Objective: Adipocyte plays important role of maintain whole body energy homeostasis by controlling lipid storage, thermogenesis and adipokine secretion in adipose tissue. Dysfunctional adipose tissue is observed in obese mouse accompanied with adipose tissue inflammation. Mitochondria is the essential role of functional adipose tissue including adipokine secretion. Mitochondria dysfunction in adipose tissue has been reported in obesity, type 2 diabetes, and the metabolic syndrome. However, mitochondrial role in adipocyte inflammation is not elucidated. In this study, we investigated the role of mitochondrial OXPHOS dysfunction in adipocytes in the regulation of adipose tissue homeostasis including immune environment and secretory proteins Methods: To explore the relationship between mitochondrial dysfunction and adipose immune environment, we develop the model of adipose-specific mitochondrial OXPHOS dysfunction by crossing CRIF1-floxed mice with adiponectin-Cre recombinase transgenic mice. These mice fed a normal chow and high fat diet for 10 weeks and 4 weeks, respectively. The metabolic phenotypes of CRIF1f/f,adipoq-Cre (AdKO) and control mice including adipose histology and immune cell population were analyzed using H&E staining and FACS Results: Adipocyte mitochondrial dysfunction mice (CRIF1f/f, adipoq-Cre, AdKO) showed decreased OXPHOS complex subunit expression in adipose tissue. AdKO mice exhibited a 5% reduction in body weight, specifically fat weight was reduced by 2-fold than control mice. Also, change of immune cell population was occurred in eWAT, iWAT of AdKO mice. But AdKO mice did not showed whole body glucose metabolism. However AdKO mice fed a high fat diet showed enhanced glucose tolerance accompanied with altered immune cell population in adipose tissue. Adipocyte derived secretory proteins were upregulated in adipose tissue and these proteins affect macrophage polarization toward M2 property Conclusion: Collectively, adipocyte specific mitochondrial dysfunction mice protects against obesity and insulin resistance. Also mitochondrial dysfunction by CRIF1 deletion induces adipose derived secretory proteins which affect adipose immune environment and it influences whole body glucose homeostasis