Insulin-like growth factor I slows the rate of denervation induced skeletal muscle atrophy

2005 ◽  
Vol 15 (2) ◽  
pp. 139-146 ◽  
Author(s):  
Thea Shavlakadze ◽  
Jason D. White ◽  
Marilyn Davies ◽  
Joseph F.Y. Hoh ◽  
Miranda D. Grounds
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

scholarly journals Insulin-Like Growth Factor-I Gene Transfer by Electroporation Prevents Skeletal Muscle Atrophy in Glucocorticoid-Treated Rats

Endocrinology ◽  
2005 ◽  
Vol 146 (4) ◽  
pp. 1789-1797 ◽  
Author(s):  
O. Schakman ◽  
H. Gilson ◽  
V. de Coninck ◽  
P. Lause ◽  
J. Verniers ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Gene Transfer ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I ◽  
I Gene

scholarly journals Skeletal and cardiac myopathy in HIV-1 transgenic rats

2008 ◽  
Vol 295 (4) ◽  
pp. E964-E973 ◽  
Author(s):  
Anne M. Pruznak ◽  
Ly Hong-Brown ◽  
Rachel Lantry ◽  
Pengxiang She ◽  
Robert A. Frost ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Growth Factor ◽  
Muscle Atrophy ◽  
Cardiac Mass ◽  
Whole Body ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I ◽  
Hiv 1

The mechanism by which human immunodeficiency virus (HIV)-1 infection in humans leads to the erosion of lean body mass is poorly defined. Therefore, the purpose of the present study was to determine whether transgenic (Tg) rats that constitutively overexpress HIV-1 viral proteins exhibit muscle wasting and to elucidate putative mechanisms. Over 7 mo, Tg rats gained less body weight than pair-fed controls exclusively as a result of a proportional reduction in lean, not fat, mass. Fast- and slow-twitch muscle atrophy in Tg rats did not result from a reduction in the in vivo-determined rate of protein synthesis. In contrast, urinary excretion of 3-methylhistidine, as well as the content of atrogin-1 and the 14-kDa actin fragment, was elevated in gastrocnemius of Tg rats, suggesting increased muscle proteolysis. Similarly, Tg rats had reduced cardiac mass, which was independent of a change in protein synthesis. This decreased cardiac mass was associated with a reduction in stroke volume, but cardiac output was maintained by a compensatory increase in heart rate. The HIV-induced muscle atrophy was associated with increased whole body energy expenditure, which was not due to an elevated body temperature or secondary bacterial infection. Furthermore, the atrophic response could not be attributed to the development of insulin resistance, decreased levels of circulating amino acids, or increased tissue cytokines. However, skeletal muscle and, to a lesser extent, circulating insulin-like growth factor I was reduced in Tg rats. Although hepatic injury was implicated by increased plasma levels of aspartate and alanine aminotransferases, hepatic protein synthesis was not different between control and Tg rats. Hence, HIV-1 Tg rats develop atrophy of cardiac and skeletal muscle, the latter of which results primarily from an increased protein degradation and may be related to the marked reduction in muscle insulin-like growth factor I.

scholarly journals Local insulin-like growth factor I prevents sepsis-induced muscle atrophy

Metabolism ◽  
2009 ◽  
Vol 58 (6) ◽  
pp. 787-797 ◽  
Author(s):  
Gerald Nystrom ◽  
Anne Pruznak ◽  
Danuta Huber ◽  
Robert A. Frost ◽  
Charles H. Lang
Keyword(s):  
Growth Factor ◽  
Muscle Atrophy ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

scholarly journals Protective Effect of Pyropia yezoensis Peptide on Dexamethasone-Induced Myotube Atrophy in C2C12 Myotubes

Marine Drugs ◽  
2019 ◽  
Vol 17 (5) ◽  
pp. 284 ◽  
Author(s):  
Min-Kyeong Lee ◽  
Jeong-Wook Choi ◽  
Youn Hee Choi ◽  
Taek-Jeong Nam
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
C2c12 Myotubes ◽  
Protective Effects ◽  
Factor I ◽  
Igf I ◽  
Foxo Signaling Pathway

