Effect of uridine on cellular UTP and glycogen synthesis in skeletal muscle: stimulation of UTP formation by insulin.

Insulin increased O2 consumption in isolated perfused rat muscle for upward of 2 h after a treadmill run. Insulin did not increase O2 consumption in nonexercised rats, nor did prior exercise increase O2 consumption in the absence of added insulin. The stimulation of glycogen synthesis by insulin was also enhanced in muscle of previously exercised rats. The additional energy required for this was not sufficient to account for the increase in O2 consumption, however. The results indicate that insulin increases thermogenesis in skeletal muscle after exercise. They also raise the possibility that in intact organisms the thermogenic effect of foods that increase insulin secretion could be increased by prior exercise.

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Long-term electrical stimulation of rabbit skeletal muscle increases growth of paired arteries and veins

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.269.2.h717 ◽

1995 ◽

Vol 269 (2) ◽

pp. H717-H724 ◽

Cited By ~ 4

Author(s):

T. H. Adair ◽

J. Hang ◽

M. L. Wells ◽

F. D. Magee ◽

J. P. Montani

Keyword(s):

Skeletal Muscle ◽

Vascular System ◽

Common Peroneal Nerve ◽

Numerical Density ◽

Muscle Stimulation ◽

Longus Muscle ◽

The Right ◽

Arteries And Veins ◽

Stimulation Of

We tested whether chronic stimulation of skeletal muscle can increase the growth of paired arteries and veins in rabbit extensor digitorum longus muscle (EDL). The right EDL of female New Zealand White rabbits was stimulated via the common peroneal nerve at 10 Hz using 300 microseconds square waves at 3-4 V. Two-hour periods of stimulation was alternated with 4-h periods of rest, 7 days/wk for approximately 60 days. The left EDL served as control. The hindlimb vascular system was maximally dilated and perfuse-fixed with 3% glutaraldehyde and 2% paraformaldehyde at arterial and venous pressures of 80-100 and 15-20 mmHg, respectively. Muscles were postfixed in OsO4 and embedded in EPOX 812 resin. One millimeter-thick transverse sections were cut at uniform locations through the entire breadth of the muscle and analyzed using videomicroscopy along with computerized morphometric and stereological techniques. All paired arteries and veins on each full muscle section were analyzed. Chronic muscle stimulation caused the wall volume of paired arteries and veins to increase by an average of approximately twofold and the lumen volume to increase by an average of approximately threefold compared with the contralateral muscles. The wall-to-lumen area ratio of the arteries and veins was not affected. Muscle stimulation also caused the numerical density of arteries having a diameter > 100 microns to increase by approximately fourfold and the density of veins having a perimeter > 500 microns to increase by approximately 10-fold.(ABSTRACT TRUNCATED AT 250 WORDS)

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A 31P-n.m.r. study of the acute effects of β-blockade on the bioenergetics of skeletal muscle during contraction

Biochemical Journal ◽

10.1042/bj2460163 ◽

1987 ◽

Vol 246 (1) ◽

pp. 163-172 ◽

Cited By ~ 4

Author(s):

R A Challiss ◽

D J Hayes ◽

G K Radda

Keyword(s):

Skeletal Muscle ◽

Gastrocnemius Muscle ◽

High Energy ◽

Muscle Stimulation ◽

Stimulation Protocol ◽

Unilateral Stimulation ◽

Short Period ◽

Supramaximal Stimulation ◽

Contractile Performance ◽

Stimulation Of

1. The effects of beta-adrenoceptor antagonist administration on skeletal muscle contractile performance and bioenergetics in vivo have been investigated during unilateral sciatic nerve stimulation in the rat. 2. Two muscle stimulation protocols have been used: supramaximal stimulation at 4 Hz, or incremental supramaximal stimulation at 1, 2 and 4 Hz. Changes in high-energy phosphate concentrations were followed using 31P-n.m.r., and gastrocnemius muscle twitch characteristics were monitored continuously. 3. Under all conditions investigated, DL-propranolol administration (2.5 mg/kg body wt.) caused a significant decrease in cyclic AMP concentrations in resting and stimulated gastrocnemius muscle, prevented an increase in heart rate upon muscle stimulation, but did not affect plasma glucose, fatty acid or lactate concentrations in comparison with values obtained in control experiments. 4. Administration of DL-propranolol 5 min or 35 min before unilateral stimulation of 4 Hz had no effect on changes in muscle phosphocreatine, ATP or Pi concentrations, intracellular pH or contractile performance. 5. In contrast, animals receiving DL-propranolol 5 min before unilateral stimulation of 1, 2 and 4 Hz showed a significant deterioration in gastrocnemius muscle tension development during 2 and 4 Hz stimulation compared with control animals. Concurrent with this change in contractile performance was a higher muscle concentration of phosphocreatine, a lower concentration of Pi and no significant change in intramuscular pH compared with control experiments. 6. The changes in muscle performance and bioenergetics observed during the incremental stimulation protocol were not observed when D-propranolol was administered and could be completely circumvented by a short period of muscle stimulation of 4 Hz prior to initiation of the incremental stimulation protocol. 7. Mechanisms are discussed which may account for the failure of gastrocnemius muscle to generate the expected force during the incremental stimulation protocol in the presence of beta-blockade.

