Physiological Adaptations in Glucose Utilization of Skeletal Muscle

2002 ◽  
pp. 169-186 ◽  
Author(s):  
Julian Mathoo ◽  
Mladen Vranic
Keyword(s):  
Skeletal Muscle ◽  
Glucose Utilization ◽  
Physiological Adaptations

scholarly journals β-Sitosterol-D-Glucopyranoside Mimics Estrogenic Properties and Stimulates Glucose Utilization in Skeletal Muscle Cells

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3129
Author(s):  
Jyotsana Pandey ◽  
Kapil Dev ◽  
Sourav Chattopadhyay ◽  
Sleman Kadan ◽  
Tanuj Sharma ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Glucose Utilization ◽  
Diabetes Management ◽  
Expression System ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Cell Periphery ◽  
Glut4 Translocation ◽  
In Silico Docking

Estrogenic molecules have been reported to regulate glucose homeostasis and may be beneficial for diabetes management. Here, we investigated the estrogenic effect of β-sitosterol-3-O-D-glucopyranoside (BSD), isolated from the fruits of Cupressus sempervirens and monitored its ability to regulate glucose utilization in skeletal muscle cells. BSD stimulated ERE-mediated luciferase activity in both ERα and ERβ-ERE luc expression system with greater response through ERβ in HEK-293T cells, and induced the expression of estrogen-regulated genes in estrogen responsive MCF-7 cells. In silico docking and molecular interaction studies revealed the affinity and interaction of BSD with ERβ through hydrophobic interaction and hydrogen bond pairing. Furthermore, prolonged exposure of L6-GLUT4myc myotubes to BSD raised the glucose uptake under basal conditions without affecting the insulin-stimulated glucose uptake, the effect associated with enhanced translocation of GLUT4 to the cell periphery. The BSD-mediated biological response to increase GLUT4 translocation was obliterated by PI-3-K inhibitor wortmannin, and BSD significantly increased the phosphorylation of AKT (Ser-473). Moreover, BSD-induced GLUT4 translocation was prevented in the presence of fulvestrant. Our findings reveal the estrogenic activity of BSD to stimulate glucose utilization in skeletal muscle cells via PI-3K/AKT-dependent mechanism.

scholarly journals An investigation of arterial insufficiency in the rat hindlimb Correlation of skeletal muscle bloodflow and glucose utilization in vivo

1986 ◽  
Vol 240 (2) ◽  
pp. 395-401 ◽  
Author(s):  
R A Challiss ◽  
D J Hayes ◽  
G K Radda
Keyword(s):  
Skeletal Muscle ◽  
Sciatic Nerve ◽  
Glucose Uptake ◽  
Nerve Stimulation ◽  
Linear Correlation ◽  
Glucose Utilization ◽  
Fold Increase ◽  
Artery Ligation ◽  
Sciatic Nerve Stimulation

Muscle bloodflow and the rate of glucose uptake and phosphorylation were measured in vivo in rats 7 days after unilateral femoral artery ligation and section. Bloodflow was determined by using radiolabelled microspheres. At rest, bloodflow to the gastrocnemius, plantaris and soleus muscles of the ligated limb was similar to their respective mean contralateral control values; however, bilateral sciatic nerve stimulation at 1 Hz caused a less pronounced hyperaemic response in the muscles of the ligated limb, being 59, 63 and 49% of their mean control values in the gastrocnemius, plantaris and soleus muscles respectively. The rate of glucose utilization was determined by using the 2-deoxy[3H]glucose method [Ferré, Leturque, Burnol, Penicaud & Girard (1985) Biochem. J. 228, 103-110]. At rest, the rate of glucose uptake and phosphorylation was statistically significantly increased in the gastrocnemius and soleus muscles of the ligated limb, being 126 and 140% of the mean control values respectively. Bilateral sciatic nerve stimulation at 1 Hz caused a 3-5-fold increase in the rate of glucose utilization by the ligated and contralateral control limbs; furthermore, the rate of glucose utilization was significantly increased in the muscles of the ligated limb, being 140, 129 and 207% of their mean control values respectively. For the range of bloodflow to normally perfused skeletal muscle at rest or during isometric contraction determined in the present study, a linear correlation between the rate of glucose utilization and bloodflow can be demonstrated. Applying similar methods of regression analysis to glucose utilization and bloodflow to muscles of the ligated limb reveals a similar linear correlation. However, the rate of glucose utilization at a given bloodflow is increased in muscles of the ligated limb, indicating an adaptation of skeletal muscle to hypoperfusion.

