Beta‐adrenoceptors and human skeletal muscle characterisation of receptor subtype and effect of age.

Elfellah,; Dalling, R.; Kantola, Ilkka; Reid, JL

doi:10.1111/j.1365-2125.1989.tb05332.x

Cited by 34 publications

(31 citation statements)

References 33 publications

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“…Kim et al [7] showed that the β1 isoform comprises only about 15–21% of the total β receptor population expressed by the soleus muscle of the adult rat and that the β2 isoform can account for essentially all β receptors in some muscles. Similar β receptor populations were found in human muscle biopsies [40, 41]. The present findings also help explain greater muscle growth efficiency in food animals supplemented with dietary β2 agonist compared to β1 agonist [42–44].…”

Section: Discussionsupporting

confidence: 80%

Acute exposure of primary rat soleus muscle to zilpaterol HCl (β2 adrenergic agonist), TNFα, or IL-6 in culture increases glucose oxidation rates independent of the impact on insulin signaling or glucose uptake

et al. 2017

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Recent studies show that adrenergic agonists and inflammatory cytokines can stimulate skeletal muscle glucose uptake, but it is unclear if glucose oxidation is similarly increased. Thus, the objective of this study was to determine the effects of ractopamine HCl (β1 agonist), zilpaterol HCl (β2 agonist), TNFα, and IL-6 on glucose uptake and oxidation rates in unstimulated and insulin-stimulated soleus muscle strips from adult Sprague-Dawley rats. Effects on phosphorylation of Akt (phospho-Akt), p38 MAPK (phospho-p38), and p44/42 MAPK (phospho-p44/42) was also determined. Incubation with insulin increased (P < 0.05) glucose uptake by ~47%, glucose oxidation by ~32%, and phospho-Akt by ~238%. Insulin also increased (P < 0.05) phospho-p38, but only after 2 hours in incubation. Muscle incubated with β2 agonist alone exhibited ~20% less (P < 0.05) glucose uptake but ~32% greater (P < 0.05) glucose oxidation than unstimulated muscle. Moreover, co-incubation with insulin + β2 agonist increased (P < 0.05) glucose oxidation and phospho-Akt compared to insulin alone. Conversely, β1 agonist did not appear to affect basal or insulin-stimulated glucose metabolism, and neither β agonist affected phospho-p44/42. TNFα and IL-6 increased (P < 0.05) glucose oxidation by ~23% and ~33%, respectively, in the absence of insulin. This coincided with increased (P < 0.05) phospho-p38 and phospho-p44/42 but not phospho-Akt. Furthermore, co-incubation of muscle with insulin + either cytokine yielded glucose oxidation rates that were similar to insulin alone, despite lower (P < 0.05) phospho-Akt. Importantly, cytokine-mediated increases in glucose oxidation rates were not concomitant with greater glucose uptake. These results show that acute β2 adrenergic stimulation, but not β1 stimulation, directly increases fractional glucose oxidation in the absence of insulin and synergistically increases glucose oxidation when combined with insulin. The cytokines, TNFα and IL-6, likewise directly increased glucose oxidation in the absence of insulin, but were not additive in combination with insulin and in fact appeared to disrupt Akt-mediated insulin signaling. Rather, cytokines appear to be acting through MAPKs to elicit effects on glucose oxidation. Regardless, stimulation of glucose oxidation by these key stress factors did not rely upon greater glucose uptake, which may promote metabolic efficiency during acute stress by increasing fractional glucose oxidation without increasing total glucose consumption by muscle.

