J
Joel K. Elmquist
Researcher at University of Texas Southwestern Medical Center
Publications - 245
Citations - 51441
Joel K. Elmquist is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Leptin & Hypothalamus. The author has an hindex of 105, co-authored 235 publications receiving 47755 citations. Previous affiliations of Joel K. Elmquist include University of Utah & Beth Israel Deaconess Medical Center.
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Journal ArticleDOI
Monitoring FoxO1 localization in chemically identified neurons.
Makoto Fukuda,Juli E. Jones,David P. Olson,Jennifer W. Hill,Charlotte E. Lee,Laurent Gautron,Michelle J. Choi,Jeffrey M. Zigman,Bradford B. Lowell,Joel K. Elmquist +9 more
TL;DR: A reporter mouse for monitoring PI3K-Akt signaling in specific populations of neurons, based on FoxO1 nucleocytoplasmic shuttling, is developed and found that insulin treatment resulted in the nuclear exclusion of FoxO 1GFP within POMC and AgRP neurons in a dose- and time-dependent manner.
Journal ArticleDOI
Induction of Leptin Resistance by Activation of cAMP-Epac Signaling
TL;DR: It is found that elevation of adenosine 3', 5'-monophosphate levels impairs multiple signaling cascades activated by leptin within the hypothalamus, and activation of hypothalamic cAMP-Epac pathway is sufficient to induce multiple indices of leptin resistance.
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PANIC-ATTAC: A Mouse Model for Inducible and Reversible β-Cell Ablation
Zhao V. Wang,James Mu,Todd Schraw,Todd Schraw,Laurent Gautron,Laurent Gautron,Joel K. Elmquist,Joel K. Elmquist,Bei B. Zhang,Michael Brownlee,Philipp E. Scherer,Philipp E. Scherer +11 more
TL;DR: The PANIC-ATTAC mouse may be used as an animal model of inducible and reversible β- cell ablation and therefore has applications in many areas of diabetes research that include identification of β-cell precursors, evaluation of glucotoxicity effects in diabetes, and examination of pharmacological interventions.
Journal ArticleDOI
Leptin: Less Is More.
TL;DR: The underlying conceptual steps that led to the exploration of partial leptin reduction as a viable therapeutic avenue are discussed and it is hoped this discussion will contribute to potential future applications ofpartial leptin reduction therapy for the treatment of obesity and type 2 diabetes.
Journal ArticleDOI
PPARγ in Vagal Neurons Regulates High-Fat Diet Induced Thermogenesis
Chen Liu,Angie L. Bookout,Syann Lee,Kai Sun,Lin Jia,Charlotte E. Lee,Swalpa Udit,Yingfeng Deng,Philipp E. Scherer,David J. Mangelsdorf,Laurent Gautron,Joel K. Elmquist +11 more
TL;DR: In conclusion, this study systematically profiled the expression of all known nuclear receptors in laser-captured nodose ganglion (NG) neurons and found PPARγ expression was reduced by high-fat-diet feeding, suggesting that the reduction ofPPARγ in NG neurons may serve as a protective mechanism against diet-induced weight gain.