Additive effects of prior exercise and insulin on glucose and AIB uptake by rat muscle

Zorzano, A.; Balon, Thomas W.; Goodman, M. N.; Ruderman, Neil B.

doi:10.1152/ajpendo.1986.251.1.e21

Cited by 45 publications

(37 citation statements)

References 24 publications

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“…The cumulative glucose uptake by perfused hindquarter in the non-supplemented experiment was significantly greater than that in the supplemented experiment (p<0.05) ( Table 2). The lactate level of perfusate during the experiment was similar to those found in previous perfusion studies [11][12][13].…”

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confidence: 87%

Ketone Body Utilization and Its Metabolic Effect in Resting Muscles of Normal and Streptozotocin-Diabetic Rats.

et al. 1991

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Abstract. By using an in situ rat hindquarter perfusion, we evaluated ketone body utilization and its metabolic effects in the resting muscle of 24 h fasted normal and streptozotocin (STZ)-diabetic rats . Under the perfusion with ketone body-supplementation(1 mM each of acetoacetic acid (AcAc) and 3-hydroxybutyric acid (3-OHB)), the AcAc and 3-OHB uptake of STZ-diabetic rats was significantly (P<0.05) smaller than that of normal rats. This might be explained by the low enzyme activity of 3-oxoacid CoA transferase demonstrated in the hindlimb muscles of STZ-diabetic rats and this reduced ketone body uptake would be one of the causes of the development of diabetic ketoacidosis . The glucose uptake and the phosphofructokinase (PFK) activity of normal rats were significantly (P<0 .05) higher than those of STZ-diabetic rats. In both normal and STZ-diabetic rats, the glucose utilization and PFK activity of the muscles in the ketone body-supplemented condition were significantly (P<0 .05) lower than those in the non-supplemented condition. This inhibition of glucose utilization by ketone bodies should be due to the mechanism by which the oxidation of ketone bodies inhibits PFK in the muscle .

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confidence: 87%

Ketone Body Utilization and Its Metabolic Effect in Resting Muscles of Normal and Streptozotocin-Diabetic Rats.

et al. 1991

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“…Data shown are the average Ϯ standard deviation of three independent experiments. translocation and glucose uptake (16,17,36,42,49,53). Although the mechanism of exercise-contraction stimulation is not known, this process occurs independently of PI 3-kinase function (30,31,50).…”

Section: Fig 8 Vamp3mentioning

confidence: 99%

VAMP3 Null Mice Display Normal Constitutive, Insulin- and Exercise-Regulated Vesicle Trafficking

Yang¹,

Mora²,

Ryder³

et al. 2001

Molecular and Cellular Biology

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To investigate the physiological function of the VAMP3 vesicle SNARE (v-SNARE) isoform in the regulation of GLUT4 vesicle trafficking, we generated homozygotic VAMP3 null mice by targeted gene disruption. The VAMP3 null mice had typical growth rate and weight gain, with normal maintenance of fasting serum glucose and insulin levels. Analysis of glucose disposal and insulin sensitivity demonstrated normal insulin and glucose tolerance, with no evidence for insulin resistance. Insulin stimulation of glucose uptake in isolated primary adipocytes was essentially the same for the wild-type and VAMP3 null mice. Similarly, insulin-, hypoxia-, and exercise-stimulated glucose uptake in isolated skeletal muscle did not differ significantly. In addition, other general membrane trafficking events including phagocytosis, pinocytosis, and transferrin receptor recycling were also found to be unaffected in the VAMP3 null mice. Taken together, these data demonstrate that VAMP3 function is not necessary for either regulated GLUT4 translocation or general constitutive membrane recycling.Insulin increases glucose uptake in adipose and striated muscle tissues primarily by recruiting the GLUT4 glucose transporter protein to the cell surface (37). In the basal noninsulin-stimulated state, the majority of GLUT4 resides in one or more intracellular compartments (44,45). Upon addition of insulin, the signaling cascade triggered by the insulin receptor leads to rapid translocation of the GLUT4 transporter to the plasma membrane, thereby increasing the number of transporters at the cell surface and the rate of glucose uptake (12,27,38,41).The process of GLUT4 translocation shares important features with the exocytosis of synaptic vesicles during neurotransmitter release. For example, the plasma membrane docking and fusion of GLUT4 vesicles appears to require the t-SNARE protein isoforms syntaxin 4 and SNAP23 (9,37,48). GLUT4 vesicles contain the v-SNARE-interacting partners VAMP2 and VAMP3, both of which translocate to the plasma membrane in parallel with GLUT4 (33,47). Recent studies using various toxins and endosomal ablation techniques have indicated that VAMP2 is the predominant v-SNARE responsible for insulin-stimulated GLUT4 translocation in cultured 3T3-L1 adipocytes and in the L6 muscle cell line (9,32,33,40). In contrast, guanosine-5Ј-O-(3-thiotriphosphate) (GTP␥S)-stimulated GLUT4 translocation was found to be dependent on VAMP3, thereby suggesting the presence of two independently regulated pools of GLUT4 storage compartments (35). In this regard, skeletal muscle has also been shown to contain two pools of GLUT4 vesicles, one that responds to insulin and another that is responsive to exercise and contraction (1,11,39).In addition, the skeletal muscle exercise-contraction subpopulation utilizes a signaling pathway independent of the phosphatidylinositol (PI) 3-kinase (30, 31, 50). Similarly, GTP␥S stimulation in adipocytes is also independent of the PI 3-kinase, suggesting that the GTP␥S and exercise-contraction pathways may util...

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“…In skeletal muscle, system A transport activity is stimulated in response to amino acid starvation by a mechanism that requires protein synthesis and microtabular function [4][5][6]. System A transport activity is rapidly activated in skeletal muscle by insulin [7], acute exercise [8], vanadate and alkalinization of intracellular pH [9]. In skeletal muscle, the effect of insulin on system A transport activity is independent of protein synthesis, adaptive regulation, microtubular function and the sodium electrochemical gradient [6,[10][11][12].…”

Section: Introductionmentioning

confidence: 99%

System A transport activity is stimulated in skeletal muscle in response to diabetes

et al. 1992

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We have studied the activity of system A transport in skeletal muscle during experimental diabetes. Five days after streptozotocin injection, rats showed a marked hyperglycemia and a substantial decrease in the content of GLUT-4 protein in skeletal muscle and adipose tissut¢, Under these conditions, basal uptake of 2-(methyl)aminoisobutyric acid (MeAl B), an index of system A transport activity, was enhanced in cxt~msor digitorum longus (EDL) muscles from diabetic rats compared to controls. Furthermore, insulin-stimulated MeAl13 uptake by the incubated EDL and soleus muscles was markedly greater in diabetic than in control rats. The derepressiv¢ phase of adaptive regulation was partially blocked in the diabetic muscle, and incubation of muscles for 3 h in the absence of amino acids led to a lower stimulation of system A tnmsport activity in muscles from diabetic groups compared to controls, We propose that the activated system A might participate in the enhanced alanine release from muscle cells that occurs in diabetes.

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Additive effects of prior exercise and insulin on glucose and AIB uptake by rat muscle

Cited by 45 publications

References 24 publications

Ketone Body Utilization and Its Metabolic Effect in Resting Muscles of Normal and Streptozotocin-Diabetic Rats.

Ketone Body Utilization and Its Metabolic Effect in Resting Muscles of Normal and Streptozotocin-Diabetic Rats.

VAMP3 Null Mice Display Normal Constitutive, Insulin- and Exercise-Regulated Vesicle Trafficking

System A transport activity is stimulated in skeletal muscle in response to diabetes

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