scholarly journals The Exercise-induced Improvement in Insulin-stimulated Glucose Uptake by Rat Skeletal Muscle Is Absent in Male AS160-Knockout Rats, Partially Restored by Muscle Expression of Phosphomutated AS160, and Fully Restored by Muscle Expression of Wildtype AS160

Diabetes ◽  
2021 ◽  
pp. db210601
Author(s):  
Amy Zheng ◽  
Edward B. Arias ◽  
Haiyan Wang ◽  
Seong Eun Kwak ◽  
Xiufang Pan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Rat Skeletal Muscle ◽  
Exercise Induced

scholarly journals Postexercise improvement in glucose uptake occurs concomitant with greater γ3-AMPK activation and AS160 phosphorylation in rat skeletal muscle

2018 ◽  
Vol 315 (5) ◽  
pp. E859-E871 ◽  
Author(s):  
Haiyan Wang ◽  
Edward B. Arias ◽  
Mark W. Pataky ◽  
Laurie J. Goodyear ◽  
Gregory D. Cartee
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Ex Vivo ◽  
Contractile Activity ◽  
Exercise Session ◽  
Ampk Activation ◽  
Rat Skeletal Muscle ◽  
Ampk Activity ◽  
Exercise Induced

A single exercise session can increase insulin-stimulated glucose uptake (GU) by skeletal muscle, concomitant with greater Akt substrate of 160 kDa (AS160) phosphorylation on Akt-phosphosites (Thr642 and Ser588) that regulate insulin-stimulated GU. Recent research using mouse skeletal muscle suggested that ex vivo 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or electrically stimulated contractile activity-inducing increased γ3-AMPK activity and AS160 phosphorylation on a consensus AMPK-motif (Ser704) resulted in greater AS160 Thr642 phosphorylation and GU by insulin-stimulated muscle. Our primary goal was to determine whether in vivo exercise that increases insulin-stimulated GU in rat skeletal muscle would also increase γ3-AMPK activity and AS160 site-selective phosphorylation (Ser588, Thr642, and Ser704) immediately postexercise (IPEX) and/or 3 h postexercise (3hPEX). Epitrochlearis muscles isolated from sedentary and exercised (2-h swim exercise; studied IPEX and 3hPEX) rats were incubated with 2-deoxyglucose to determine GU (without insulin at IPEX; without or with insulin at 3hPEX). Muscles were also assessed for γ1-AMPK activity, γ3-AMPK activity, phosphorylated AMPK (pAMPK), and phosphorylated AS160 (pAS160). IPEX versus sedentary had greater γ3-AMPK activity, pAS160 (Ser588, Thr642, Ser704), and GU with unaltered γ1-AMPK activity. 3hPEX versus sedentary had greater γ3-AMPK activity, pAS160 Ser704, and GU with or without insulin; greater pAS160 Thr642 only with insulin; and unaltered γ1-AMPK activity. These results using an in vivo exercise protocol that increased insulin-stimulated GU in rat skeletal muscle are consistent with the hypothesis that in vivo exercise-induced enhancement of γ3-AMPK activation and AS160 Ser704 IPEX and 3hPEX are important for greater pAS160 Thr642 and enhanced insulin-stimulated GU by skeletal muscle.

scholarly journals The Exercise-induced Improvement in Insulin-stimulated Glucose Uptake by Rat Skeletal Muscle Is Absent in Male AS160-Knockout Rats, Partially Restored by Muscle Expression of Phosphomutated AS160, and Fully Restored by Muscle Expression of Wildtype AS160

2021 ◽  
Author(s):  
Amy Zheng ◽  
Edward B. Arias ◽  
Haiyan Wang ◽  
Seong Eun Kwak ◽  
Xiufang Pan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Exercise Session ◽  
Rat Skeletal Muscle ◽  
Initial Experiment ◽  
Adeno Associated Virus ◽  
Glut4 Expression ◽  
Exercise Effect ◽  
Key Sites ◽  
Exercise Induced

One exercise session can elevate insulin-stimulated glucose uptake (ISGU) in skeletal muscle, but the mechanisms remain elusive. Circumstantial evidence suggests a role for Akt substrate of 160 kDa (AS160 or TBC1D4). We used genetic approaches to rigorously test this idea. The initial experiment evaluated AS160’s role for the postexercise increase in ISGU using muscles from male wildtype (WT) and AS160-knockout (AS160-KO) rats. The next experiment used AS160-KO rats with an adeno-associated virus (AAV) approach to determine if rescuing muscle AS160 deficiency could restore exercise’s ability to improve ISGU. The third experiment tested if eliminating the muscle GLUT4 deficit in AS160-KO rats via AAV-delivered GLUT4 would enable postexercise enhancement of ISGU. The final experiment employed AS160-KO rats and AAV-delivery of AS160 mutated to prevent phosphorylation of Ser588, Thr642, and Ser704 to evaluate their role in postexercise ISGU. We discovered: 1) AS160 expression was essential for postexercise increase in ISGU; 2) rescuing muscle AS160 expression of AS160-KO rats restored postexercise enhancement of ISGU; 3) restoring GLUT4 expression in AS160-KO muscle did not rescue the postexercise increase in ISGU; and 4) although AS160 phosphorylation on 3 key sites was not required for postexercise elevation in ISGU, it was essential for the full-exercise effect.

