Disease relevance of Planipart

• Food poisoning following consumption of clenbuterol-treated veal in Italy [1].
• The results showed that the increase in body weight did not differ significantly between the clenbuterol-treated and control groups (P > .5) [2].
• Clenbuterol induces hypertrophy of the latissimus dorsi muscle and heart in the rat with molecular and phenotypic changes [2].
• RNA analyses indicate that ventricles of clenbuterol-treated rats express elevated levels of mRNA to atrial natriuretic factor without a concomitant increase in skeletal alpha-actin and beta-myosin heavy chain, consistent with a "physiological" form of cardiac hypertrophy [2].
• In C6-2B glioma cells, whose NGF expression is induced by BAR agonists, (i) CLE increased C/EBPdelta-binding activity, (ii) NGF mRNA levels were increased by overexpressing C/EBPdelta, and (iii) C/EBPdelta increased the activity of an NGF promoter-reporter construct [3].

Psychiatry related information on Planipart

• Complete tolerance occurred within 4 days to the effects of clenbuterol and salbutamol on lever-pressing ICSS and to the effects of clenbuterol on motor activity [4].
• Repeated administration to rats of desipramine (5 mg kg-1, twice daily for 14 days), clenbuterol (5 mg kg-1, twice daily for 14 days) or electroconvulsive shocks (5 ECS over 10 days) decreased the number of beta-adrenoceptors in the cortex [5].
• The experiments also identified that Clenbuterol activated a very sensitive beta 2-adrenergic system for the regulation of feeding behavior [6].
• Effects of the beta 2-adrenoceptor agonist, clenbuterol, on muscle atrophy due to food deprivation in the rat [7].
• It is considered, therefore, that twice daily regimens of clenbuterol can be as effective as salbutamol given 3-times daily and this may help to improve patient compliance [8].

High impact information on Planipart

• One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values [9].
• The same dose of clenbuterol significantly increased Arc protein levels in the dorsal hippocampus [10].
• Although the NGF promoter contains an AP-1 element, AP-1-binding activity in the cerebral cortex was not induced by CLE, suggesting that other transcription factors govern the brain area-specific induction of NGF [3].
• The beta2-adrenergic receptor agonist clenbuterol has been shown to induce CH without such adverse effects to the rat heart [11].
• In vivo, clenbuterol protected rat hippocampus in a model of transient forebrain ischemia and reduced the infarct volume in a rat model of permanent middle cerebral artery occlusion (MCAo) [12].

Chemical compound and disease context of Planipart

• The serum gamma-globulin fraction from patients with allergic bronchial asthma (8/8), in contrast to the fraction from nonatopic control subjects (10/10), was found to inhibit the positive chronotropic action of the beta 2-selective adrenergic agonist, clenbuterol, on pyruvate- or lactate-treated cultured neonatal rat heart myocytes [13].
• Effects of clenbuterol and propranolol on muscle mass. Evidence that clenbuterol stimulates muscle beta-adrenoceptors to induce hypertrophy [14].
• The effects of repeated electroconvulsive shock (ECS) administration, repeated desmethylimipramine injection (5 mg kg-1, twice daily for 14 days) and acute administration of the beta-adrenoceptor, clenbuterol, on 5-hydroxytryptamine (5-HT)- and dopamine-mediated behaviours in mice have been examined [15].
• Both nifedipine and clenbuterol-induced hypertrophy increased total protein content of the soleus and left ventricle, with no change in protein concentration [16].
• Effects of the cyclo-oxygenase inhibitor, fenbufen, on clenbuterol-induced hypertrophy of cardiac and skeletal muscle of rats [17].

Biological context of Planipart

• CONCLUSIONS: Clenbuterol induces significant hypertrophy of the LDM associated with specific changes in cardiac gene expression [2].
• In the present study, we examined whether clenbuterol was capable of inhibiting apoptosis caused by ischemia [18].
• Importantly, clenbuterol use-dependently inhibited action potential firing in rat skeletal muscle fibers, owing to beta-adrenoceptor-independent I(Na) block [19].
• 5) The results focus on the interest in some beta 2-agonist drugs (zinterol, clenbuterol) as partial inductors of lipolysis, with the lipolytic efficacies of these compounds being well correlated with their efficacies at 125I-labeled CYP sites [20].
• By contrast, the antidepressant-like effect of the beta-2 adrenergic agonist clenbuterol was attenuated by down-regulation of beta-2 adrenergic receptors [21].

