In vivo regulation of muscle glycogen synthase and the control of glycogen synthesis.

Shulman, Robert G.; Bloch, G; Rothman, Douglas L.

doi:10.1073/pnas.92.19.8535

Cited by 136 publications

(85 citation statements)

References 63 publications

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“…These observations suggest also that the lack of glycogen deposition in the starved state may be determined primarily by the low levels of glucose 6-phosphate. Overall, our findings are consistent with the model put forward by Shulman et al [1] that the rate of glycogen synthase is controlled at the level of glucose transport\hexokinase by the concentration of glucose 6-phosphate. On the basis of this model, one may propose that the increase in glucose 6-phosphate levels is linked to increases in glucose uptake and phosphorylation that result from the high postprandial blood glucose and insulin levels that accompany re-feeding.…”

Section: Metabolitessupporting

confidence: 93%

“…The control of the rate of glycogen synthesis from glucose in skeletal muscle involves a number of regulatory steps, namely glucose transport via the insulin-sensitive glucose transporter GLUT 4, hexokinase, glycogen synthase, and glycogen phosphorylase [1][2][3]. The relative contribution of each of these potential control sites to the acute control of glycogen synthesis flux in muscle is dependent on the physiological state of the animal.…”

Section: Introductionmentioning

confidence: 99%

“…In other physiological conditions, this dual mechanism of control is not observed, rather the rate of glycogen synthesis is predominantly controlled either by an increase in the fractional velocity of glycogen synthase through dephosphorylation or by an increase in glucose 6-phosphate levels consecutive to an increase in glucose transport\hexokinase activity. Using the glucose clamp technique, in response to hyperglycaemia, dephosphorylation of glycogen synthase is not observed [5][6][7][8], suggesting that glucose transport\hexokinase activity produces an increase in glucose 6-phosphate levels which in turn controls the rate of glycogen synthesis via activation of glycogen synthase [1]. There are other physiological conditions where changes in the phosphorylation state of glycogen synthase have been proposed to play the major role in the control of glycogen synthesis.…”

Section: Introductionmentioning

confidence: 99%

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Re-feeding after starvation involves a temporal shift in the control site of glycogen synthesis in rat muscle

James

Flynn²,

Jones³

et al. 1998

Biochemical Journal

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The starved-to-fed transition is accompanied by rapid glycogen deposition in skeletal muscles. On the basis of recent findings [Bra$ u, Ferreira, Nikolovski, Raja, Palmer and Fournier (1997) Biochem. J. 322, [303][304][305][306][307][308] that during recovery from exercise there is a shift from a glucose 6-phosphate\phosphorylation-based control of glycogen synthesis to a phosphorylation-based control alone, this paper seeks to establish whether a similar shift occurs in muscle during re-feeding after starvation in the rat. Chow re-feeding after 48 h of starvation resulted in glycogen deposition in all muscles examined (white, red and mixed quadriceps, soleus and diaphragm) to levels higher than those in the fed state. Although the early phase of re-feeding was associated with increases in glucose 6-phosphate levels in all muscles, there was no accompanying increase in the fractional

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Section: Metabolitessupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Re-feeding after starvation involves a temporal shift in the control site of glycogen synthesis in rat muscle

James

Flynn²,

Jones³

et al. 1998

Biochemical Journal

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“…The data was also analyzed quantitively using metabolic control analysis 56 and a similar conclusion was reached. 57 In order to distinguish between the glucose transporter and hexokinase as the key rate controlling enzyme, 13 C MRS was used to directly measure muscle glucose concentration. 58 A problem in measuring intracellular glucose concentrations is to distinguish the signal from glucose in the blood and extracellular space.…”

Section: Mrs Studies Of Insulin-stimulated Mus-cle Glucose Transport mentioning

confidence: 99%

Studies of metabolic compartmentation and glucose transport using in vivo MRS

Rothman

2001

NMR in Biomedicine

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Organs consist of several types of cells with specialized functions. This cellular localization of function is often referred to as compartmentation. Due to the intrinsic low sensitivity of MR methods it is generally not possible in vivo to obtain images or spectra of single cells. Instead the MRS signal is the sum of the signal from millions of cells and multiple cell types. A major challenge in using MRS to study biological processes such as metabolism and transport is to devise measurements that provide cell-specific information from this mix. Fortunately nature has helped the MR scientist by in several cases nearly completely localizing metabolic pathways and their associated metabolites in specific cell types. The chemical specificity of MRS allows the concentrations and synthesis rates of these metabolites to be measured, providing information about the compartmentation of metabolism and function. In this review examples are presented from MRS studies of metabolic trafficking between neurons and astrocytes in the brain, brain glucose transport, and the role of muscle glucose transport in insulin resistance and diabetes. The concepts and approaches used in these studies are generally applicable for studying cellular metabolic compartmentation in a wide range of systems.

