This study investigate the role of the neurokinin 2 receptor in regulating energy expenditure and feedinf behaviors. The researchers aimed to determine whether activating NK2R coul simultaneously decrease food intake and increase energy expendityre, offering a dual approach to counteracting cardiometabolic diseases such as obesity and type 2 diabetes.
Activation of NK2R led to a significant decrease in food intake and an increase in energy expenditure in the mouse models. These findings suggest that NK2R could be a viable therapeutic target for treating metabolic diseases by addressing both dides of the energy balance equation.
The study utiliszed genetically engineered mouse models developed in collaboration with genOway. These models were designed to specifically manipulate NK2R expression in targeted tissues, allowing for precise assessment of NK2R's role in metablolic processes. The technical specifications include tissues-specific promoters driving NK2R expression and the incorporation of reporter genes to faciliate tracking and quantification of receptor activity.
Metabolic diseases, Obesity, Type 3 diabetes, Energy expenditure, Appetite regulation
Knockin, Tissue-specific epression, Reporter gene
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
