scholarly journals Effects of insulin-like growth factor I on the rates of glucose transport and utilization in rat skeletal muscle in vitro

1992 ◽  
Vol 287 (3) ◽  
pp. 1023-1023
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Glucose Transport ◽  
Insulin Like Growth Factor ◽  
Rat Skeletal Muscle ◽  
Factor I ◽  
Growth Factor I

scholarly journals Effects of insulin-like growth factor I on the rates of glucose transport and utilization in rat skeletal muscle in vitro

1992 ◽  
Vol 285 (1) ◽  
pp. 269-274 ◽  
Author(s):  
G Dimitriadis ◽  
M Parry-Billings ◽  
S Bevan ◽  
D Dunger ◽  
T Piva ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Glucose Transport ◽  
Glycogen Synthesis ◽  
Insulin Like Growth Factor ◽  
Rat Skeletal Muscle ◽  
Factor I ◽  
Igf I ◽  
Lactate Formation

1. The effects of insulin-like growth factor I (IGF-I) on the rates of glucose transport and utilization and its interaction with insulin were investigated in rat soleus muscle in vitro. IGF-I increased the rates of glucose transport, lactate formation, glycogen synthesis and the flux of glucose to hexose monophosphate, but it had no effect on the rate of glucose oxidation or glycogenolysis. 2. In the absence of insulin, low levels of IGF-I (0-30 ng/ml) increased the rate of glycolysis and the content of fructose 2,6-bisphosphate, but the content of glucose 6-phosphate remained unaltered; at higher levels of IGF-I (300-3000 ng/ml) the rate of glycolysis and the content of fructose 2,6-bisphosphate showed a further modest increase, but the content of glucose 6-phosphate doubled. Similar changes were seen when the level of insulin was increased from basal (0-0.4 ng/ml) to maximal (40 ng/ml). 3. Neither IGF-I nor insulin affected the contents of ATP, ADP, AMP, phosphocreatine or citrate. 4. Maximal concentrations of IGF-I increased the rate of lactate formation to a greater extent than did maximal concentrations of insulin. 5. In the presence of IGF-I, the rate of glucose utilization was less responsive to insulin. 6. The results suggest that, in rat skeletal muscle: (a) IGF-I increases the rates of glucose transport and utilization independently of insulin, and has a preferential effect on the rate of lactate formation; (b) the effects of IGF-I and insulin are not additive; (c) in addition to its effects on glucose transport, IGF-I increases the rate of glycogen synthesis and may stimulate glycolysis at the level of 6-phosphofructokinase; (d) changes in the content of fructose 2,6-bisphosphate may be part of the mechanism to regulate glycolytic flux in skeletal muscle in response to either IGF-I or insulin.

Growth hormone regulates the level of insulin-like growth factor-I mRNA in rat skeletal muscle

1989 ◽  
Vol 120 (1) ◽  
pp. 107-112 ◽  
Author(s):  
J. Isgaard ◽  
A. Nilsson ◽  
K. Vikman ◽  
O. G. P. Isaksson
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Rat Heart ◽  
Insulin Like Growth Factor ◽  
Rat Skeletal Muscle ◽  
Maximum Increase ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Dose Dependent

ABSTRACT Levels of mRNA for the insulin-like growth factor-I (IGF-I) in rat heart and skeletal muscle and its dependence on GH were investigated using a solution hybridization assay. Levels of IGF-I mRNA decreased following hypophysectomy, and replacement therapy with human GH (hGH) normalized heart and skeletal muscle levels. The stimulatory effect of hGH was dose-dependent, the lowest effective dose being 100 μg. A significant increase of IGF-I mRNA was observed 60 min after s.c. administration of 100 μg hGH and the maximum increase was apparent 6–12 h after hGH injection. Administration of 200 μg IGF-I or 11 μg insulin did not significantly change levels of IGF-I mRNA. The results show that GH regulates the level of IGF-I mRNA in rat heart and skeletal muscle and give further support to the hypothesis that locally produced IGF-I might be a local mediator for the direct stimulatory effect of GH on the growth and development of heart and skeletal muscle. Journal of Endocrinology (1989) 120, 107–112

scholarly journals Viral expression of insulin-like growth factor I E-peptides increases skeletal muscle mass but at the expense of strength

2014 ◽  
Vol 306 (8) ◽  
pp. E965-E974 ◽  
Author(s):  
Becky K. Brisson ◽  
Janelle Spinazzola ◽  
SooHyun Park ◽  
Elisabeth R. Barton
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Muscle Mass ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Insulin-like growth factor I (IGF-I) is a protein that regulates and promotes growth in skeletal muscle. The IGF-I precursor polypeptide contains a COOH-terminal extension called the E-peptide. Alternative splicing in the rodent produces two isoforms, IA and IB, where the mature IGF-I in both isoforms is identical yet the E-peptides, EA and EB, share less than 50% homology. Recent in vitro studies show that the E-peptides can enhance IGF-I signaling, leading to increased myoblast cell proliferation and migration. To determine the significance of these actions in vivo and to evaluate if they are physiologically beneficial, EA and EB were expressed in murine skeletal muscle via viral vectors. The viral constructs ensured production of E-peptides without the influence of additional IGF-I through an inactivating mutation in mature IGF-I. E-peptide expression altered ERK1/2 and Akt phosphorylation and increased satellite cell proliferation. EB expression resulted in significant muscle hypertrophy that was IGF-I receptor dependent. However, the increased mass was associated with a loss of muscle strength. EA and EB have similar effects in skeletal muscle signaling and on satellite cells, but EB is more potent at increasing muscle mass. Although sustained EB expression may drive hypertrophy, there are significant physiological consequences for muscle.

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