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“…An improved method of assessing ADP recovery after exercise has recently been reported (Chen et al 1999). Results from MRS studies of human skeletal muscle have also been interpreted in terms of metabolic control analysis (Shulman et al 1995) or metabolic control theory (Jeneson et al 1999).…”

Section: Muscle Bioenergetics As Observed By Dynamic 31 P Magnetic Rementioning

confidence: 99%

Introduction toin vivo³¹P magnetic resonance spectroscopy of (human) skeletal muscle

et al. 1999

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fax +31 24 3540 866, email a.heerschap@rdiag.azn.nl 31 P magnetic resonance spectroscopy (MRS) offers a unique non-invasive window on energy metabolism in skeletal muscle, with possibilities for longitudinal studies and of obtaining important bioenergetic data continuously and with sufficient time resolution during muscle exercise. The present paper provides an introductory overview of the current status of in vivo 31 P MRS of skeletal muscle, focusing on human applications, but with some illustrative examples from studies on transgenic mice. Topics which are described in the present paper are the information content of the 31 P magnetic resonance spectrum of skeletal muscle, some practical issues in the performance of this MRS methodology, related muscle biochemistry and the validity of interpreting results in terms of biochemical processes, the possibility of investigating reaction kinetics in vivo and some indications for fibre-type heterogeneity as seen in spectra obtained during exercise. P magnetic resonance spectroscopy: Skeletal muscle: High-energy phosphates: Energy metabolism: ExerciseFollowing initial experiments on animal tissue (Hoult et al. 1974;Ackerman et al. 1980), magnetic resonance (MR) spectroscopy (MRS) was first applied to human subjects in the early 1980s, using the 31 P nucleus to monitor the levels and fate of high-energy phosphates in skeletal muscle (Chance et al. 1981;Cresshull et al. 1981;Ross et al. 1981). From these first experiments it was clear that 31 P MRS offers a unique non-invasive window on energy metabolism in skeletal muscle. Of particular interest is the possibility of obtaining important bioenergetic data continuously and with sufficient time resolution during muscle exercise. Another important aspect is that longitudinal monitoring is possible. Numerous studies applying this technique to human subjects have been published, and several reviews are available addressing specific results obtained in this way (for example, see Barbiroli, 1992;Cozzone & Bendahan, 1994;Kemp & Radda, 1994;McCully et al. 1994;Radda et al. 1995).The present paper provides an introduction to 31 P MRS as applied to skeletal muscle of human subjects, and also gives some illustrative examples from our recent studies on skeletal muscle of transgenic mouse models lacking creatine kinase (EC 2.7.3.2). Information content of the 31 P magnetic resonance spectrum of skeletal muscleTo appreciate the potential of the method, first, the information content of a spectrum obtained from human skeletal muscle at rest should be examined (see Fig. 1(A)).The most dominant signals in the spectrum are from phosphocreatine (PCr) and the three non-equivalent phosphate groups of ATP. Usually also a signal for inorganic phosphate (Pi) can be observed, and under favourable conditions signals for phosphomonoesters and phosphodiesters are observable as well. What is the origin of the distinct resonance frequencies of the 31 P nuclei in these compounds? In a first approximation the resonance frequency of the nuclear spins is...

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In vivo regulation of muscle glycogen synthase and the control of glycogen synthesis.

Cited by 136 publications

References 63 publications

Re-feeding after starvation involves a temporal shift in the control site of glycogen synthesis in rat muscle

Re-feeding after starvation involves a temporal shift in the control site of glycogen synthesis in rat muscle

Studies of metabolic compartmentation and glucose transport using in vivo MRS

Introduction toin vivo³¹P magnetic resonance spectroscopy of (human) skeletal muscle

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In vivo regulation of muscle glycogen synthase and the control of glycogen synthesis.

Cited by 136 publications

References 63 publications

Re-feeding after starvation involves a temporal shift in the control site of glycogen synthesis in rat muscle

Re-feeding after starvation involves a temporal shift in the control site of glycogen synthesis in rat muscle

Studies of metabolic compartmentation and glucose transport using in vivo MRS

Introduction toin vivo31P magnetic resonance spectroscopy of (human) skeletal muscle

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Product

Resources

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Introduction toin vivo³¹P magnetic resonance spectroscopy of (human) skeletal muscle