D
Diego Perez-Tilve
Researcher at University of Cincinnati Academic Health Center
Publications - 120
Citations - 10449
Diego Perez-Tilve is an academic researcher from University of Cincinnati Academic Health Center. The author has contributed to research in topics: Ghrelin & Receptor. The author has an hindex of 48, co-authored 116 publications receiving 8743 citations. Previous affiliations of Diego Perez-Tilve include University of Cincinnati & University of Vigo.
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Journal ArticleDOI
Glucagon-like peptide 1 (GLP-1)
Timo D. Müller,Brian Finan,Stephen R. Bloom,David A. D'Alessio,Daniel J. Drucker,Peter R. Flatt,Andreas Fritsche,Fiona M. Gribble,Harvey J. Grill,Joel F. Habener,Jens J. Holst,Wolfgang Langhans,Juris J. Meier,Michael A. Nauck,Diego Perez-Tilve,Alessandro Pocai,Frank Reimann,Darleen A. Sandoval,Thue W. Schwartz,Randy J. Seeley,Kerstin Stemmer,Mads Tang-Christensen,Stephen C. Woods,Richard D. DiMarchi,M.H. Tschöp +24 more
TL;DR: The numerous beneficial effects of GLP-1 render this hormone an interesting candidate for the development of pharmacotherapies to treat obesity, diabetes, and neurodegenerative disorders.
Journal ArticleDOI
A new glucagon and GLP-1 co-agonist eliminates obesity in rodents
Jonathan Day,Nickki Ottaway,James Patterson,Vasily M. Gelfanov,David L. Smiley,Jas Gidda,Hannes M. Findeisen,Dennis Bruemmer,Daniel J. Drucker,Nilika Chaudhary,Jenna Holland,Jazzminn Hembree,William Abplanalp,Erin Grant,Jennifer Ruehl,Hilary Wilson,Henriette Kirchner,Sarah Kathleen Haas Lockie,Susanna M. Hofmann,Stephen C. Woods,Rubén Nogueiras,Paul T. Pfluger,Diego Perez-Tilve,Richard D. DiMarchi,Matthias H. Tschöp +24 more
TL;DR: Preclinical studies indicate that when full GLP-1 agonism is augmented with an appropriate degree of glucagon receptor activation, body fat reduction can be substantially enhanced without any overt adverse effects.
Journal ArticleDOI
Unimolecular Dual Incretins Maximize Metabolic Benefits in Rodents, Monkeys, and Humans
Brian Finan,Brian Finan,Tao Ma,Nickki Ottaway,Timo D. Müller,Kirk M. Habegger,Kristy M. Heppner,Henriette Kirchner,Jenna Holland,Jazzminn Hembree,Christine Raver,Sarah Kathleen Haas Lockie,David L. Smiley,Vasily M. Gelfanov,Bin Yang,Susanna M. Hofmann,Dennis Bruemmer,Daniel J. Drucker,Paul T. Pfluger,Paul T. Pfluger,Diego Perez-Tilve,Jaswant Gidda,Louis Vignati,Lianshan Zhang,Jonathan Hauptman,Michele Lau,Mathieu Brecheisen,Sabine Uhles,William Riboulet,Emmanuelle Hainaut,Elena Sebokova,Karin Conde-Knape,Anish Konkar,Richard D. DiMarchi,Matthias H. Tschöp,Matthias H. Tschöp +35 more
TL;DR: This discovery and validation of a balanced and high-potency dual incretin agonist enables a more physiological approach to management of diseases associated with impaired glucose tolerance and represents a new class of drug candidates for the treatment of metabolic diseases.
Journal ArticleDOI
A rationally designed monomeric peptide triagonist corrects obesity and diabetes in rodents
Brian Finan,Bin Yang,Nickki Ottaway,David L. Smiley,Tao Ma,Christoffer Clemmensen,Joseph Chabenne,Lianshan Zhang,Kirk M. Habegger,Katrin Fischer,Jonathan E. Campbell,Darleen A. Sandoval,Randy J. Seeley,Konrad Bleicher,Sabine Uhles,William Riboulet,Jürgen Funk,Cornelia Hertel,Sara Belli,Elena Sebokova,Karin Conde-Knape,Anish Konkar,Daniel J. Drucker,Vasily M. Gelfanov,Paul T. Pfluger,Timo D. Müller,Diego Perez-Tilve,Richard D. DiMarchi,Matthias H. Tschöp +28 more
TL;DR: It is demonstrated that these individual constituent activities harmonize to govern the overall metabolic efficacy, which predominantly results from synergistic glucagon action to increase energy expenditure, GLP-1 action to reduce caloric intake and improve glucose control, and GIP action to potentiate the incretin effect and buffer against the diabetogenic effect of inherent glucagon activity.
Journal ArticleDOI
Hypothalamic fatty acid metabolism mediates the orexigenic action of ghrelin.
Miguel López,Ricardo Lage,Asish K. Saha,Diego Perez-Tilve,María del Carmen Saavedra Vázquez,Luis M. Varela,Susana Sangiao-Alvarellos,Sulay Tovar,Kawtar Raghay,Sergio Rodriguez-Cuenca,Rosangela Deoliveira,Tamara R. Castañeda,Rakesh Datta,Jesse Z. Dong,Michael D. Culler,Mark W. Sleeman,Clara V. Alvarez,Rosalía Gallego,Christopher J. Lelliott,David Carling,Matthias H. Tschöp,Carlos Dieguez,Antonio Vidal-Puig +22 more
TL;DR: Modulation of hypothalamic fatty acid metabolism specifically in the VMH in response to ghrelin is a physiological mechanism that controls feeding, and decreasing AMPK activity in the ventromedial nucleus of the hypothalamus (VMH) is sufficient to inhibit gh Relin's effects on FAS expression and feeding.