Skip to Content
Merck
  • Insulin increases reendothelialization and inhibits cell migration and neointimal growth after arterial injury.

Insulin increases reendothelialization and inhibits cell migration and neointimal growth after arterial injury.

Arteriosclerosis, thrombosis, and vascular biology (2009-04-11)
Danna M Breen, Kalam K Chan, Jiwanjeet K Dhaliwall, Michael R Ward, Nael Al Koudsi, Loretta Lam, Melissa De Souza, Husam Ghanim, Paresh Dandona, Duncan J Stewart, Michelle P Bendeck, Adria Giacca
ABSTRACT

Insulin has both growth-promoting and protective vascular effects in vitro, however the predominant effect in vivo is unclear. We investigated the effects of insulin in vivo on neointimal growth after arterial injury. Rats were given subcutaneous control (C) or insulin implants (3U/d;I) 3 days before arterial (carotid or aortic) balloon catheter injury. Normoglycemia was maintained by oral glucose and, after surgery, by intraperitoneal glucose infusion (saline in C). Insulin decreased intimal area (P<0.01) but did not change intimal cell proliferation or apoptosis. However, insulin inhibited cell migration into the intima (P<0.01) and increased expression of smooth muscle cell (SMC) differentiation markers (P<0.05). Insulin also increased reendothelialization (P<0.01) and the number of circulating progenitor cells (P<0.05). These results are the first demonstration that insulin has a protective effect on both SMC and endothelium in vivo, resulting in inhibition of neointimal growth after vessel injury.