α-Adrenergic receptors in rat skeletal muscle

Rattigan, Stephen; Appleby, Geoffrey J.; Edwards, Susan; McKinstry, William J.; Colquhoun, Eric Q.; Clark, Michael G.; Richter, Erik A.

doi:10.1016/0006-291x(86)90442-0

Cited by 31 publications

(19 citation statements)

References 10 publications

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“…This review focuses primarily on ␤-adrenoceptor signaling, since the ␤-adrenoceptors are the predominant subtype in skeletal muscle (226,370). However, a sparse population of ␣-adrenoceptors has been identified in skeletal muscle and is usually expressed in higher proportions in muscles that are highly vascularized (370).…”

Section: B the ␣-Adrenoceptorsmentioning

confidence: 99%

“…However, very little work has focused on the role of this pathway in normal muscle growth and development, muscle fiber regeneration after injury, or its involvement in pathological conditions where muscle wasting and weakness are indicated. Thus the aim of this review will be to describe the potential role(s) of this novel signaling pathway in skeletal muscle structure and function, with particular emphasis on the ␤ 2 -adrenoceptor, which is the predominant skeletal muscle subtype (226,370).…”

Section: Adrenoceptors and The Sympathetic Nervous Systemmentioning

confidence: 99%

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Role of β-Adrenoceptor Signaling in Skeletal Muscle: Implications for Muscle Wasting and Disease

Lynch¹,

Ryall²

2008

Physiological Reviews

362

356

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The importance of beta-adrenergic signaling in the heart has been well documented, but it is only more recently that we have begun to understand the importance of this signaling pathway in skeletal muscle. There is considerable evidence regarding the stimulation of the beta-adrenergic system with beta-adrenoceptor agonists (beta-agonists). Although traditionally used for treating bronchospasm, it became apparent that some beta-agonists could increase skeletal muscle mass and decrease body fat. These so-called "repartitioning effects" proved desirable for the livestock industry trying to improve feed efficiency and meat quality. Studying beta-agonist effects on skeletal muscle has identified potential therapeutic applications for muscle wasting conditions such as sarcopenia, cancer cachexia, denervation, and neuromuscular diseases, aiming to attenuate (or potentially reverse) the muscle wasting and associated muscle weakness, and to enhance muscle growth and repair after injury. Some undesirable cardiovascular side effects of beta-agonists have so far limited their therapeutic potential. This review describes the physiological significance of beta-adrenergic signaling in skeletal muscle and examines the effects of beta-agonists on skeletal muscle structure and function. In addition, we examine the proposed beneficial effects of beta-agonist administration on skeletal muscle along with some of the less desirable cardiovascular effects. Understanding beta-adrenergic signaling in skeletal muscle is important for identifying new therapeutic targets and identifying novel approaches to attenuate the muscle wasting concomitant with many diseases.

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Section: B the ␣-Adrenoceptorsmentioning

confidence: 99%

Section: Adrenoceptors and The Sympathetic Nervous Systemmentioning

confidence: 99%

Role of β-Adrenoceptor Signaling in Skeletal Muscle: Implications for Muscle Wasting and Disease

Lynch¹,

Ryall²

2008

Physiological Reviews

362

356

View full text Add to dashboard Cite

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“…We ruled out a role for b 1 -or b 3 -adrenoceptors, because the in vivo effect of b-adrenergic agonists on glucose uptake in skeletal muscle is absent in b 1 /b 2 KO mice and the selective b 2 -adrenoceptor agonist clenbuterol displayed the same efficacy as isoproterenol in L6 muscle cells. Previous studies show that b 2 -adrenoceptors are the primary target for catecholamines in skeletal muscle (6,41), and studies in L6 cells demonstrate that b-adrenoceptor agonist effects are mediated by b 2 -adrenoceptors (6), clearly suggesting that the effects of b-adrenergic agonists on glucose uptake are mediated primarily by b 2 -adrenoceptors.…”

