M
Mark A. Magnuson
Researcher at Vanderbilt University
Publications - 260
Citations - 32767
Mark A. Magnuson is an academic researcher from Vanderbilt University. The author has contributed to research in topics: Glucokinase & Insulin. The author has an hindex of 100, co-authored 249 publications receiving 30668 citations. Previous affiliations of Mark A. Magnuson include Ninewells Hospital & University of Texas Southwestern Medical Center.
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Journal ArticleDOI
PDX-1 is required for pancreatic outgrowth and differentiation of the rostral duodenum
Martin F. Offield,T. L. Jetton,Patricia A. Labosky,Michael Ray,Roland Stein,Mark A. Magnuson,Brigid L.M. Hogan,Christopher V.E. Wright +7 more
TL;DR: The pdx-1/beta-galactosidase fusion allele is expressed in pancreatic and duodenal cells in the absence of functional PDX-1, with expression continuing into perinatal stages with similar boundaries and expression levels, and offers additional insight into the role of p dx-1 in the determination and differentiation of the posterior foregut.
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Loss of Insulin Signaling in Hepatocytes Leads to Severe Insulin Resistance and Progressive Hepatic Dysfunction
M. Dodson Michael,Rohit N. Kulkarni,Catherine Postic,Steven F. Previs,Gerald I. Shulman,Mark A. Magnuson,C. Ronald Kahn +6 more
TL;DR: In this paper, the Cre-loxP system was used to inactivate the insulin receptor gene in hepatocytes, and the effect of the loss of direct insulin action in liver was investigated.
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Dual roles for glucokinase in glucose homeostasis as determined by liver and pancreatic beta cell-specific gene knock-outs using Cre recombinase.
Catherine Postic,Masakazu Shiota,Kevin D. Niswender,T. L. Jetton,Yeujin Chen,J. M. Moates,Kathy D. Shelton,Jill Lindner,Alan D. Cherrington,Mark A. Magnuson +9 more
TL;DR: These studies indicate that deficiencies in both β cell and hepatic GK contribute to the hyperglycemia of MODY-2, and suggest that heterozygous null for GK, either globally or just in the β cell, survive but are moderately hyperglycemic.
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Tissue-Specific Knockout of the Insulin Receptor in Pancreatic β Cells Creates an Insulin Secretory Defect Similar to that in Type 2 Diabetes
Rohit N. Kulkarni,Jens C. Brüning,Jonathon N. Winnay,Catherine Postic,Mark A. Magnuson,C R Kahn +5 more
TL;DR: An important functional role for the insulin receptor in glucose sensing by the pancreatic beta cell is indicated and it is suggested that defects in insulin signaling at the level of the beta cell may contribute to the observed alterations in insulin secretion in type 2 diabetes.
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Thiazolidinediones expand body fluid volume through PPARγ stimulation of ENaC-mediated renal salt absorption
You Fei Guan,Chuan-Ming Hao,Dae Ryong Cha,Reena Rao,Wendell J. Lu,Donald E. Kohan,Donald E. Kohan,Donald E. Kohan,Mark A. Magnuson,Reyadh Redha,Yahua Zhang,Matthew D. Breyer,Matthew D. Breyer +12 more
TL;DR: It is shown that mice treated with TZDs experience early weight gain from increased total body water, and it is suggested amiloride might provide a specific therapy.