Insulin-like growth factor 1 (IGF1) is a key factor for tissue growth and fuel metabolism. The potential function of central IGF1 remains unclear. We previously observed that IGF1 expression is increased in the hypothalamus of obese mice lacking STAT5 in the central nervous system (CNS). In this study, we explored the potential metabolic function of central IGF1 by intracerebroventricular (ICV) injection of IGF1, over-expression of central IGF1 by administering an adeno-associated virus (AAV), and ICV injection of an anti-IGF1 antibody. Mice that over-expressed central IGF1 displayed increased appetite, improved glucose tolerance and insulin sensitivity, decreased Pomc levels in the hypothalamus, and increased UCP1 expression in brown fat tissue. This is the first study demonstrating that central IGF1 regulates several important metabolic functions.

Central IGF1 improves glucose tolerance and insulin sensitivity in mice

Rossi M;
2017

Abstract

Insulin-like growth factor 1 (IGF1) is a key factor for tissue growth and fuel metabolism. The potential function of central IGF1 remains unclear. We previously observed that IGF1 expression is increased in the hypothalamus of obese mice lacking STAT5 in the central nervous system (CNS). In this study, we explored the potential metabolic function of central IGF1 by intracerebroventricular (ICV) injection of IGF1, over-expression of central IGF1 by administering an adeno-associated virus (AAV), and ICV injection of an anti-IGF1 antibody. Mice that over-expressed central IGF1 displayed increased appetite, improved glucose tolerance and insulin sensitivity, decreased Pomc levels in the hypothalamus, and increased UCP1 expression in brown fat tissue. This is the first study demonstrating that central IGF1 regulates several important metabolic functions.
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11697/180181
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 22
  • ???jsp.display-item.citation.isi??? 23
social impact