Open Access<p>Obesity of G2e3 Knockout Mice Suggests That Obesity-Associated Variants Near Human G2E3 Decrease G2E3 Activity</p>
Author(s) -
David R. Powell,
Deon Doree,
Christopher M. DaCosta,
Kenneth A. Platt,
Gwenn M. Hansen,
Isaac Van Sligtenhorst,
ZhiMing Ding,
JeanPierre Revelli,
Robert Brommage
Publication year - 2020
Publication title -
diabetes, metabolic syndrome and obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.853
H-Index - 43
ISSN - 1178-7007
DOI - 10.2147/dmso.s259546
Subject(s) - medicine , endocrinology , weaning , obesity , glucose homeostasis , biology , knockout mouse , single nucleotide polymorphism , gene , insulin resistance , genetics , receptor , genotype
In humans, single nucleotide polymorphisms (SNPs) near the adjacent protein kinase D1 ( PRKD1 ) and G2/M-phase-specific E3 ubiquitin protein ligase ( G2E3 ) genes on chromosome 14 are associated with obesity. To date, no published evidence links inactivation of either gene to changes in body fat. These two genes are also adjacent on mouse chromosome 12. Because obesity genes are highly conserved between humans and mice, we analyzed body fat in adult G2e3 and Prkd1 knockout (KO) mice to determine whether inactivating either gene leads to obesity in mice and, by inference, probably in humans.