Fibroblast activation protein (FAP) as a novel metabolic target
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- 作者：Miguel Angel Sá ; nchez-Garrido1 ; 2 ; 3 ; Kirk M. Habegger4 ; Christoffer Clemmensen1 ; 2 ; 3 ; Cassie Holleman4 ; Timo D. Mü ; ller1 ; 2 ; 3 ; Diego Perez-Tilve5 ; Pengyun Li7 ; Archita S. Agrawal7 ; Brian Finan1 ; 2 ; 3 ; Daniel J. Drucker6 ; Matthias H. Tschö ; p1 ; 2 ; 3 ; Richard D. DiMarchi7 ; rdimarch@indiana.edu" class="auth_mail" title="E-mail the corresponding author ; Alexei Kharitonenkov7 ; alexkhar@indiana.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：FAP ; FGF21 ; DPP4 ; Metabolic regulation ; Obesity ; Diabetes
- 刊名：Molecular Metabolism
- 出版年：2016
- 出版时间：October 2016
- 年：2016
- 卷：5
- 期：10
- 页码：1015-1024
- 全文大小：1002 K
文摘
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Pharmacological inhibition of FAP reduces weight, improves glucose and lipid metabolism in obese, but not lean mice.
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FAP inhibitor Talabostat at higher doses lessens food intake, without any apparent adverse effects in short term studies.
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Obese FGF21 deficient mice did not exhibit meaningful change in metabolic regulation when treated with Talabostat.
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The mechanism of Talabostat in vivo action appears to center on an increase in total and active levels of plasma FGF21.
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FAP inhibition alone, or in combination with DPP4 is proposed as a novel approach to treat metabolic diseases.