This study examines the role of Tmem117 in AVP neurons concerning the counterregulatory response to hypoglycemia. The findings indicate that Tmem117 is expressed in AVP magnocellular neurons, and its inactivation leads to increased AVP secretion during hypoglycemia, resulting in higher glucagon levels in male mice, with effects dependent on the estrous cycle phase in female mice.
Inactivation of Tmem117 in AVP neurons increased AVP and glucagon secretion in response to hypoglycemia. This effect was sex-dependent, observed in male mice and during the proestrus phase in female mice. Tmem117 inactivation increased ER stress, ROS production, and intracellular calcium levels, leading to enhanced AVP production and secretion.
Tmem117fl/fl conditional Knockout mouse model generated by homologous recombination in embryonic stem cells. The model includes a FLEx system for exon 3 targeting, flanked by loxP sites and a mutated loxP variant for Cre-dependent deletion monitoring.
Hypoglycemia, Counterregulatory response, Vasopressin neurons, Glucagon secretion, ER stress, ROS production
Conditional Knockout mouse model, FLEx technology, LoxP sites, Cre recombinase system, AVP neuron-specific inactivation, ER stress assessment, ROS measurement, Intracellular calcium imaging
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
