SOMATOMEDINS = Insulin-like factors promoting growth

[Nicholas Cheong]

I have a doubt.

Growth hormone (GH) antagonizes actions of insulin, thus increasing glucose levels in blood. Another fact is that GH effects/actions are mostly mediated  by insulin-like growth factor (IGF). But why does IGF cause hypoglycemia? "Shouldn't" it cause hyperglycemia, since it is supposed to mediate the actions of GH? Going by its name, I understand why IGF causes hypoglycemia. But since it is also known as somatomedin, "shouldn't' it cause hyperglycemia like GH?  Please enlighten me.

GH is lipolytic while IGF is antilipolytic - another confusion for me.

Attached is the diagram showing the correlation of GH and IGF obtained from Ganong.

Thank you for your help.

Joyce Lim

MBBS Batch 15 (Year 2)



Dear Joyce,

Insulin-like growth factors are thus named because it has functional and structural similarities with Insulin.  IGF’s and insulin cross react with each others’ receptors. Some tissues express hybrid receptors that combine insulin and IGF-I receptor subunits.

Since insulin facilitates glucose entry into cells, one would expect IGF to do the same.

IGF was initially named somatomedin…mediator of somatotropin (GH) because of its action on the bones and cartilage, and not so much because of its actions on the intermediary metabolism.

We can say that IGF-1 is a growth promoting hormone and its metabolic actions appear similar to that of insulin. I'd like to think of IGF's as insulin-like factors which promote growth.

IGF’s or somatomedins have an inhibitory effect on GH secretion by stimulating somatostatin release from the neuroendocrine neurons of the periventricular nucleus of the hypothalamus. If IGF is reduced for whatever reasons, the negative feedback on GH secretion is lost and GH secretion increases. GH increases glucose output and decreases insulin sensitivity.  There is a compensatory increase of insulin secretion by the endocrine pancreas, giving rise to a hyperinsulinemic state. What we see here is a case of insulin resistance (elevated basal as well as glucose-induced insulin levels but normal glucose levels). What is worse is that the pancreas might be overworked due to excess GH secretion and pancreatic beta cells might be damaged. The significance of this is that, decreased IGF production or defective IGF signaling may predispose an individual to diabetes. And IGF-1 administration could be an option for treatment of DM type-2.

Experimental rats with deleted IGF genes show hyperinsulinemic state. http://diabetes.diabetesjournals.org/content/50/7/1539.full

The antilipolytic effect was demonstrated by the deletion of IGF genes in lab rats. These rats appeared leaner. This implies that IGF is lipogenic.

In experimental rats with deleted IGF genes, leptin levels were found to be increased. Leptin is known to decrease adiposity ( one way it does so is by acting on higher center to decease appetite).

In these rats, IGF’s produced by liver were absent. Hence Insulin may surge secondary to GH oversecretion. Insulin has been shown to increase plasma leptin.(please follow the link I have included above for further reading)

Dr Prakash will be able to provide a better explanation. In the mean time, I hope this helps a little.

All the best,

Nicholas Cheong

MBBS Batch 14 (Year 3)