Adrenergic control of protein metabolism in skeletal muscle

被引:57
作者
Navegantes, LCC
Migliorini, RH
Kettelhut, ID
机构
[1] Univ Sao Paulo, Dept Biochem & Immunol, Sch Med Ribeirao Preto, BR-14049900 Ribeirao Preto, SP, Brazil
[2] Univ Sao Paulo, Dept Physiol, Sch Med, BR-14049900 Ribeirao Preto, SP, Brazil
关键词
D O I
10.1097/00075197-200205000-00007
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
This review summarizes evidence indicating that the sympathetic nervous system, through hormonal and neurotransmitter actions, produces anabolic, protein-sparing effects on skeletal muscle protein metabolism. Studies are reviewed which indicate that catecholamines secreted by the adrenal medulla have an inhibitory effect on muscle Ca2+-dependent protein degradation independently of other hormones. In addition, norepinephrine released from adrenergic terminals may increase the rate of protein synthesis in oxidative muscles, leading to increased protein accretion. Evidence is also presented that these effects seem to be mediated by beta(2)-adrenoceptors and cyclic adenosine monophosphate-dependent pathways, The understanding of the precise mechanisms by which endogenous catecholamines promote muscle anabolic effects may bring new perspectives for efficient treatment of muscle-wasting conditions and enhancement of growth efficacy in farm species. (C) 2002 Lippincott Williams Wilkins.
引用
收藏
页码:281 / 286
页数:6
相关论文
共 55 条
[1]   Calcium influx through calcium leak channels is responsible for the elevated levels of calcium-dependent proteolysis in dystrophic myotubes [J].
Alderton, JM ;
Steinhardt, RA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (13) :9452-9460
[2]   Metabolic interrelationships between liver and skeletal muscle in pathological states [J].
Argilés, JM ;
Busquets, S ;
López-Soriano, FJ .
LIFE SCIENCES, 2001, 69 (12) :1345-1361
[3]   Changes in intracellular calpastatin localization are mediated by reversible phosphorylation [J].
Averna, M ;
de Tullio, R ;
Passalacqua, M ;
Salamino, F ;
Pontremoli, S ;
Melloni, E .
BIOCHEMICAL JOURNAL, 2001, 354 :25-30
[4]   EFFECT OF BETA-AGONISTS ON EXPRESSION OF CALPAIN AND CALPASTATIN ACTIVITY IN SKELETAL-MUSCLE [J].
BARDSLEY, RG ;
ALLCOCK, SMJ ;
DAWSON, JM ;
DUMELOW, NW ;
HIGGINS, JA ;
LASSLETT, YV ;
LOCKLEY, AK ;
PARR, T ;
BUTTERY, PJ .
BIOCHIMIE, 1992, 74 (03) :267-273
[5]   Calpain-3 gene expression is decreased during experimental cancer cachexia [J].
Busquets, S ;
García-Martínez, C ;
Alvarez, B ;
Carbó, N ;
López-Soriano, FJ ;
Argilés, JM .
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, 2000, 1475 (01) :5-9
[6]   EFFECT OF CLENBUTEROL ON RECOVERY OF MUSCLE MASS AND CARCASS PROTEIN-CONTENT FOLLOWING EXPERIMENTAL HYPERTHYROIDISM IN OLD RATS [J].
CARTER, WJ ;
LYNCH, ME .
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-PHYSIOLOGY, 1994, 108 (2-3) :387-394
[7]  
Chen KD, 2001, MUSCLE NERVE, V24, P211, DOI 10.1002/1097-4598(200102)24:2<211::AID-MUS60>3.3.CO
[8]  
2-4
[9]   MUSCLE WASTING ASSOCIATED WITH ENDOTOXEMIA IN THE RAT - MODIFICATION BY THE BETA-2-ADRENOCEPTOR AGONIST CLENBUTEROL [J].
CHOO, JJ ;
HORAN, MA ;
LITTLE, RA ;
ROTHWELL, NJ .
BIOSCIENCE REPORTS, 1989, 9 (05) :615-621
[10]   ANABOLIC EFFECTS OF CLENBUTEROL ON SKELETAL-MUSCLE ARE MEDIATED BY BETA(2)-ADRENOCEPTOR ACTIVATION [J].
CHOO, JJ ;
HORAN, MA ;
LITTLE, RA ;
ROTHWELL, NJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 263 (01) :E50-E56