New Findings What is the topic of this review?The review covers basic knowledge about the role of mitochondria in the homeostatic function of adipose tissue. It also provide a comprehensive analysis of how mitochondrial function is affected during obesity and lipoatrophies and discuss the results of recent studies that targeted mitochondrial function specifically in adipose tissue or in fat cells and how these interventions affected whole body adiposity and peripheral insulin sensitivity. What advances does it highlight?The review provides specific highlights of the major roles of mitochondria in key metabolic processes that occur in adipose tissue including its role in adipogenesis, adipokine secretion, lipogenesis, fatty acid esterification, branched‐chain amino acid catabolism and lipolysis. Furthermore, we provide the reader with an update on the specific defects that affect mitochondrial function in adipose tissue during obesity and lipoatrophies. Finally, we discuss the latest mouse studies that specifically targeted mitochondrial function in adipose tissue to assess its contribution to the pathogenesis of obesity and insulin resistance. The role of mitochondria in white adipocytes has long been neglected due in part to their lower abundance in these cells. However, accumulating evidence suggests that mitochondria are vital for maintaining metabolic homeostasis in white adipocytes because of their involvement in adipogenesis, fatty acid synthesis and esterification, branched‐chain amino acid catabolism and lipolysis. It is therefore not surprising that white adipose tissue function can be perturbed by altering mitochondrial components or oxidative capacity. Moreover, studies in humans and animals with significantly altered fat mass, such as in obesity or lipoatrophy, indicate that impaired mitochondrial function in adipocytes may be linked directly to the development of metabolic diseases such as diabetes and insulin resistance. However, recent studies that specifically targeted mitochondrial function in adipocytes indicated dissociation between impaired mitochondrial oxidative capacity and systemic insulin sensitivity.