Anatomical context of Planipart

• The hypertrophy was more pronounced for hindlimb skeletal muscle (21% to 35% for GPS), and the effects of this relatively high dose of clenbuterol on the heart were less marked (18% to 20% hypertrophy) [2].
• The beta 2-adrenoceptor agonist clenbuterol was used to investigate its potential to selectively induce skeletal muscle hypertrophy, particularly the latissimus dorsi muscle (LDM), independent of adverse effects on cardiac muscle [2].
• Stimulation of beta-adrenoceptors with clenbuterol led to increased NGF synthesis in cultured central nervous system (CNS) cells and rat brain tissue [12].
• Hypertrophy of soleus and plantaris muscles was induced either by severance of the tendon to the synergistic gastrocnemius (tenotomy) or by administration of the beta-adrenoceptor agonist clenbuterol [22].
• Increased association of ribosomes with myofibrils during the skeletal-muscle hypertrophy induced either by the beta-adrenoceptor agonist clenbuterol or by tenotomy [23].

Associations of Planipart with other chemical compounds

• Looking for potential modulation of these channels by beta(2)-adrenergic pathway using patch-clamp technique, we found that clenbuterol blocked sodium currents (I(Na)) in rat skeletal muscle fibers and in tsA201 cells transfected with the human channel isoform, whereas salbutamol did not [19].
• Moreover, in adrenalectomized rats, isoproterenol failed to increase bFGF and NGF mRNA, whereas clenbuterol elicited a 2-fold increase in bFGF mRNA in the cortex and hippocampus [24].
• These changes are characteristic of muscle beta-adrenoceptor stimulation and were abolished by intraperitoneal injection of propranolol (12.5 mg/kg) 15 min before clenbuterol administration [14].
• A comparative study for the enantiomeric separation of terbutaline, clenbuterol, salbutamol and dobutamine was performed by capillary electrophoresis using cyclodextrins and their derivatives as chiral selectors [25].
• The present study was conducted to determine the effect of chronic administration of the long-acting beta(2)-adrenergic agonist clenbuterol on rats that are genetically prone to insulin resistance and impaired glucose tolerance [26].

Gene context of Planipart

• These data show that muscle hypertrophy induced by clenbuterol is associated with a local increase in muscle IGF-I content [27].
• We report herein the effects of the beta-adrenergic agonist clenbuterol on desipramine (DMI)-induced growth hormone (GH), prolactin (PRL) and cortisol secretion in healthy male subjects [28].
• DMI alone caused GH stimulation (mean maximum = 15.7 +/- 3.4 ng/ml), which was significantly lower after combined administration of DMI and clenbuterol (mean maximum = 7.7 +/- 1.6 ng/ml) (p less than or equal to 0.01) [28].
• That for IGFBP3 only exhibited a clenbuterol-induced decrease and a strong negative correlation with the weight of masseter muscle [29].
• RESULTS: The mRNA expression levels for IGF-I and II, IGFR1 and 2, and IGFBP4 and 6 showed clenbuterol-induced elevations and positive correlations with the weight of masseter muscle [29].

Analytical, diagnostic and therapeutic context of Planipart

• Determination of clenbuterol in bovine liver by combining matrix solid-phase dispersion and molecular imprinted solid-phase extraction followed by liquid chromatography/electrospray ion trap multiple-stage mass spectrometry [30].
• Clenbuterol and beta-adrenergic drugs detected in hair of treated animals by ELISA [31].
• Detection of the anabolic beta 2-adrenoceptor agonist clenbuterol in human scalp hair by HPLC/EIA [32].
• Mechanistic study on the opposite migration order of clenbuterol enantiomers in capillary electrophoresis with beta-cyclodextrin and single-isomer heptakis(2,3-diacetyl-6-sulfo)-beta-cyclodextrin [33].
• 2. We measured the mRNA expression levels for TGFbetas, FGFs, HGF, and PDGFs in rat masseter muscle hypertrophied by oral administration of clenbuterol for 3 weeks and determined correlations between the weight of masseter muscle and mRNA expression levels by regression analysis [34].

References