Glucose and Weight Control in Mice with a Designed Ghrelin O-Acyltransferase Inhibitor

Brad P. Barnett(Johns Hopkins University), Yousang Hwang(Johns Hopkins University), Martin S. Taylor(Johns Hopkins University), Henriette Kirchner(German Institute of Human Nutrition), Paul T. Pfluger(University of Cincinnati), Vincent Bernard(Johns Hopkins University), Yu-Yi Lin(Johns Hopkins University), Erin M. Bowers(Johns Hopkins University), Chandrani Mukherjee(Johns Hopkins University), Woo‐Jin Song(Johns Hopkins University), Patti A. Longo(Johns Hopkins University), Daniel J. Leahy(Johns Hopkins University), Mehboob A. Hussain(Johns Hopkins University), Matthias H. Tschöp(German Institute of Human Nutrition), Jef D. Boeke(Johns Hopkins University), Philip A. Cole(Johns Hopkins University)
Science
November 19, 2010
Cited by 259

Abstract

Ghrelin is a gastric peptide hormone that stimulates weight gain in vertebrates. The biological activities of ghrelin require octanoylation of the peptide on Ser(3), an unusual posttranslational modification that is catalyzed by the enzyme ghrelin O-acyltransferase (GOAT). Here, we describe the design, synthesis, and characterization of GO-CoA-Tat, a peptide-based bisubstrate analog that antagonizes GOAT. GO-CoA-Tat potently inhibits GOAT in vitro, in cultured cells, and in mice. Intraperitoneal administration of GO-CoA-Tat improves glucose tolerance and reduces weight gain in wild-type mice but not in ghrelin-deficient mice, supporting the concept that its beneficial metabolic effects are due specifically to GOAT inhibition. In addition to serving as a research tool for mapping ghrelin actions, GO-CoA-Tat may help pave the way for clinical targeting of GOAT in metabolic diseases.


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