M. Sayeed ◽  
Arthur E. Baue
Keyword(s):  
Hemorrhagic Shock ◽  
Glucose Uptake ◽  
Soleus Muscle ◽  
Anaerobic Conditions ◽  
Maximal Stimulation ◽  
Carrier Mechanism ◽  
Insulin Responsiveness ◽  
Glucose Carrier ◽  
Basal Glucose Uptake ◽  
Stimulation Of

Hemorrhagic shock was produced by bleeding conscious rats to a mean arterial pressure of 40 mm Hg, which was maintained for 2 h. Basal glucose uptake by isolated soleus muscle from normal rats and rats subjected to hemorrhagic shock ('shock' muscles) increased with the increase in medium glucose concentration. Uptake values were similar in both groups of muscles. This indicates that there were no alterations in the basal glucose carrier mechanism during shock. Whereas insulin (0.1 U/ml) stimulated glucose uptake in control muscles under aerobic as well as under anaerobic conditions, it had no stimulatory effect in 'shock' muscles under either environment. Maximal stimulation of glucose uptake in 'shock' muscles was observed at an insulin concentration of 0.2 U/ml. The ability of muscle to bind insulin was not altered during shock. The present experiments indicate that insulin responsiveness to tissues is altered in shock. This could be due to alterations in the insulin sensitivity of the glucose carrier mechanism during shock.

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