Objective: The molecular mechanism by which obesity and type 2 diabetes develops is not fully understood. We have shown that bromodomain containing protein 7 (BRD7) levels are significantly reduced in the liver of genetically obese ob/ob and high fat diet (HFD)-induced obese mouse models. The objective of this study is to understand the association between the onset of obesity and type 2 diabetes and discover whether reduced BRD7 in the liver is a risk factor for developing obesity and consequent glucose intolerance and insulin resistance. Methods: We generated a heterozygous whole body BRD7 knockout mouse model and liver-specific BRD7 knockout mouse model. We placed them on a normal chow diet (NCD) and also challenged them with a HFD for 22 weeks. We monitored various parameters of glucose metabolism. Results: Both the heterozygous whole body BRD7 knockout mouse model and the liver-specific BRD7 knockout mouse model resulted in increased body weights with no significant difference in their food intake, which was further augmented when mice were challenged with HFD. Blood glucose levels and hepatic triglyceride levels were significantly higher in both animal lines compared to their control animals. However, BRD7 deficiency did not lead to disturbed glucose tolerance and insulin resistance. Lack of BRD7 led to decreased phosphorylation of glycogen synthase kinase 3b (GSK3b) in response to activation of the insulin receptor signaling pathway following insulin stimulation and the nutrient-sensing pathway after feeding conditions. Of interest, BRD7 mediated phosphorylation of GSK3b can occur independent of AKT activity in the insulin signaling pathway. Conclusion: Our results provide the first evidence that BRD7 is involved in the development of obesity and the insulin signaling pathway.