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Insulin action in denervated skeletal muscle. Evidence that the reduced stimulation of glycogen synthesis does not involve decreased insulin binding.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(18)89727-7 ◽

1985 ◽

Vol 260 (1) ◽

pp. 273-278 ◽

Cited By ~ 3

Author(s):

R L Smith ◽

J C Lawrence

Keyword(s):

Skeletal Muscle ◽

Insulin Action ◽

Glycogen Synthesis ◽

Insulin Binding ◽

Stimulation Of

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Selectivity of the insulin-like actions of vanadate on glucose and protein metabolism in skeletal muscle

Biochemical Journal ◽

10.1042/bj2320273 ◽

1985 ◽

Vol 232 (1) ◽

pp. 273-276 ◽

Cited By ~ 95

Author(s):

A S Clark ◽

J M Fagan ◽

W E Mitch

Keyword(s):

Skeletal Muscle ◽

Protein Synthesis ◽

Insulin Receptor ◽

Glucose Uptake ◽

Protein Metabolism ◽

Glucose Oxidation ◽

Glycogen Synthesis ◽

Metabolic Responses ◽

Receptor Phosphorylation ◽

Stimulation Of

To determine if vanadate has insulin-like actions in skeletal muscle, we measured its effects on glucose and protein metabolism in epitrochlearis muscles of rats. Compared with insulin, vanadate increased glucose uptake, glycogen synthesis and glycolysis to a lesser degree, but caused a greater stimulation of lactate and glucose oxidation. Unlike insulin, vanadate did not change either protein synthesis or degradation. These different metabolic responses could be related to the different pattern of insulin-receptor phosphorylation caused by insulin and vanadate.

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Elevated glucose uptake in skeletal muscle with increased sarcolemma translocation of GLUT4 and glycogen synthesis contributes to bariatric surgery mediated diabetes remission

Endocrine Abstracts ◽

10.1530/endoabs.63.oc2.2 ◽

2019 ◽

Author(s):

Qiaoran Liu ◽

Xin Huang ◽

Yugang Cheng ◽

Teng Liu ◽

Mingwei Zhong ◽

...

Keyword(s):

Bariatric Surgery ◽

Skeletal Muscle ◽

Glucose Uptake ◽

Glycogen Synthesis ◽

Diabetes Remission ◽

Elevated Glucose

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Evidence for the coordinate control of glycogen synthesis, glucose utilization, and glycolysis in Escherichia coli. II. Quantitative correlation of the inhibition of glycogen synthesis and the stimulation of glucose utilization by 2,4-dinitrophenol with the effects on the cellular levels of glucose 6-phosphate, fructose, 1,6-diphosphate, and total adenylates.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(19)40928-9 ◽

1975 ◽

Vol 250 (18) ◽

pp. 7194-7203

Author(s):

D N Dietzler ◽

M P Leckie ◽

J L Magnani ◽

M J Sughrue ◽

P E Bergstein

Keyword(s):

Escherichia Coli ◽

Glucose Utilization ◽

Glycogen Synthesis ◽

Quantitative Correlation ◽

Coordinate Control ◽

Stimulation Of

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Stimulation of glycogen phosphorylase kinase from rabbit skeletal muscle by organic solvents.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(19)86914-4 ◽

1979 ◽

Vol 254 (17) ◽

pp. 8466-8472

Author(s):

T.J. Singh ◽

J.H. Wang

Keyword(s):

Skeletal Muscle ◽

Organic Solvents ◽

Glycogen Phosphorylase ◽

Rabbit Skeletal Muscle ◽

Phosphorylase Kinase ◽

Stimulation Of

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Glycogenin is Dispensable for Glycogen Synthesis in Human Muscle, and Glycogenin Deficiency Causes Polyglucosan Storage

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/clinem/dgz075 ◽

2019 ◽

Vol 105 (2) ◽

pp. 557-566 ◽

Cited By ~ 3

Author(s):

Kittichate Visuttijai ◽

Carola Hedberg-Oldfors ◽

Christer Thomsen ◽

Emma Glamuzina ◽

Cornelia Kornblum ◽

...

Keyword(s):

Mass Spectrometry ◽

Skeletal Muscle ◽

Western Blot ◽

Cardiac Muscle ◽

Glycogen Synthesis ◽

Muscle Fibers ◽

Human Muscle ◽

Missense Mutations ◽

Skeletal Muscle Fibers ◽

Glycogen Biosynthesis

Abstract Context Glycogenin is considered to be an essential primer for glycogen biosynthesis. Nevertheless, patients with glycogenin-1 deficiency due to biallelic GYG1 (NM_004130.3) mutations can store glycogen in muscle. Glycogenin-2 has been suggested as an alternative primer for glycogen synthesis in patients with glycogenin-1 deficiency. Objective The objective of this article is to investigate the importance of glycogenin-1 and glycogenin-2 for glycogen synthesis in skeletal and cardiac muscle. Design, Setting, and Patients Glycogenin-1 and glycogenin-2 expression was analyzed by Western blot, mass spectrometry, and immunohistochemistry in liver, heart, and skeletal muscle from controls and in skeletal and cardiac muscle from patients with glycogenin-1 deficiency. Results Glycogenin-1 and glycogenin-2 both were found to be expressed in the liver, but only glycogenin-1 was identified in heart and skeletal muscle from controls. In patients with truncating GYG1 mutations, neither glycogenin-1 nor glycogenin-2 was expressed in skeletal muscle. However, nonfunctional glycogenin-1 but not glycogenin-2 was identified in cardiac muscle from patients with cardiomyopathy due to GYG1 missense mutations. By immunohistochemistry, the mutated glycogenin-1 colocalized with the storage of glycogen and polyglucosan in cardiomyocytes. Conclusions Glycogen can be synthesized in the absence of glycogenin, and glycogenin-1 deficiency is not compensated for by upregulation of functional glycogenin-2. Absence of glycogenin-1 leads to the focal accumulation of glycogen and polyglucosan in skeletal muscle fibers. Expression of mutated glycogenin-1 in the heart is deleterious, and it leads to storage of abnormal glycogen and cardiomyopathy.

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