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Patricia L. Brubaker

Researcher at University of Toronto

Publications -  198
Citations -  15783

Patricia L. Brubaker is an academic researcher from University of Toronto. The author has contributed to research in topics: Glucagon-like peptide-2 & Glucagon-like peptide-1. The author has an hindex of 68, co-authored 191 publications receiving 14810 citations. Previous affiliations of Patricia L. Brubaker include Toronto General Hospital.

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Induction of intestinal epithelial proliferation by glucagon-like peptide 2

TL;DR: It is demonstrated that nude mice bearing subcutaneous proglucagon-producing tumors exhibit marked proliferation of the small intestinal epithelium, defining a novel biological role for GLP-2 as an intestinal-derived peptide stimulator of small bowel epithelial proliferation.
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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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Minireview: Glucagon-Like Peptides Regulate Cell Proliferation and Apoptosis in the Pancreas, Gut, and Central Nervous System

TL;DR: This article showed that glucagon-like peptides (GLP-1 and GLP-2) directly regulate signaling pathways coupled to cell proliferation and apoptosis, which may be mediated by direct or indirect effects on target cells.
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Role of the vagus nerve in mediating proximal nutrient-induced glucagon-like peptide-1 secretion.

TL;DR: The results of these experiments demonstrate that the secretion of GLP-1 and gGLI from the ileal L cell in response to fat is regulated by a complex neuroendocrine loop, involving the enteric nervous system, the afferent and efferent vagus nerves, as well as the duodenal hormone GIP.
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TCF-4 Mediates Cell Type-specific Regulation of Proglucagon Gene Expression by β-Catenin and Glycogen Synthase Kinase-3β

TL;DR: It is shown that β-catenin and the glycogen synthase kinase-3β inhibitor lithium do not activate glu mRNA or glu promoter expression in pancreatic cell lines, and stable introduction of dominant-negative TCF-4 into the GLUTag cell line repressed basal glu RNA expression and abolished the effect of lithium onglu mRNA expression and GLP-1 synthesis.