The Larry L. Hillblom Center for the Immunobiology of Type 2 Diabetes
A chronic low-grade inflammatory state contributes to the co-morbid conditions associated with obesity, including insulin resistance and diabetes. Recent studies indicate that increase in adiposity results in recruitment of macrophages to adipose tissue, leading to tissue inflammation and insulin resistance. However, immune cells are also found in metabolic tissues of lean mice and humans.
These findings lead us to hypothesize that immune cells residing in adipose tissue and liver might directly orchestrate cellular and peripheral metabolism. Thus, to further explore this postulate, we propose to form a new network that will bring together the strengths and expertise of two labs in these disparate areas. Our network is composed of Dr. Chawla’s laboratory at Stanford University and Dr. Richard Locksley’s laboratory at UCSF. This brings together expertise in metabolism and gene regulation (Chawla laboratory) with expertise in tracking of the immune system as it undergoes activation (Locksley laboratory).
This network will address three fundamental questions: what signals lead to recruitment and activation of immune cells in metabolic tissues, how do factors secreted by immune cells regulate glucose metabolism, and how do immune cells control nutrient and energy balance in the context of the whole organism. This will be accomplished by employing genetically modified mice and exploiting highly complementary techniques available in the two laboratories. It is anticipated that insights derived from these studies will identify new cellular and molecular targets to treat inflammation, obesity and diabetes.