Insulin - A growth hormone

Endocrinology and Diabetes Research Unit, Schneider Children's Medical Center of Israel, WHO Collaborating Center for the Study of Diabetes in Youth, Sackler Faculty of Medicine, Tel Aviv University, Petah Tikva, Israel.
Archives of Physiology and Biochemistry (Impact Factor: 1.76). 03/2008; 114(1):11-6. DOI: 10.1080/13813450801928356
Source: PubMed


Insulin is a peptide hormone with a high degree of homology with the insulin-like growth factor I (IGF-I). Its biological actions are interlaced with those of GH and IGF-I. The objective of this study is to review the growth promoting actions of insulin. The experimental evidence consists of the use of organ cultures of neonatal mice condilar cartilage insulin which stimulates the cartilage cell differentiation and maturation. Injection of insulin to hypohysectomized rats stimulated tibial growth. Clinical evidence is manifold. Babies with diabetes and hypoinsulinemia are short, whereas babies with hyperinsulinism are big. Children with idiopathic short stature have low insulin whereas obese children with hyperinsulinism are tall. Hypo-insulinized children with diabetes slow their growth until the insulin dose is optimized. It remains to be clarified whether insulin exerts its growth promoting actions via its own receptors, via the IGF-I receptors, or via a hybrid (insulin--IGF-I) receptor.

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Available from: Zvi Laron, Dec 29, 2014
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    • "The traditional view is that the metabolic impacts of insulin are primarily achieved through the INSR, while IGFs promote mitogenic effects through the IGF1R. Yet, there is crosstalk between the ligands and receptors, and evidence indicates that insulin and IGFs can induce similar effects on metabolism and growth [11] [12] [13] [14]. Upon ligand binding, INSR and IGF1R are activated through tyrosine kinase-mediated autophosphorylation, thereby stimulating various downstream pathways, the two best-characterized being the PI3K/Akt/mTOR and the mitogen-activated protein kinase (MAPK) pathways, the latter of which involves Ras, Raf, MEK, and ERK signaling molecules. "
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    • "More recently, HCV core protein seems to increase the serine phosphorylation of insulin receptor substrate (IRS)-1 and to activate c-Jun N-terminal kinase signaling and the proteasome activator 28γ, all of which are associated with insulin resistance [28–30]. Such hyperinsulinemia from insulin resistance—by its action on hepatic stellate cells, extracellular matrix, endothelial cells or connective growth factors—not only can accelerate the progression of fibrosis [31, 32], but also can increase accumulation of free fatty acids in the liver, leading to activation of some kinases, such as protein kinase C delta, inhibitor kappa B kinase, JNK, or mammalian target of rapamycin (mTOR) that are known to promote carcinogenesis [33, 34]. "
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