Fibroblast activation protein enzyme deficiency prevents liver steatosis, insulin resistance and glucose intolerance and increases fibroblast growth factor-21 in diet induced obese mice

  title={Fibroblast activation protein enzyme deficiency prevents liver steatosis, insulin resistance and glucose intolerance and increases fibroblast growth factor-21 in diet induced obese mice},
  author={Sumaiya Islam Chowdhury and Sunmi Song and Hui Emma Zhang and Xin Maggie Wang and Margaret G. Gall and Denise Ming Tse Yu and Angelina J. Lay and Michelle Sui Wen Xiang and Kathryn A Evans and S Wetzel and Yolanda Liu and Belinda Yau and Andrew L. Coppage and Lisa W-Y Lo and Rebecca A. Stokes and Wayne J. Hawthorne and Gregory J. Cooney and Susan V. Mclennan and Jenny E. Gunton and William W. Bachovchin and Nigel Turner and Melkam A. Kebede and Geoffrey W McCaughan and Stephen Morris Twigg and Mark D. Gorrell},
Background & Aims Fibroblast activation protein-a (FAP) is a post-proline peptidase closely related to dipeptidyl peptidase-4. FAP degrades bioactive peptides including fibroblast growth factor-21 (FGF-21) and neuropeptide Y. We examined metabolic outcomes of specific genetic ablation of FAP and its enzyme activity in a mouse model of diet-induced obesity (DIO) causing fatty liver. Methods Wildtype (WT) and genetically modified FAP deficient mice that specifically lacked either the FAP protein… 
2 Citations
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This study greatly expands the repertoire of FAP substrates and shows that FAP has a role in coagulation in the mouse and provides insight into the physiological and potential pathological roles of this enigmatic protease.


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