scholarly journals The Exercise-induced Improvement in Insulin-stimulated Glucose Uptake by Rat Skeletal Muscle Is Absent in Male AS160-Knockout Rats, Partially Restored by Muscle Expression of Phosphomutated AS160, and Fully Restored by Muscle Expression of Wildtype AS160

2021 ◽  
Author(s):  
Amy Zheng ◽  
Edward B. Arias ◽  
Haiyan Wang ◽  
Seong Eun Kwak ◽  
Xiufang Pan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Exercise Session ◽  
Rat Skeletal Muscle ◽  
Initial Experiment ◽  
Adeno Associated Virus ◽  
Glut4 Expression ◽  
Exercise Effect ◽  
Key Sites ◽  
Exercise Induced

One exercise session can elevate insulin-stimulated glucose uptake (ISGU) in skeletal muscle, but the mechanisms remain elusive. Circumstantial evidence suggests a role for Akt substrate of 160 kDa (AS160 or TBC1D4). We used genetic approaches to rigorously test this idea. The initial experiment evaluated AS160’s role for the postexercise increase in ISGU using muscles from male wildtype (WT) and AS160-knockout (AS160-KO) rats. The next experiment used AS160-KO rats with an adeno-associated virus (AAV) approach to determine if rescuing muscle AS160 deficiency could restore exercise’s ability to improve ISGU. The third experiment tested if eliminating the muscle GLUT4 deficit in AS160-KO rats via AAV-delivered GLUT4 would enable postexercise enhancement of ISGU. The final experiment employed AS160-KO rats and AAV-delivery of AS160 mutated to prevent phosphorylation of Ser588, Thr642, and Ser704 to evaluate their role in postexercise ISGU. We discovered: 1) AS160 expression was essential for postexercise increase in ISGU; 2) rescuing muscle AS160 expression of AS160-KO rats restored postexercise enhancement of ISGU; 3) restoring GLUT4 expression in AS160-KO muscle did not rescue the postexercise increase in ISGU; and 4) although AS160 phosphorylation on 3 key sites was not required for postexercise elevation in ISGU, it was essential for the full-exercise effect.

Impaired plasma FFA oxidation imposed by extreme CHO deficiency in contracting rat skeletal muscle

1994 ◽  
Vol 77 (2) ◽  
pp. 517-525 ◽  
Author(s):  
L. P. Turcotte ◽  
P. J. Hespel ◽  
T. E. Graham ◽  
E. A. Richter
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Glucose Uptake ◽  
Swimming Exercise ◽  
Rat Skeletal Muscle ◽  
Palmitate Oxidation ◽  
Plasma Ffa ◽  
Ffa Metabolism ◽  
Palmitate Uptake

The extent to which carbohydrate (CHO) availability affects free fatty acid (FFA) metabolism in contracting skeletal muscle is not well characterized. To study this question, rats were depleted of glycogen by swimming exercise and lard feeding 24 h before perfusion of their isolated hindquarters. After 20 min of preperfusion with a medium containing no glucose, palmitate (600 or 2,000 microM), and [1–14C]palmitate, flow was restricted to one hindlimb, which was electrically stimulated for 2 min to further deplete muscles of glycogen. After 2 min of recovery, glucose was added to the perfusate at final concentrations of 0, 6, or 20 mM, and after another 3 min muscles were stimulated for 30 min. At 6 and 2,000 microM palmitate, glucose uptake after 30 min of stimulation averaged 23.5 +/- 9.3 and 45.9 +/- 10.6 mumol.g-1.h-1 with 6 and 20 mM glucose, respectively. At 6 and 2,000 microM palmitate, palmitate uptake was lower (30–37%, P < 0.05) with 0 than with 6 or 20 mM glucose. At 600 microM palmitate, percent palmitate oxidation was higher (27%, P < 0.05) with 0 than with 6 or 20 mM glucose, resulting in similar total palmitate oxidation with the three glucose concentrations (0.28 +/- 0.01 mumol.g-1.h-1). At 2,000 microM palmitate, percent palmitate oxidation was not significantly different among glucose concentrations, resulting in a significantly lower rate of palmitate oxidation with 0 (0.62 +/- 0.18 mumol.g-1.h-1) than with 6 or 20 mM glucose (0.77 +/- 0.25 and 0.78 +/- 0.20 mumol.g-1.h-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Proteomic Investigation of Changes in Rat Skeletal Muscle after Exercise-Induced Fatigue

2012 ◽  
Vol 45 (1) ◽  
pp. 75-80 ◽  
Author(s):  
Liping Zhao ◽  
Wenhui Yan ◽  
Heng Xiang ◽  
Xiaoyang Wang ◽  
Haixuan Qiao
Keyword(s):  
Skeletal Muscle ◽  
Rat Skeletal Muscle ◽  
Proteomic Investigation ◽  
Exercise Induced

