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.
Highlights
Insulin-like growth factors (IGFs) regulate a very large number of important physiological processes
To test the hypothesis that Insulin-like growth factor 1 (IGF1) expression is increased in other obese mouse-models, we studied mice that had been maintained on a high-fat diet
We examined for IGF1 over-expression efficiency after associated virus (AAV)-GFP and AAV-Igf[1] virus injection in the hypothalamus of the mice using immunostaining and western blot
Summary
Insulin-like growth factors (IGFs) regulate a very large number of important physiological processes. IGF1 has multiple biological effects, including promoting cell growth and proliferation[2] and regulating fuel metabolism peripherally[3]. IGF1 is primarily secreted by the liver and mediates the endocrine actions of growth hormone (GH). GH, the main regulator of circulating IGF1 level in mammals, has an intricate regulatory relationship with IGF1. Mice lacking IGF1 in the liver have shown to display enhanced insulin sensitivity and glucose homeostasis[5]. IGF1 plays an important role in childhood growth and continues to havee brainrowth hormone (GH). Low serum IGF1 levels are associated with reduced insulin sensitivity, metabolic syndrome, glucose intolerance, and the development of type 2 diabetes[9]
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