Clenbuterol-induced muscle growth: investigation of possible mediation by insulin
| Autor: | M. A. Mcelligott, J. E. Mulder, Lee-Yuh Chaung, A. Barreto |
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| Rok vydání: | 1987 |
| Předmět: |
Agonist
Blood Glucose Male medicine.medical_specialty Normal diet Physiology medicine.drug_class Endocrinology Diabetes and Metabolism medicine.medical_treatment Biology Muscle Development Muscle hypertrophy Cathepsin B Eating Physiology (medical) Diabetes mellitus Internal medicine Acetylglucosaminidase medicine Animals Insulin Clenbuterol Muscles Body Weight Rats Inbred Strains Streptozotocin medicine.disease Rats Endocrinology Ethanolamines medicine.symptom Weight gain medicine.drug |
| Zdroj: | The American journal of physiology. 253(4 Pt 1) |
| ISSN: | 0002-9513 |
| Popis: | The role of insulin as a possible mediator of the beta-adrenergic agonist stimulation of muscle growth was investigated. To exclude possible action of the beta-agonist on the pancreatic release of insulin, diabetes was induced in rats by a streptozotocin injection (100 mg/kg). Insulin levels were almost not detectable in these rats. Feeding either normal diet or diet containing the beta-adrenergic agonist clenbuterol (10 parts/million) did not alter plasma insulin concentrations. The effects of clenbuterol on muscle and weight gain were determined in diabetic rats given daily insulin replacement (D + I) and fed either a normal diet or clenbuterol-treated diet. Clenbuterol, fed for 1 wk, increased the wet weight of the gastrocnemius, soleus, and extensor digitorum longus muscles (15-23%) in both normal and D + I rats. Although clenbuterol increased body weight gain, it did not alter feed consumption and, therefore, feed efficiency (g gain/g food) was improved. Activities of cathepsin B and N-acetyl-beta-glucosaminidase, but not cathepsin D, were elevated in the soleus muscles of clenbuterol-treated rats. The clenbuterol-induced increase in muscle growth in the insulin-replaced diabetic rats indicated that this beta-adrenergic agonist effect was not mediated by an alteration of circulating levels of insulin, secondary to beta-agonist action on pancreatic insulin release. |
| Databáze: | OpenAIRE |
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