AMP-activated protein kinase activity and glucose uptake in rat skeletal muscle

2001 ◽  
Vol 280 (5) ◽  
pp. E677-E684 ◽  
Author(s):  
Nicolas Musi ◽  
Tatsuya Hayashi ◽  
Nobuharu Fujii ◽  
Michael F. Hirshman ◽  
Lee A. Witters ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Muscle Contractions ◽  
Treadmill Running ◽  
Dependent Manner ◽  
Rat Skeletal Muscle ◽  
Amp Activated Protein Kinase ◽  
Dose Dependent

The AMP-activated protein kinase (AMPK) has been hypothesized to mediate contraction and 5-aminoimidazole-4-carboxamide 1-β-d-ribonucleoside (AICAR)-induced increases in glucose uptake in skeletal muscle. The purpose of the current study was to determine whether treadmill exercise and isolated muscle contractions in rat skeletal muscle increase the activity of the AMPKα1 and AMPKα2 catalytic subunits in a dose-dependent manner and to evaluate the effects of the putative AMPK inhibitors adenine 9-β-d-arabinofuranoside (ara-A), 8-bromo-AMP, and iodotubercidin on AMPK activity and 3- O-methyl-d-glucose (3-MG) uptake. There were dose-dependent increases in AMPKα2 activity and 3-MG uptake in rat epitrochlearis muscles with treadmill running exercise but no effect of exercise on AMPKα1 activity. Tetanic contractions of isolated epitrochlearis muscles in vitro significantly increased the activity of both AMPK isoforms in a dose-dependent manner and at a similar rate compared with increases in 3-MG uptake. In isolated muscles, the putative AMPK inhibitors ara-A, 8-bromo-AMP, and iodotubercidin fully inhibited AICAR-stimulated AMPKα2 activity and 3-MG uptake but had little effect on AMPKα1 activity. In contrast, these compounds had absent or minimal effects on contraction-stimulated AMPKα1 and -α2 activity and 3-MG uptake. Although the AMPKα1 and -α2 isoforms are activated during tetanic muscle contractions in vitro, in fast-glycolytic fibers, the activation of AMPKα2-containing complexes may be more important in regulating exercise-mediated skeletal muscle metabolism in vivo. Development of new compounds will be required to study contraction regulation of AMPK by pharmacological inhibition.

Exercise-induced apoptosis of rat skeletal muscle and the effect of meloxicam

2001 ◽  
Vol 21 (4) ◽  
pp. 133-136 ◽  
Author(s):  
Sule Arslan ◽  
Sevim Erdem ◽  
Aysen Sivri ◽  
Zafer Hasçelik ◽  
Ersin Tan
Keyword(s):  
Skeletal Muscle ◽  
Rat Skeletal Muscle ◽  
Exercise Induced ◽  
Induced Apoptosis

scholarly journals The B2 Receptor of Bradykinin Is Not Essential for the Post-Exercise Increase in Glucose Uptake by Insulin-Stimulated Mouse Skeletal Muscle

2011 ◽  
pp. 511-519 ◽  
Author(s):  
G. G. SCHWEITZER ◽  
C. M. CASTORENA ◽  
T. HAMADA ◽  
K. FUNAI ◽  
E. B. ARIAS ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Plasma Insulin ◽  
Treadmill Exercise ◽  
Post Exercise ◽  
Skeletal Muscle Glucose Uptake ◽  
Glucose Plasma ◽  
Exercise Induced

Bradykinin can enhance skeletal muscle glucose uptake (GU), and exercise increases both bradykinin production and muscle insulin sensitivity, but bradykinin’s relationship with post-exercise insulin action is uncertain. Our primary aim was to determine if the B2 receptor of bradykinin (B2R) is essential for the post-exercise increase in GU by insulin-stimulated mouse soleus muscles. Wildtype (WT) and B2R knockout (B2RKO) mice were sedentary or performed 60 minutes of treadmill exercise. Isolated soleus muscles were incubated with [3H]-2-deoxyglucose ±insulin (60 or 100 μU/ml). GU tended to be greater for WT vs. B2RKO soleus with 60 μU/ml insulin (P=0.166) and was significantly greater for muscles with 100 μU/ml insulin (P<0.05). Both genotypes had significant exercise-induced reductions (P<0.05) in glycemia and insulinemia, and the decrements for glucose (~14 %) and insulin (~55 %) were similar between genotypes. GU tended to be greater for exercised vs. sedentary soleus with 60 μU/ml insulin (P=0.063) and was significantly greater for muscles with 100 μU/ml insulin (P<0.05). There were no significant interactions between genotype and exercise for blood glucose, plasma insulin or GU. These results indicate that the B2R is not essential for the exercise-induced decrements in blood glucose or plasma insulin or for the post-exercise increase in GU by insulin-stimulated mouse soleus muscle.

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