Concerted Regulation of Glycogen Metabolism and Muscle Contraction

Author(s):  
E. H. Fischer ◽  
H. E. Blum ◽  
B. Byers ◽  
C. Heizmann ◽  
G. W. Kerrick ◽  
...  
1976 ◽  
pp. 137-158 ◽  
Author(s):  
E. H. Fischer ◽  
J.-U. Becker ◽  
H. E. Blum ◽  
B. Byers ◽  
C. Heizmann ◽  
...  

1982 ◽  
Vol 242 (5) ◽  
pp. R514-R521
Author(s):  
M. J. Donahue ◽  
N. J. Yacoub ◽  
B. G. Harris

Isolated muscle segments from the parasitic roundworm Ascaris suum were shown to contract when perfused with acetylcholine (ACh). The muscle responded to ACh concentrations of 1 microM and was maximally contracted at 50 microM ACh. In fed muscle segments perfused with saturating levels of ACh the glycogen synthase Ka values for glucose 6-phosphate increased from 0.5 to 0.95 mM. In starved segments stimulated by ACh, the muscle utilized glycogen at a rate that was 1.41 micrograms.min-1.g tissue-1 greater than the saline-perfused controls. The cyclic AMP (cAMP) levels remained relatively constant at 0.34 +/- 0.08 nmol/g muscle during perfusion with ACh. Contraction in the muscle could be inhibited in a dose-dependent manner by gamma-aminobutyric acid (GABA). The presence of GABA in starved muscle prevented the decrease in Ka values and phosphorylase activity ratios brought about by glucose. Perfusion of GABA did not change cAMP levels in the muscle. Starved muscle perfused with GABA utilized glycogen at a rate that was 0.41 microgram.min-1.g-1 greater than saline-perfused controls. The results indicated that muscle contraction could be elicited by ACh, and that the energy for this process was derived from endogenous glycogen stores, which were depleted during contraction. Muscle contraction was also correlated with inactivation of glycogen synthase and activation of phosphorylase. These processes appeared to function via a cAMP-independent mechanisms.


1991 ◽  
Vol 260 (6) ◽  
pp. E927-E932 ◽  
Author(s):  
L. Coderre ◽  
A. K. Srivastava ◽  
J. L. Chiasson

With the use of the hindlimb perfusion technique, the effect of glucocorticoid on the regulation of glycogen metabolism was studied in rat skeletal muscle. Rats were adrenalectomized (ADX) or sham operated (controls) 14 days before the study. The ADX animals were treated with either saline or corticosterone, and the hindlimbs were perfused at rest or during muscle contraction with saline or epinephrine (10(-7) M). In the resting state, the glycogen content was 33.0 +/- 1.9 mumol/g in the controls, and the activity ratios of glycogen phosphorylase (GPase) and glycogen synthase (GSase) were 0.27 +/- 0.03 and 0.15 +/- 0.02, respectively. Epinephrine treatment increased GPase activity (0.78 +/- 0.03) and decreased GSase activity (0.05 +/- 0.01), which resulted in decreased glycogen content (25.7 +/- 0.9 mumol/g; P less than 0.01). Adrenalectomy induced a 35% reduction in glycogen content but had no effect on the activities of basal enzymes. Under these conditions, however, epinephrine had no effect on GPase activity, had a diminished effect on GSase activity (0.11 +/- 0.01), and did not induce further glycogen breakdown. Corticosterone replacement normalized muscle glycogen content in ADX rats as well as the response of the enzymes to epinephrine. Muscle contraction resulted in a decrease in glycogen content (8.9 +/- 1.3 mumol/g) and in GPase activity (0.14 +/- 0.02) and an increase in GSase activity (0.25 +/- 0.01); this was not affected by adrenalectomy nor by epinephrine. In conclusion, these data indicate that glucocorticoid is essential for the effects of epinephrine on GPase activation. on GSase inhibition, and consequently on glycogen breakdown in resting muscle.(ABSTRACT TRUNCATED AT 250 WORDS)


Author(s):  
H. Mohri

In 1959, Afzelius observed the presence of two rows of arms projecting from each outer doublet microtubule of the so-called 9 + 2 pattern of cilia and flagella, and suggested a possibility that the outer doublet microtubules slide with respect to each other with the aid of these arms during ciliary and flagellar movement. The identification of the arms as an ATPase, dynein, by Gibbons (1963)strengthened this hypothesis, since the ATPase-bearing heads of myosin molecules projecting from the thick filaments pull the thin filaments by cross-bridge formation during muscle contraction. The first experimental evidence for the sliding mechanism in cilia and flagella was obtained by examining the tip patterns of molluscan gill cilia by Satir (1965) who observed constant length of the microtubules during ciliary bending. Further evidence for the sliding-tubule mechanism was given by Summers and Gibbons (1971), using trypsin-treated axonemal fragments of sea urchin spermatozoa. Upon the addition of ATP, the outer doublets telescoped out from these fragments and the total length reached up to seven or more times that of the original fragment. Thus, the arms on a certain doublet microtubule can walk along the adjacent doublet when the doublet microtubules are disconnected by digestion of the interdoublet links which connect them with each other, or the radial spokes which connect them with the central pair-central sheath complex as illustrated in Fig. 1. On the basis of these pioneer works, the sliding-tubule mechanism has been established as one of the basic mechanisms for ciliary and flagellar movement.


Diabetes ◽  
1985 ◽  
Vol 34 (4) ◽  
pp. 395-402 ◽  
Author(s):  
W. J. Roesler ◽  
R. L. Khandelwal

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