Abstract
ABSTRACT: Insulin is a potent mitogen for many cell types in vitro. During tissue culture, supraphysiological concentrations of insulin are necessary to promote cell replication in connective or musculoskeletal tissues. Insulin promotes the growth of these cells by binding, with low affinity, to the type I insulin-like growth factor (IGF) receptor, not through the high affinity insulin receptor. In other cell types, such as hepatocytes, embryonal carcinoma cells, or mammary tumor cells, the type I IGF receptor is virtually absent, and insulin stimulates the growth of these cells at physiological concentrations by binding to the high affinity insulin receptor. Both receptor systems activate phosphorylation reactions within the cell which extend to ribosomal proteins. Insulin acts synergistically with other factors, such as platelet-derived growth factor and epidermal growth factor, to stimulate the progression of cells through the cycle of proliferation. Abnormal insulin secretion or action, before or after birth, often is associated with disordered growth suggesting that insulin may function as a growth factor in vitro. Poor growth follows impaired insulin secretion in diabetes mellitus. This is associated with reduced circulating levels of IGF's which may be partly responsible for the growth failure. Insulin has a direct action on release of IGF's from the liver in vitro. but during experimental diabetes there is a reduced number of hepatic somatotropic receptors which could limit the ability of growth hormone to regulate IGF release. Diabetic children, treated conventionally, have normal circulating IGF levels, but both growth rate and serum IGF concentration may increase dramatically when diabetic control is optimized. Hyperinsulinaemia in the human fetus of a diabetic mother may result in somatic overgrowth as well as adiposity, whereas experimental fetal (animal) hyperinsulinaemia does not result in skeletal overgrowth, and promotes IGF release only at extreme levels. Conversely hypoinsulinemia, with or without nutritional deprivation, is associated with fetal growth retardation accompanied by low circulating IGF levels. It can be concluded that insulin functions as a growth factor in both normal and abnormal development. Insulin promotes the growth of selected tissues by a direct action; in others, such as the musculoskeletal system, the action is indirect via the regulation of IGF release.
Similar content being viewed by others
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Hill, D., Milner, R. Insulin as a Growth Factor. Pediatr Res 19, 879–886 (1985). https://doi.org/10.1203/00006450-198509000-00001
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1203/00006450-198509000-00001
This article is cited by
-
The metastatic spread of breast cancer accelerates during sleep
Nature (2022)
-
The interaction between glycemic index, glycemic load, and the genetic variant ADIPOQ T45G (rs2241766) in the risk of colorectal cancer: a case–control study in a Korean population
European Journal of Nutrition (2022)
-
Local islet remodelling associated with duct lesion–islet complex in adult human pancreas
Diabetologia (2021)
-
Maternal exposure to diluted diesel engine exhaust alters placental function and induces intergenerational effects in rabbits
Particle and Fibre Toxicology (2015)
-
Poor pregnancy outcome after octreotide treatment during pregnancy for familial hyperinsulinemic hypoglycemia: a case report
BMC Research Notes (2014)