scholarly journals AUTORADIOGRAPHIC LOCALIZATION OF NEW RNA SYNTHESIS IN HYPERTROPHYING SKELETAL MUSCLE

1973 ◽  
Vol 57 (3) ◽  
pp. 743-759 ◽  
Author(s):  
Charles K. Jablecki ◽  
John E. Heuser ◽  
Seymour Kaufman
Keyword(s):  
Skeletal Muscle ◽  
Connective Tissue ◽  
Rna Synthesis ◽  
Proliferating Cells ◽  
Quantitative Studies ◽  
Physiological Adaptations ◽  
Rat Soleus Muscle ◽  
Tissue Cells ◽  
A Site ◽  
Silver Grains

Work-induced growth of rat soleus muscle is accompanied by an early increase in new RNA synthesis. To determine the cell type(s) responsible for the increased RNA synthesis, we compared light autoradiographs of control and hypertrophying muscles from rats injected with tritiated uridine 12, 24, and 48 h after inducing hypertrophy. There was an increased number of silver grains over autoradiographs of hypertrophied muscle. This increase occurred over connective tissue cells; there was no increase in the number of silver grains over the muscle fibers. Quantitative studies demonstrated that between 70 and 80% of the radioactivity in the muscle that survived fixation and washing was in RNA. Pretreatment of the animals with actinomycin D reduced in parallel both the radioactivity in RNA and the number of silver grains over autoradiographs. Proliferation of the connective tissue in hypertrophying muscle was evident in light micrographs, and electron micrographs identified the proliferating cells as enlarged fibroblasts and macrophages; the connective tissue cells remained after hypertrophy was completed. Thus, proliferating connective tissue cells are the major site of the increase in new RNA synthesis during acute work-induced growth of skeletal muscle. It is suggested that in the analysis of physiological adaptations of muscle, the connective tissue cells deserve consideration as a site of significant molecular activity.

scholarly journals Hypoglycemic activity of Phaseolus vulgaris (L.) aqueous extract in type 1 diabetic rats

2019 ◽  
Vol 32 (4) ◽  
pp. 210-218
Author(s):  
Tetiana Halenova ◽  
Natalia Raksha ◽  
Olha Kravchenko ◽  
Tetiana Vovk ◽  
Alona Yurchenko ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Phaseolus Vulgaris ◽  
Aqueous Extract ◽  
Glucose Transporter ◽  
Glucose Utilization ◽  
Muscle Cells ◽  
Diabetic Rats ◽  
Hypoglycemic Activity ◽  
Skeletal Muscle Cells ◽  
Glut 4

Abstract The aim of the present study was to evaluate the hypoglycemic activity of the aqueous extract from the fruit walls of Phaseolus vulgaris pods and to examine the potential mechanism underlying the improvement of the glycemic level. In the course of the study, diabetes mellitus was induced in rats with a single intraperitoneal injection of streptozotocin (45 mg·kg−1 b.w.). Diabetic and control rats were then orally administered with a single-dose or repeated-dose (28 day) of P. vulgaris extract (200 mg·kg−1). Results show that the extract was found to possess significant hypoglycemic activity, and the study of glucose utilization by isolated rat hemidiaphragm suggests that the aqueous extract may enhance the peripheral utilization of glucose. The subsequent experiments have revealed that the P. vulgaris extract could increase glucose transporter 4 (GLUT-4) content in skeletal muscle cells of control and diabetic rats. Our data also indicate that the P. vulgaris extract did not affect the content of the insulin receptor, but significantly reduced the total tyrosine kinase activity in skeletal muscle cells of both experimental groups of rats. The present results clearly indicated that P. vulgaris extract may be beneficial for reducing hyperglycemia through its potency in regulation of glucose utilization via GLUT-4, but the current mechanism remains to be unidentified.

scholarly journals Glucose utilization and disposal in cardiothoracic and skeletal muscles during the starved-to-fed transition in the rat

