ArticlePflugers Archiv : European journal of physiology2006
CL 316,243, a selective beta3-adrenergic agonist, inhibits protein breakdown in rat skeletal muscle.
Article in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- The β3 Adrenergic Receptor Agonist CL316243 Ameliorates the Metabolic Abnormalities of High-Fat Diet-Fed Rats by Activating AMPK/PGC-1α Signaling in Skeletal Muscle.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- CL316,243, a β3-adrenergic receptor agonist, induces muscle hypertrophy and increased strength.Scientific reports · 2016Article
- CL316,243, a selective β3-adrenoceptor agonist, activates protein translation through mTOR/p70S6K signaling pathway in rat skeletal muscle cells.Pflugers Archiv : European journal of physiology · 2013Article
- Comparative effects of oleoyl-estrone and a specific beta3-adrenergic agonist (CL316, 243) on the expression of genes involved in energy metabolism of rat white adipose tissue.Nutrition & metabolism · 2010Article
- Expression profiling of skeletal muscle following acute and chronic beta2-adrenergic stimulation: implications for hypertrophy, metabolism and circadian rhythm.BMC genomics · 2009Article
- Beta3-adrenoceptor agonist stimulation of the Na+, K+ -pump in rat skeletal muscle is mediated by beta2- rather than beta3-adrenoceptors.British journal of pharmacology · 2006Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The in vitro effect of CL 316,243 (CL), a selective beta3-adrenoceptor agonist in the rate of overall proteolysis, the activity of proteolytic systems (lysosomal, Ca2+-dependent, ATP-dependent, and ATP-independent) and in the process of protein synthesis was investigated in rat skeletal muscles. The rate of overall proteolysis in soleus muscle from rats incubated with CL (10(-4) and 10(-5) M) or epinephrine (10(-5) M) was significantly decreased. In vitro rates of maximal activity of Ca2+-dependent proteolysis in soleus muscles were decreased by about 41% in the presence of 10(-5) M CL. No change was observed in the activities of the lysosomal, ATP-dependent or ATP-independent proteolytic systems. The anti-proteolytic effect of CL or epinephrine was partially prevented by 10(-5) M SR 59230A, a selective beta3-adrenoceptor antagonist. The increase of proteolysis induced by food deprivation in soleus was abolished by in vitro addition of 10(-5) M CL. No change in proteolysis was observed in extensor digitorum longus (EDL) muscles incubated with any concentration of the beta3-adrenoceptor agonist tested. Rates of protein synthesis were not affected by 10(-4) M CL neither in soleus nor EDL. The data suggest that a beta3-adrenoceptor-mediated inhibition of Ca2+-dependent proteolysis participates of the antiproteolytic effect of catecholamines in oxidative muscles.
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