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We have reported a correlation between hypothalamic expression of Creb-binding protein ( Cbp ) and lifespan, and that inhibition of  Cbp  prevents protective effects of dietary restriction during aging, suggesting that hypothalamic  Cbp  plays a role in responses to nutritional status and energy balance. Recent GWAS and network analyses have also implicated  Cbp  as the most connected gene in protein-protein interactions in human Type 2 diabetes. The present studies address mechanisms mediating the role of  Cbp  in diabetes by inhibiting hypothalamic  Cbp  using a Cre-lox strategy. Inhibition of hypothalamic  Cbp  results in profound obesity and impaired glucose homeostasis, increased food intake, and decreased body temperature. In addition, these changes are accompanied by molecular evidence in the hypothalamus for impaired leptin and insulin signaling, a shift from glucose to lipid metabolism, and decreased  Pomc  mRNA, with no effect on locomotion. Further assessment of the significance of the metabolic switch demonstrated that enhanced expression of hypothalamic  Cpt1a , which promotes lipid metabolism, similarly resulted in increased body weight and reduced  Pomc  mRNA.

Role of Hypothalamic Creb-Binding Protein in Obesity and Molecular Reprogramming of Metabolic Substrates