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Adropin Enhances Glucose Disposal and Cardiovascular Function in Rats (LB761)
Author(s) -
Stein Lauren,
Samson Willis,
Yosten Gina
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb761
Subject(s) - medicine , endocrinology , glucose homeostasis , receptor , homeostasis , carbohydrate metabolism , basal (medicine) , hormone , energy homeostasis , biology , insulin , chemistry , insulin resistance
Adropin, a hormone encoded by the Energy Homeostasis Associated gene, has been demonstrated in mice to enhance glucose tolerance (Cell Metabolism 8:468, 2008) and in cultured, human endothelial cells to exert a protective role via up‐regulation of endothelial NO synthase expression in a manner consistent with activation of a G protein‐coupled receptor (Circulation 122:S185, 2010). We examined potential effects of adropin in conscious male rats and observed a significant effect of intravenously applied adropin on glucose disposal in a modified glucose tolerance test. A rapid and significant effect of adropin to lower basal glucose levels was observed. A similar dose of adropin, given i.v., significantly elevated mean arterial pressure in unrestrained male rats, with slow onset (circa 7 minutes) and relatively long duration (circa 30 min). Thus in the rat, as in mice, adropin appears to enhance insulin sensitivity and, in the rat at least, cardiovascular actions can be predicted. While existing gene compromise and over expression models also support a role for adropin in glucose homeostasis and metabolism, we believe the ultimate physiologic relevance of the hormone, and all of its potential actions, will be established only once its cognate receptor is identified, its localization mapped and consequences of its deletion determined.