1 results match your criteria: "USAThird Institute of OceanographyState Oceanic Administration[Affiliation]"
Glucagon receptor inactivation leads to α-cell hyperplasia in zebrafish.
J Endocrinol
November 2015
Departments of Molecular Physiology and BiophysicsVanderbilt University School of Medicine, Light Hall, Room 711, 2215 Garland Avenue, Nashville, Tennessee 37232, USADivision of DiabetesEndocrinology, and Metabolism, Department of Medicine, Vanderbilt University, Nashville, Tennessee 37232, USAThird Institute of OceanographyState Oceanic Administration, Xiamen 361005, ChinaVeterans Affairs Tennessee Valley Healthcare SystemNashville, Tennessee 37212, USA
Glucagon antagonism is a potential treatment for diabetes. One potential side effect is α-cell hyperplasia, which has been noted in several approaches to antagonize glucagon action. To investigate the molecular mechanism of the α-cell hyperplasia and to identify the responsible factor, we created a zebrafish model in which glucagon receptor (gcgr) signaling has been interrupted.
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