H
Harvey J. Grill
Researcher at University of Pennsylvania
Publications - 172
Citations - 15156
Harvey J. Grill is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Leptin & Forebrain. The author has an hindex of 63, co-authored 168 publications receiving 13834 citations. Previous affiliations of Harvey J. Grill include Beth Israel Deaconess Medical Center & Rockefeller University.
Papers
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Journal ArticleDOI
Hypophagia induced by salmon calcitonin, but not by amylin, is partially driven by malaise and is mediated by CGRP neurons
Lavinia Boccia,Tito Borner,Misgana Y. Ghidewon,Patricia Kulka,Chiara Piffaretti,Sarah Doebley,Bart C. De Jonghe,Harvey J. Grill,Thomas A. Lutz,Christelle Le Foll +9 more
TL;DR: In this article , the authors investigated the role of calcitonin gene-related peptide (CGRP) lateral parabrachial nucleus (LPBN) neurons in reducing food intake in mice.
Hyperphagic Effects of Brainstem Ghrelin
TL;DR: The results affirm a caudal brainstem site of action and recommend further investigation into multisite interactions underlying the modulation of ingestive behavior by ghrelin.
Journal ArticleDOI
Tim Bartness, Ph.D. (1953-2015)
TL;DR: Tim Bartness was a friend, mentor, collaborator and leader to many scientists, younger and older, across a variety of disciplines, and challenged us to think critically and to laugh heartily about both the bad and the good the authors experienced in life.
Book ChapterDOI
Neural Controls of Energy Homeostasis Caudal to the Forebrain
TL;DR: The forebrain,particularly the hypothalamus, has loomed large in thinking about the neural control of motivational states, particularly the behavioral and autonomic responses of energy balance in mammals.
Journal ArticleDOI
The caudal brainstem is sufficient to mediate inhibition of gastric emptying by peripheral glucagon-like-peptide-1 receptor activation.
Matthew R. Hayes,Harvey J. Grill +1 more
TL;DR: These studies demonstrate that the caudal brainstem is sufficient to mediate GLP-1R-mediated inhibition of GE and that forebrain processing is not required.