Obesity is a net result of an imbalance between energy intake and expenditure. AMP-dependent protein kinase (AMPK) is an enzyme that plays a role in energy homeostasis. AMPK is activated in response to an increase in the AMP/ATP ratio under low nutrient conditions. These functions are partly mediated by its role in glucose sensing by hypothalamic neurons. SAD-A, also known as BRSK2 (Brain Specific Kinase 2) is exclusively expressed in the brain and pancreas and is a serine/theronine protein kinase related to the AMPK family of kinases. In order to understand the role of Sad-A in energy metabolism, tissue specific knockout of the Sad-A gene was generated using a Cre-lox mediated approach in Pomc neurons, a cell type primarily involved in food intake and energy metabolism. Pomc-cre+/null mice were bred with Sad-Aflox/flox mice to generate a Pomc neuron-specific Sad-A knockout line. The generation of tissue specific Sad-A knockout line was confirmed by genotyping. Metabolic studies were conducted using the genetically modified Sad-A knockout mouse line to determine its role in energy and glucose homeostasis.
