This invention describes a method of treatment of type-2 diabetes using activators of adipose-resident type 1 natural killer T (NKT) such as lipid antigens and cytokines that promote M2 macrophage polarization.
Approximately 29.1 million people in the U.S. are living with diabetes in 2012, that being 9.3% of the population. 95% of them suffer from type 2 diabetes mellitus, the most common form of diabetes.
The present method offers a breakthrough in treatment options for diabetes patients. Cornell researchers discovered that adipose tissue contains a unique and previously unidentified population of lipid-sensing NKT cells that play a key role in modulating immune cell response, macrophage polarization, and glucose homeostasis. This population of CD1d-restricted type 1 NKT cells has been shown to decrease while the body mass index and glucose intolerance increase consequently (Fig.1). Thus, it is proven that the activation of these NKT cells is able to lead to the reduction of inflammation in the adipose environment and improve glucose homeostasis.
In experiments, the method significantly improved glucose tolerance in diet-induced obesity mice (HFD) that received a lipid antigen such as α-galactosylceramide (αGalCer). The inventors demonstrated that the effect of α-GalCer was NKT cells-depend (Fig.2) and HFD mice challenged with α-GalCer had an improved glucose tolerance, approaching the LFD level (Fig.3).由于技术保密工作限制,技术信息无法完全展现,请通过邮箱或短信联系我们,获取更多技术资料。
cornell researchers discovered
body mass index
diet-induced obesity mice
glucose intolerance increase
improved glucose tolerance