Section: Diabetesdiabetesjournalsorg Sato and Associatesmentioning

confidence: 99%

Improving Type 2 Diabetes Through a Distinct Adrenergic Signaling Pathway Involving mTORC2 That Mediates Glucose Uptake in Skeletal Muscle

et al. 2014

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There is an increasing worldwide epidemic of type 2 diabetes that poses major health problems. We have identified a novel physiological system that increases glucose uptake in skeletal muscle but not in white adipocytes. Activation of this system improves glucose tolerance in Goto-Kakizaki rats or mice fed a high-fat diet, which are established models for type 2 diabetes. The pathway involves activation of β2-adrenoceptors that increase cAMP levels and activate cAMP-dependent protein kinase, which phosphorylates mammalian target of rapamycin complex 2 (mTORC2) at S2481. The active mTORC2 causes translocation of GLUT4 to the plasma membrane and glucose uptake without the involvement of Akt or AS160. Stimulation of glucose uptake into skeletal muscle after activation of the sympathetic nervous system is likely to be of high physiological relevance because mTORC2 activation was observed at the cellular, tissue, and whole-animal level in rodent and human systems. This signaling pathway provides new opportunities for the treatment of type 2 diabetes.

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“…[23], or by dihydropyridine binding assayed with 0.5 nM [3H]PN 200/110 (New England Nuclear) as ligand as described by Muscarine receptors were assayed as described previously with quinuclidinyl[phen~~l-4-~H]benzilate as ligand [24]. a'-Adrenergic receptors were assayed by the protocol of Rattigan et al [25] with [3H]prazosine as ligand. Protein was determined by the method of Bradford [26] using bovine serum albumin as standard.…”

Section: Methodsmentioning

confidence: 99%

Intracellular localization of inositol‐phospholipid‐metabolizing enzymes in rabbit fast‐twitch skeletal muscle

Varsányi

Messer

Brandt

1989

European Journal of Biochemistry

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Rabbit fast-twitch skeletal muscle microsomes have been separated by isopycnic centrifugation on a linear sucrose gradient into triads and light sarcoplasmic reticulum. In both fractions phosphatidylinositol-kinase activity is found [Varsanyi et al. (1986) Biochem. Biophys. Rex Commun. 138, 13951. In contrast, phosphatidylinositol-4-phosphate kinase is nearly exclusively associated with triads. The phosphatidylinositol-4,5-bisphosphatephosphodiesterase activity shows a biphasic distribution : approximately 50% of the activity is associated with triads and 50% appears in the overlay.Triads have been broken mechanically into transverse tubules and terminal cisternae, then separated by isopycnic sucrose-gradient centrifugation. Both fractions exhibit phosphatidylinositol-kinase activity; the activities of phosphatidylinositol-4-phosphate kinase and phosphatidylinositol-4,5-bisphosphate phosphodiesterase are associated mainly with the transverse tubules. Consequently, in rabbit fast-twitch skeletal muscle all necessary enzymes for production of D-myo-inositol 1,4,5-trisphosphate are associated with transverse tubules.Phosphatidylinositol-4,5-bisphosphate phosphodiesterase associated with triads shows a pH optimum at 6.8. The enzyme is maximally active between pCa 5 and pCa 4.Mg2+ inhibits the enzyme activity half-maximally at about 1 mM. Guanine-nucleotide-binding proteins seem not to be involved in the regulation of enzyme activity; guanosine 5'-[y-thio]triphosphate does not influence phosphatidylinositol-4,5-bisphosphate phosphodiesterase activity. It correlates well with the observation that neither cr,-adrenergic nor muscarinic receptors have been found in fast-twitch rabbit skeletal muscle. On basis of the respective enzyme activities estimations on maximal phosphatidylinositol turnover were made and a possible involvement of this signal pathway in excitation-contraction coupling has been discussed. Furthermore, calculations show that during a single twitch D-myo-inositol 1,4,5-trisphosphate concentration does not reach more than 2 nM. However, during a 4-s tetanus D-myo-inositol 1,4,5-trisphosphate can accumulate to a level which could effect force generation [Thieleczek and Heilmeyer (1 986) Biochem. Biophys. Res. Commun. 135, 6621 and aldolase distribution (Thieleczek et al., unpublished results).

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α-Adrenergic receptors in rat skeletal muscle

Cited by 31 publications

References 10 publications

Role of β-Adrenoceptor Signaling in Skeletal Muscle: Implications for Muscle Wasting and Disease

Role of β-Adrenoceptor Signaling in Skeletal Muscle: Implications for Muscle Wasting and Disease

Improving Type 2 Diabetes Through a Distinct Adrenergic Signaling Pathway Involving mTORC2 That Mediates Glucose Uptake in Skeletal Muscle

Intracellular localization of inositol‐phospholipid‐metabolizing enzymes in rabbit fast‐twitch skeletal muscle

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