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Theodore J. Brown

Researcher at Lunenfeld-Tanenbaum Research Institute

Publications -  139
Citations -  7910

Theodore J. Brown is an academic researcher from Lunenfeld-Tanenbaum Research Institute. The author has contributed to research in topics: Receptor & Estrogen. The author has an hindex of 44, co-authored 138 publications receiving 7537 citations. Previous affiliations of Theodore J. Brown include Iowa State University & Mount Sinai Hospital.

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Glucose intolerance but normal satiety in mice with a null mutation in the glucagon-like peptide 1 receptor gene.

TL;DR: It is demonstrated that GLP1 plays a central role in the regulation of glycemia; however, disruption of GLP 1/GLP1R signaling in the central nervous system is not associated with perturbation of feeding behavior or obesity in vivo.
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Estrogen receptors colocalize with low-affinity nerve growth factor receptors in cholinergic neurons of the basal forebrain.

TL;DR: Colocalization of estrogen and low-affinity nerve growth factor receptors implies that their ligands may act on the same neuron, perhaps synergistically, to regulate the expression of specific genes or gene networks that may influence neuronal survival, differentiation, regeneration, and plasticity.
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A Recombinant Human Glucagon-Like Peptide (GLP)-1–Albumin Protein (Albugon) Mimics Peptidergic Activation of GLP-1 Receptor–Dependent Pathways Coupled With Satiety, Gastrointestinal Motility, and Glucose Homeostasis

TL;DR: Findings illustrate that peripheral administration of a larger peptide-albumin recombinant protein mimics GLP-1R-dependent activation of central and peripheral pathways regulating energy intake and glucose homeostasis in vivo.
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Oxyntomodulin and glucagon-like peptide-1 differentially regulate murine food intake and energy expenditure.

TL;DR: It is demonstrated that structurally distinct PGDPs differentially regulate food intake and energy expenditure by interacting with a GLP-1R-dependent pathway.
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Corticotropin-Releasing Factor, But Not Corticosterone, Is Involved in Stress-Induced Relapse to Heroin-Seeking in Rats

TL;DR: It is suggested that CRF, a major brain peptide involved in stress, contributes to relapse to heroin-seeking induced by stressors.