1990 ◽  
Vol 272 (1) ◽  
pp. 133-137 ◽  
Author(s):  
M C Sugden ◽  
Y L Liu ◽  
M J Holness
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Glucose Utilization ◽  
Glycogen Deposition ◽  
Total Glucose

Glucose utilization indices (GUI) increased to fed values in diaphragm and oxidative skeletal muscles and exceeded fed values in non-oxidative muscles within 2 h of re-feeding chow to 48 h-starved rats. Cardiac GUI reached fed values only after 7 h. Glycogen deposition accounted for most of the glucose phosphorylated in skeletal muscle over the first 2 h in oxidative muscles and over the first 4 h in non-oxidative muscles. In oxidative muscles, the contribution of glycogen deposition to total glucose 6-phosphate disposal diminished as re-feeding was extended from 2 to 6 h.

Effects of blockade of fatty acid oxidation on whole body and tissue-specific glucose metabolism in rats

1993 ◽  
Vol 265 (4) ◽  
pp. E592-E600 ◽  
Author(s):  
A. B. Jenkins ◽  
L. H. Storlien ◽  
G. J. Cooney ◽  
G. S. Denyer ◽  
I. D. Caterson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Glucose Metabolism ◽  
Fatty Acid Oxidation ◽  
Pyruvate Dehydrogenase ◽  
Glucose Utilization ◽  
Whole Body ◽  
Acid Oxidation ◽  
Tissue Specific ◽  
Glucose Output

We examined the effect of the long-chain fatty acid oxidation blocker methyl palmoxirate (methyl 2-tetradecyloxiranecarboxylate, McN-3716) on glucose metabolism in conscious rats. Fasted animals [5 h with or without hyperinsulinemia (100 mU/l) and 24 h] received methyl palmoxirate (30 or 100 mg/kg body wt po) or vehicle 30 min before a euglycemic glucose clamp. Whole body and tissue-specific glucose metabolism were calculated from 2-deoxy-[3H]-glucose kinetics and accumulation. Oxidative metabolism was assessed by respiratory gas exchange in 24-h fasted animals. Pyruvate dehydrogenase complex activation was determined in selected tissues. Methyl palmoxirate suppressed whole body lipid oxidation by 40-50% in 24-h fasted animals, whereas carbohydrate oxidation was stimulated 8- to 10-fold. Whole body glucose utilization was not significantly affected by methyl palmoxirate under any conditions; hepatic glucose output was suppressed only in the predominantly gluconeogenic 24-h fasted animals. Methyl palmoxirate stimulated glucose uptake in heart in 24-h fasted animals [15 +/- 5 vs. 220 +/- 28 (SE) mumol x 100 g-1 x min-1], with smaller effects in 5-h fasted animals with or without hyperinsulinemia. Methyl palmoxirate induced significant activation of pyruvate dehydrogenase in heart in the basal state, but not during hyperinsulinemia. In skeletal muscles, methyl palmoxirate suppressed glucose utilization in the basal state but had no effect during hyperinsulinemia; pyruvate dehydrogenase activation in skeletal muscle was not affected by methyl palmoxirate under any conditions. The responses in skeletal muscle are consistent with the operation of a mechanism similar to the Pasteur effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhancement of maximal thermogenesis by reducing endogenous adenosine activity in the rat

1990 ◽  
Vol 68 (2) ◽  
pp. 580-585 ◽  
Author(s):  
L. C. Wang ◽  
T. F. Lee
Keyword(s):  
Skeletal Muscle ◽  
Cold Exposure ◽  
Adenosine Receptor ◽  
Glucose Utilization ◽  
Cold Resistance ◽  
Atp Hydrolysis ◽  
A1 Receptor ◽  
Thermogenic Capacity

