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The Xiao Lab for Diabetes Research

The Xiao Lab for Diabetes Research

Developing a Better Understanding of Diabetes, Immunology, and Disease Interactions

Produced by pancreatic beta cells, insulin is a key regulator of glucose homeostasis. Insufficient insulin leads to diabetes mellitus, a metabolic disease that affects over 300 million people worldwide. As beta cell replacement can be an efficient therapy for all types of diabetes, Principal Investigator Xiangwei Xiao, MD, PhD, and his research team are exploring the mechanisms that govern beta cell regeneration at both cellular level and molecular level in search of new therapies to prevent and treat diabetes.

Diabetes includes the two most common kinds, type 1 (T1D) and type 2 (T2D), as well as some uncommon types, including chronic pancreatitis-related diabetes (CPRD) and type 3 diabetes (T3D), which has been linked to losses in cognitive function.

The most prevalent form of diabetes, T2D, is believed to result from the loss of sensitivity of other cells to insulin. It is often associated with insulin resistance, inadequate insulin production and secretion by the pancreatic beta cells, beta cell dysfunction, and eventual beta cell loss. Believed to result from autoimmune destruction of the insulin-producing beta cells in the pancreas, T1D is usually diagnosed in children and young adults. While it is accompanied by more severe symptoms and complications than T2D, it constitutes only about 5% of all diabetes cases.

The lab team has found that pancreatic macrophages play a pivotal role in the initiation and progression of diabetes, and it is now dissecting the precise molecular interaction between macrophages and beta cells. Xiao Lab researchers are also trying to develop practical treatments of various diabetes through manipulating macrophages in vivo.

Crosstalk Between Beta Cells and Macrophages

Macrophages mediate the response of beta cells to metabolic needs and inflammatory insults.

Macrophages mediate the response of beta cells to metabolic needs and inflammatory insults.