scholarly journals Nutritional dependence of insulin-like growth factor (IGF) receptors in skeletal muscle: measurement by light microscopic autoradiography.

1993 ◽  
Vol 41 (3) ◽  
pp. 415-421 ◽  
Author(s):  
J M Oldham ◽  
A K Hodges ◽  
P N Schaare ◽  
P C Molan ◽  
J J Bass
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Connective Tissue ◽  
Blood Vessels ◽  
Muscle Fiber ◽  
Insulin Like Growth Factor ◽  
Igf Receptors

To determine the cellular location, capacity, and nutritional sensitivity of insulin-like growth factor (IGF) receptors, we measured the in vitro binding of [125I]-IGFs to skeletal muscle using light microscopic autoradiography. Muscle was collected from 8-month lambs that had received high or low nutrition diets (3% and 1.25% of body weight/day in pellets, respectively). Half of each group had also received growth hormone (0.25 mg/kg/day). Cryosections were incubated with [125I]-IGF alone or with unlabeled IGF-1, IGF-2, or insulin to characterize binding sites as probable Type 1 IGF, Type 2 IGF, or insulin receptors. [125I]-IGF-1 was found to bind to blood vessels and Type 1 receptors in connective tissue (p < or = 0.001), but not to muscle fiber or nerves. In muscle from 6-month lambs that were fed or fasted, [125I]-IGF-1 bound to Type 1 receptors in connective tissue (p < or = 0.01 fed; p < or = 0.05 fasted) and muscle fiber (p < or = 0.05). The binding to connective tissue was also greater in fasted than in fed animals (p < or = 0.05). Binding of [125I]-IGF-2 to the Type 2 receptor was located in blood vessels and connective tissue (p < or = 0.01) and did not alter with fasting. Therefore, these experiments have demonstrated that Type 1 and Type 2 receptors vary in their distribution and nutritional sensitivity in skeletal muscle.

1559-P: Differential Effects of Type 1 (T1D) and Type 2 Diabetes (T2D) on the Growth Hormone (GH)-Insulin-Like Growth Factor (IGF) Axis in Youth

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1559-P
Author(s):  
JANET K. SNELL-BERGEON ◽  
JANE E.B. REUSCH ◽  
AMY D. BAUMGARTNER ◽  
MELANIE CREE-GREEN ◽  
KRISTEN J. NADEAU
Keyword(s):  
Type 2 Diabetes ◽  
Growth Hormone ◽  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Differential Effects

scholarly journals Insulin-Like Growth Factor Binding Protein-6 Promotes the Differentiation of Placental Mesenchymal Stem Cells into Skeletal Muscle Independent of Insulin-Like Growth Factor Receptor-1 and Insulin Receptor

2019 ◽  
Vol 2019 ◽  
pp. 1-18 ◽  
Author(s):  
Doaa Aboalola ◽  
Victor K. M. Han
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Growth Factor ◽  
Muscle Differentiation ◽  
Insulin Like Growth Factor ◽  
Differentiation Process ◽  
Placental Mesenchymal Stem Cells

As mesenchymal stem cells (MSCs) are being investigated for regenerative therapies to be used in the clinic, delineating the roles of the IGF system in MSC growth and differentiation, in vitro, is vital in developing these cellular therapies to treat degenerative diseases. Muscle differentiation is a multistep process, starting with commitment to the muscle lineage and ending with the formation of multinucleated fibers. Insulin-like growth factor binding protein-6 (IGFBP-6), relative to other IGFBPs, has high affinity for IGF-2. However, the role of IGFBP-6 in muscle development has not been clearly defined. Our previous studies showed that in vitro extracellular IGFBP-6 increased myogenesis in early stages and could enhance the muscle differentiation process in the absence of IGF-2. In this study, we identified the signal transduction mechanisms of IGFBP-6 on muscle differentiation by placental mesenchymal stem cells (PMSCs). We showed that muscle differentiation required activation of both AKT and MAPK pathways. Interestingly, we demonstrated that IGFBP-6 could compensate for IGF-2 loss and help enhance the muscle differentiation process by triggering predominantly the MAPK pathway independent of activating either IGF-1R or the insulin receptor (IR). These findings indicate the complex interactions between IGFBP-6 and IGFs in PMSC differentiation into the skeletal muscle and that the IGF signaling axis, specifically involving IGFBP-6, is important in muscle differentiation. Moreover, although the major role of IGFBP-6 is IGF-2 inhibition, it is not necessarily the case that IGFBP-6 is the main modulator of IGF-2.

scholarly journals The effect of insulin-like growth factor II on glucose uptake and metabolism in rat skeletal muscle in vitro

1992 ◽  
Vol 286 (2) ◽  
pp. 561-565 ◽  
Author(s):  
S J Bevan ◽  
M Parry-Billings ◽  
E Opara ◽  
C T Liu ◽  
D B Dunger ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Glucose Uptake ◽  
Glycogen Synthesis ◽  
Insulin Like Growth Factor ◽  
Rat Skeletal Muscle ◽  
Factor Ii ◽  
Igf Binding ◽  
Uptake And Metabolism

The effect of insulin-like growth factor II (IGF II) on the rates of lactate formation, glycogen synthesis and glucose transport in the presence of a range of concentrations of insulin were investigated using an isolated preparation of rat skeletal muscle. IGF II, at a concentration of 65 ng/ml, caused a small but significant increase in the rates of these processes at a basal physiological insulin concentration (10 muunits/ml), but was without effect in the presence of 1, 100, 1000 or 10,000 muunits of insulin/ml. Hence IGF II increased the insulin sensitivity of this tissue. This effect was removed if the incubation medium was supplemented with an equimolar concentration of IGF binding protein 1 (BP1). It is suggested that changes in the concentration of IGF II and/or BP1 may regulate glucose uptake and metabolism in skeletal muscle and have physiological significance in the control of blood glucose level.

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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