Obesity, Diabetes, and Metabolic tissue engineering

lab members

Our research is focused on the roles of extracellular matrix (ECM) proteins and proteinases in the pathogenesis of obesity, insulin resistance and metabolic syndrome. In the body, metabolically active cells are surrounded by a fibrous composite of extracellular matrix proteins (e.g., type I collagen, elastin, and fibronectin). While being embedded within these dense matrices, adipocytes and their precursor cells constantly change their shape and function in adaptation to nutritional cues by remodeling pericellular ECM environment. We have identified a novel role played by a membrane-type matrix metalloproteinase, MMP14, in the regulation of obesity and diabetes (Chun et al., Diabetes 2010). MMP14-dependent collagen degradation promotes the epigenetic histone modifications necessary for adipogenesis (Sato-Kusubata et al., Mol. Endocrinol. 2011). Most recently we have identified a novel role played by thrombospondin-1 (THBS1) in the pathogenesis of insulin resistance and tissue fibrosis (Inoue et al., Endocrinology 2013 and Matsuo et al, Metabolism 2015). We also have characterized fat depot-dependent ECM remodeling mediated by the distinct expression profile of adipose stem cell population in each fat depot (Tokunaga et al., Matrix Biology 2014). 
In collaboration with researchers of tissue engineering, material sciences, and stem cell biology at Biointerfaces Institute of NCRC (Moraes C et al., Integr Biol 2013), our group aims to develop human metabolic network on-a-chip to dissect the critical crosstalk that regulates human metabolism.
Our lab is now located at NCRC Building 20, part of Biointerfaces Institute

Publication Link


  • August, 2015. Masashi Hasebe, a medical student from Kyoto University, joined the lab for summer research internship. Welcome, Masa!
  • Mar 13, 2015. Published a paper that demonstrates a novel role of the exocyst complex in regulating free fatty acid uptake. Inoue et al., The Exocyst complex regulates fatty acid uptake by adipocytes. PLoS ONE, 2015 Mar. 10(3): e0120289

Methods and Reviews
Chun TH, Inoue M. 3-D adipocyte differentiation and peri-adipocyte collagen turnover. Methods Enzymol. 2014;538:15-34.