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Section: Discussionsupporting

confidence: 80%

Acute exposure of primary rat soleus muscle to zilpaterol HCl (β2 adrenergic agonist), TNFα, or IL-6 in culture increases glucose oxidation rates independent of the impact on insulin signaling or glucose uptake

et al. 2017

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“…Thus, in terms of tachycardia response, if the elderly are less sensitive to the effects of isoprenaline (a non-selective 13-adrenoceptor agonist) but the effects of salbutamol (a selective P2-adrenoceptor agonist) are unchanged, this may suggest that 13-adrenoceptor responses are attenuated with preservation of 12 responses. Such a conclusion would be supported by two other recent studies (Elfellah et al, 1989;Klein et al, 1988). Klein and co-workers (1988) The heart rate response to exercise and its attenuation by ,B-adrenoceptor blockade are reduced in the elderly (Conway et al, 1971): this is probably the most reliable indicator of cardiac 1l-adrenoceptor activity.…”

Section: Discussionsupporting

confidence: 68%

Beta‐adrenoceptor responses to inhaled salbutamol in the elderly.

Lipworth

Tregaskis

McDevitt

1989

Brit J Clinical Pharma

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The purpose of the present study was to evaluate and compare the responsiveness of 32-adrenoceptors in elderly and young subjects. Seven healthy elderly volunteers (72 ± 3 years) were given cumulative doses of inhaled salbutamol (100 ±g-4000 ,ug) or placebo, following pre-treatment with propranolol 40 mg or placebo. Finger tremor (Tr), plasma potassium (K), and heart rate (HR) were measured at each dose step. There were dosedependent increases in Tr (P < 0.001) and HR (P < 0.001) and falls in K (P < 0.001), which were completely attenuated by propranolol (P < 0.001). Comparison with doseresponse curves in a group of young (Y)

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“…In skeletal muscle, as much as 80-95% of the β-adrenergic receptors are of the β 2 -subtype, although most studies have detected β 1 -adrenergic receptors also (Elfellah et al 1989;Kim et al 1991;. The responsiveness to β-adrenergic stimulation depends on the density of β-adrenoceptors in the cell membrane (Böhm et al 1997;Grady et al 1997).…”

mentioning

confidence: 97%

Quantitative determination of cell surface β-adrenoceptors in different rat skeletal muscles

Jensen

Brennesvik

Bergersen

et al. 2002

Pflügers Arch - Eur J Physiol

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In the present study, the density of cell surface beta-adrenergic receptors was determined in different skeletal muscles using the hydrophilic ligand [3H]CGP 12177. The density of beta-adrenergic receptors was highest in the slow-twitch soleus muscle (32.8+/-0.9 fmol mg dw(-1)) and lowest in the fast-twitch glycolytic white gastrocnemius (10.4+/-0.5 fmol mg dw(-1)) beta-Adrenoceptor density correlated closely with the percentage of type-I fibres (r=0.979; P<0.0001) and inversely with the percentage of type-IIB fibres (r=696; P<0.03). Incubation with isoprenaline (10 microM) for 30 min decreased the density of beta-adrenergic receptors in the cell surface from 32.9+/-0.8 to 19.3+/-0.7 fmol mg dw(-1) in the soleus and from 16.8+/-1.0 to 12.0+/-0.7 fmol mg dw(-1) in the epitrochlearis. Internalisation appeared rapid (half-time less than 5 min). To study externalisation of beta-adrenergic receptors, soleus strips were incubated 30 min with 10 microM isoprenaline and then transferred to buffer without agonist. The first incubation reduced the density to approximately 50%, the subsequent incubation without agonist increased cell surface receptor density to approximately 80% of the initial density after 1 h. No further increase was observed over the next 2 h, suggesting that some of the receptors had been degraded. Insulin or contractile activity did not influence rate of externalisation.

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Beta‐adrenoceptors and human skeletal muscle characterisation of receptor subtype and effect of age.

Cited by 34 publications

References 33 publications

Acute exposure of primary rat soleus muscle to zilpaterol HCl (β2 adrenergic agonist), TNFα, or IL-6 in culture increases glucose oxidation rates independent of the impact on insulin signaling or glucose uptake

Acute exposure of primary rat soleus muscle to zilpaterol HCl (β2 adrenergic agonist), TNFα, or IL-6 in culture increases glucose oxidation rates independent of the impact on insulin signaling or glucose uptake

Beta‐adrenoceptor responses to inhaled salbutamol in the elderly.

Quantitative determination of cell surface β-adrenoceptors in different rat skeletal muscles

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