E
Eva B. Nygaard
Researcher at University of Copenhagen
Publications - 7
Citations - 1214
Eva B. Nygaard is an academic researcher from University of Copenhagen. The author has contributed to research in topics: FGF21 & Receptor. The author has an hindex of 7, co-authored 7 publications receiving 1037 citations. Previous affiliations of Eva B. Nygaard include Novo Nordisk.
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Journal ArticleDOI
Brown adipose tissue regulates glucose homeostasis and insulin sensitivity
Kristin I. Stanford,Roeland J.W. Middelbeek,Kristy L. Townsend,Ding An,Eva B. Nygaard,Kristen M. Hitchcox,Kathleen R. Markan,Kazuhiro Nakano,Michael F. Hirshman,Yu-Hua Tseng,Laurie J. Goodyear +10 more
TL;DR: A previously under-appreciated role for BAT in glucose metabolism is revealed, demonstrating that BAT-derived IL-6 is required for the profound effects of BAT transplantation on glucose homeostasis and insulin sensitivity.
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Increased fibroblast growth factor 21 expression in high-fat diet-sensitive non-human primates ( Macaca mulatta )
TL;DR: This study demonstrates that HFD changes FGF 21 and FGF21 receptor expression in a tissue-specific manner in rhesus monkeys; differential regulation is moreover observed between HFD-sensitive and -resistant monkeys.
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Transcriptional and Functional Characterization of the G Protein-Coupled Receptor Repertoire of Gastric Somatostatin Cells
Kristoffer L. Egerod,Maja S. Engelstoft,Mari L. Lund,Kaare V. Grunddal,Mirabella Zhao,Dominique Barir-Jensen,Eva B. Nygaard,Natalia Petersen,Jens J. Holst,Thue W. Schwartz +9 more
TL;DR: A comprehensive map of receptors through which SST secretion is regulated by hormones, neurotransmitters, neuropeptides and metabolites that act directly on the SST cells in the gastric mucosa is provided.
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Metformin stimulates FGF21 expression in primary hepatocytes.
TL;DR: The study shows that meetformin is a potent inducer of hepatic FGF21 expression and that the effect of metformin seems to be mediated through AMPK activation, which might play an important role in met formin's antidiabetic effect.
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NHE1 inhibition by amiloride- and benzoylguanidine-type compounds. Inhibitor binding loci deduced from chimeras of NHE1 homologues with endogenous differences in inhibitor sensitivity.
TL;DR: It is concluded that regions within TM4 and TM10–11 contribute to amiloride and HOE sensitivity, with both regions imparting partial inhibitor sensitivity to NHE1.