Dexamethasone (DEX), a synthetic glucocorticoid, causes skeletal muscle atrophy. This study examined the protective effects of Pyropia yezoensis peptide (PYP15) against DEX-induced myotube atrophy and its association with insulin-like growth factor-I (IGF-I) and the Akt/mammalian target of rapamycin (mTOR)-forkhead box O (FoxO) signaling pathway. To elucidate the molecular mechanisms underlying the effects of PYP15 on DEX-induced myotube atrophy, C2C12 myotubes were treated for 24 h with 100 μM DEX in the presence or absence of 500 ng/mL PYP15. Cell viability assays revealed no PYP15 toxicity in C2C12 myotubes. PYP15 activated the insulin-like growth factor-I receptor (IGF-IR) and Akt-mTORC1 signaling pathway in DEX-induced myotube atrophy. In addition, PYP15 markedly downregulated the nuclear translocation of transcription factors FoxO1 and FoxO3a, and inhibited 20S proteasome activity. Furthermore, PYP15 inhibited the autophagy-lysosomal pathway in DEX-stimulated myotube atrophy. Our findings suggest that PYP15 treatment protected against myotube atrophy by regulating IGF-I and the Akt-mTORC1-FoxO signaling pathway in skeletal muscle. Therefore, PYP15 treatment appears to exert protective effects against skeletal muscle atrophy.

scholarly journals Intact Insulin and Insulin-Like Growth Factor-I Receptor Signaling Is Required for Growth Hormone Effects on Skeletal Muscle Growth and Functionin Vivo

Endocrinology ◽  
2005 ◽  
Vol 146 (4) ◽  
pp. 1772-1779 ◽  
Author(s):  
Hyunsook Kim ◽  
Elisabeth Barton ◽  
Naser Muja ◽  
Shoshana Yakar ◽  
Patricia Pennisi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Growth Hormone ◽  
Growth Factor ◽  
Muscle Growth ◽  
Insulin Like Growth Factor ◽  
Receptor Signaling ◽  
Skeletal Muscle Growth ◽  
Factor I ◽  
Hormone Effects ◽  
Growth Factor I

scholarly journals Insulin-like growth factor I stimulates degradation of an mRNA transcript encoding the 14 kDa ubiquitin-conjugating enzyme

1996 ◽  
Vol 319 (2) ◽  
pp. 455-461 ◽  
Author(s):  
Simon S WING ◽  
Nathalie BEDARD
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Binding Proteins ◽  
Mrna Levels ◽  
Insulin Like Growth Factor ◽  
Mrna Transcript ◽  
Factor I ◽  
Igf I ◽  
Ubiquitin Conjugating Enzyme ◽  
Growth Factor I

Upon fasting, the ubiquitin-dependent proteolytic system is activated in skeletal muscle in parallel with the increases in rates of proteolysis. Levels of mRNA encoding the 14 kDa ubiquitin-conjugating enzyme (E214k), which can catalyse the first irreversible reaction in this pathway, rise and fall in parallel with the rates of proteolysis [Wing and Banville (1994) Am. J. Physiol. 267, E39-E48], indicating that the conjugation of ubiquitin to proteins is a regulated step. To characterize the mechanisms of this regulation, we have examined the effects of insulin, insulin-like growth factor I (IGF-I) and des(1–3) insulin-like growth factor I (DES-IGF-I), which does not bind IGF-binding proteins, on E214k mRNA levels in L6 myotubes. Insulin suppressed levels of E214k mRNA with an IC50 of 4×10-9 M, but had no effects on mRNAs encoding polyubiquitin and proteasome subunits C2 and C8, which, like E214k, also increase in skeletal muscle upon fasting. Reduction of E214k mRNA levels was more sensitive to IGF-I with an IC50 of approx. 5×10-10 M. During the incubation of these cells for 12 h there was significant secretion of IGF-I-binding proteins into the medium. DES-IGF-I, which has markedly reduced affinity for these binding proteins, was found to potently reduce E214k mRNA levels with an IC50 of 3×10-11 M. DES-IGF-I did not alter rates of transcription of the E214k gene, but enhanced the rate of degradation of the 1.2 kb mRNA transcript. The half-life of the 1.2 kb transcript was approximately one-third that of the 1.8 kb transcript and can explain the more marked regulation of this transcript observed previously. This indicates that the additional 3´ non-coding sequence in the 1.8 kb transcript confers stability. These observations suggest that IGF-I is an important regulator of E214k expression and demonstrate, for the first time, stimulation of degradation of a specific mRNA transcript by this hormone, while overall RNA accumulates.

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