Effects of Caloric Restriction and Growth Hormone Treatment on Insulin‐Related Intermediates in The Skeletal Muscle

2008 ◽  
Vol 22 (S2) ◽  
pp. 116-116
Author(s):  
Khalid A Al‐Regaiey ◽  
Michal M Masternak ◽  
Zhihui Wang ◽  
Jacob Panici ◽  
Andrzej Bartke
1978 ◽  
Vol 234 (1) ◽  
pp. E38 ◽  
Author(s):  
K E Flaim ◽  
J B Li ◽  
L S Jefferson

The role of growth hormone in regulating protein turnover was examined in a perfused preparation of rat skeletal muscle. The perfused muscle maintained in vivo levels of ATP and creatine phosphate and exhibited constant rates of oxygen consumption and protein synthesis. Hypophysectomy reduced the rate of protein synthesis, the concentration of RNA, and the efficiency of protein synthesis in gastrocnemius muscle to 30, 46, and 66 percent of normal, respectively. In vivo treatment of hypophysectomized (hypox) rats with bovine growth hormone (250 microgram/day for 5 days) resulted in small increases in protein synthesis and RNA, whereas synthesis/RNA was returned to near normal. Elevation of ribosomal subunits in psoas muscle indicated an inhibition of peptide-chain initiation in hypox rats that was reversed by in vivo growth hormone treatment. Thus, hypox rats exhibited both a decreased capacity and a decreased efficiency of protein synthesis. Growth hormone replacement primarily increased efficiency of protein synthesis. The rate of protein degradation and the activity of cathepsin D in gastrocnemius muscle were decreased by hypophysectomy. Growth hormone treatment had no significant effect on degradation.


1997 ◽  
Vol 150 ◽  
pp. S178
Author(s):  
A. Leal-Cerro ◽  
J. Guerra ◽  
D. Segura ◽  
I. Chinchón ◽  
E. Rafel ◽  
...  

2002 ◽  
Vol 58 (6) ◽  
pp. 287-291 ◽  
Author(s):  
C. Peyreigne ◽  
E. Raynaud ◽  
C. Fedou ◽  
C. Prefaut ◽  
J.-F. Brun ◽  
...  

2000 ◽  
Vol 231 (4) ◽  
pp. 577-586 ◽  
Author(s):  
Lena Gamrin ◽  
Pia Essén ◽  
Eric Hultman ◽  
Margaret A. McNurlan ◽  
Peter J. Garlick ◽  
...  

1996 ◽  
Vol 315 (3) ◽  
pp. 959-963 ◽  
Author(s):  
Raffaele NAPOLI ◽  
Antonio CITTADINI ◽  
Jesse C. CHOW ◽  
Michael F. HIRSHMAN ◽  
Robert J. SMITH ◽  
...  

Whether skeletal muscle glucose transport system is impaired in the basal, post-prandial state during chronic growth hormone treatment is unknown. The current study was designed to determine whether 4 weeks of human growth hormone (hGH) treatment (3.5 mg/kg per day) would impair glucose transport and/or the number of glucose transporters in plasma membrane vesicles isolated from hindlimb skeletal muscle of Sprague–Dawley rats under basal, post-prandial conditions. hGH treatment was shown to have no effect on glucose influx (Vmax or Km) determined under equilibrium exchange conditions in isolated plasma membrane vesicles. Plasma membrane glucose transporter number (Ro) measured by cytochalasin B binding was also unchanged by hGH treatment. Consequently, glucose transporter turnover number (Vmax/Ro), a measure of average glucose transporter intrinsic activity, was similar in hGH-treated and control rats. hGH did not change GLUT4 protein content in whole muscle or in the plasma membrane, and muscle content of GLUT4 mRNA also was unchanged. In contrast, GLUT1 protein content in the plasma membrane fraction was significantly reduced by hGH treatment. This was associated with a modest, although not significant, decrease in muscle content of GLUT1 mRNA. In conclusion, high-dose hGH treatment for 4 weeks did not alter post-prandial skeletal muscle glucose transport activity. Neither the muscle level nor the intracellular localization of GLUT4 was changed by the hormone treatment. On the contrary, the basal post-prandial level of GLUT1 in the plasma membrane was reduced by hGH. The mRNA data suggest that this reduction might result from a decrease in the synthesis of GLUT1.


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