Project Description:

The classic ACE/AngII/AT₁ receptor axis of the Renin Angiotensin System (RAS) regulates cardio­vascular and metabolic functions. Blockade of AT₁ receptors prevents development of obesity by normalizing energy homeo­stasis via leptin, brain, and gut related mechanisms. An alternative RAS pathway (ACE2/Ang(1-7)/Mas) is estab­lished to also be involved although it remains unknown whether due to an adipocyte or brain related mecha­nism. We aim to investigate tissue specificity by using transgenic mouse models with an adipocyte and brain selective overexpression or deficiency of Mas or Ang(1-7). We further want to clarify whether the Ang(1-7)-dependent weight loss after ARB treatment is not only related to Mas but also to MrgD receptors.

Experimental Methods:

• Working with genetically modified mice including breeding strategies
• Chronic treatment of animals with drugs
• Phenotyping of mice including measurement of blood pressure, heart rate, glucose control, energy expenditure, body weight and fat mass
• Multiplex, ELISA, RIA analyses of adipokines and endocrine parameters
• DNA and RNA extraction
• PCR, qPCR (e.g. for analyzing components of the RAS in different tissue)