Adenosine has been shown in vitro to be a potent antilipolytic agent and an inhibitor of insulin-stimulated glucose utilization in skeletal muscle. To test whether endogenously produced adenosine (e.g., from ATP hydrolysis) shares these deleterious effects on substrate mobilization and utilization and thus limits maximum thermogenesis in vivo, adenosine deaminase (converts adenosine to inosine) was given to rats 15 min before cold exposure. Significant (P less than 0.05) increases in thermogenesis were observed under both well-fed (100 units/kg ip) and food-rationed (200 units/kg ip) states. Significant (P less than 0.05) increases in thermogenesis and cold resistance were also observed after pretreatment with selective adenosine receptor antagonists [8-cyclopentyltheophylline (1 microgram/kg ip) greater than 1,3-dipropyl-8-p-sulfophenylxanthine (1.25 mg/kg ip) greater than aminophylline (18.7 mg/kg ip)], indicating an A1-receptor-mediated effect. These results indicate that endogenously released adenosine can indeed attenuate the thermogenic capacity in severe cold and that adenosine antagonists, especially those selective for A1-receptor, are useful in improving cold resistance under varying nutritional states.

Increased uptake and phosphorylation of 2-deoxyglucose by skeletal muscles in endotoxin-treated rats

1987 ◽  
Vol 253 (1) ◽  
pp. E33-E39 ◽  
Author(s):  
K. Meszaros ◽  
G. J. Bagby ◽  
C. H. Lang ◽  
J. J. Spitzer
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Skeletal Muscle Mass ◽  
Glucose Utilization ◽  
Abdominal Muscle ◽  
Whole Body ◽  
Fiber Types ◽  
Double Labeling ◽  
Lumped Constant ◽  
And Control

Glucose metabolism of respiratory and nonrespiratory muscles of different fiber composition was investigated in conscious rats. The accumulation of phosphorylated 2-deoxyglucose (2DGP) was increased in skeletal muscles by 56-102% and in diaphragm by 236% at 3 h after treatment with 100 micrograms/100 g endotoxin. The increase was still marked at 24 h, whereas it diminished at 48 h in the diaphragm, abdominal muscle, and white portion of the quadriceps. In the red portion of this muscle 2DGP accumulation was less than that in time-matched controls at 24 and 48 h. Whole gastrocnemius (mixed-fiber types) showed no changes after 24 h. The high 2DGP accumulation in brain remained stable. The retention of 2DGP in tissues, studied by sequential double labeling, did not change 3 h after endotoxin. The lumped constant was similar in the isolated epitrochlear muscles of endotoxemic and control rats. Whole-body glucose utilization (Rd) was increased by 68% 3 h after endotoxin, but it was normal at 24 and 48 h. The increase of glucose utilization by the entire skeletal muscle mass was responsible for approximately 25% of the increase in Rd; therefore it appears that other tissues also contributed significantly to the endotoxin-induced alterations in carbohydrate metabolism.

Reversion of insulin resistance in the rat during late pregnancy by 72-h glucose infusion

1995 ◽  
Vol 269 (5) ◽  
pp. E858-E863 ◽  
Author(s):  
P. Ramos ◽  
E. Herrera
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Glucose Utilization ◽  
Late Pregnancy ◽  
Glucose Infusion ◽  
Continuous Intravenous Infusion ◽  
Pregnant Rats ◽  
Bidistilled Water ◽  
Insulin Responsiveness

To determine whether sustained exaggerated hyperinsulinemia in normoglycemic rats modifies insulin responsiveness during pregnancy, 17-day-pregnant and virgin rats were studied after receiving a continuous intravenous infusion (35 ml/day) of either 50% glucose or bidistilled water (controls) for 72 h. Plasma glucose was unchanged, whereas insulin was highly increased, and the effect was more marked in pregnant than in virgin rats. Insulin responsiveness, estimated under the hyperinsulinemic euglycemic clamp with 0.8 IU insulin.h-1.kg-1, was lower in control pregnant than in virgin rats but higher in pregnant than in virgin rats in those that had received the glucose infusion. The tissue glucose utilization metabolic index (GUI) was estimated with 2-deoxy-D-[1-3H]glucose in the clamped rats. The GUI was lower in heart, white- and red-fiber skeletal muscle, and adipose tissue in control pregnant rats than in control virgin rats, and, although the glucose infusion decreased that index in both red-fiber muscle and adipose tissue in virgin rats, glucose increased the index in red-fiber muscle in pregnant rats to the level found in virgin controls. Results therefore show that, when unaccompanied by hypoglycemia, sustained exaggerated hyperinsulinemia decreases insulin responsiveness in virgin rats but reverts insulin resistance in late-pregnant rats.

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