There is an ongoing worldwide obesity epidemic. As a consequence, prevalence of obesity- related diseases and conditions are rapidly increasing. One of these related conditions is type 2 diabetes (T2D), which alone caused 1.5 million deaths in 2012. Thus, it is of upmost importance to develop a more complete understanding of these interrelated diseases. At the heart of all these diseases lies the adipose tissue. This tissue is a major endocrine organ, and one of the key secreted cytokines is adiponectin. Adiponectin interplays with the complex insulin signaling network, and adiponectin levels are inversely related with increased adiposity. The presence of these complex dependencies argues for the usage of mathematical modelling. In the work of Brännmark et al, a model of short-term adiponectin release has been validated. However, this model did not include adrenergic signaling, which is the canonical pathway for in situ regulation of adiponectin secretion. To fill this gap, herein, a mechanistic model describing adrenaline-induced short-term adiponectin exocytosis in white adipocytes has been constructed. The newly constructed model is capable of describing experimental data depicting adiponectin release due to adrenergic stimulation as well as data for different mediator combinations. By implementing adrenergic receptor components, the transition to a more physiological model has been initiated. By finding the smallest possible model capable of describing data, one can argue that the model depicts, to some degree, the fundamental mechanisms for short-term adiponectin secretion. Thus, this work has contributed to solidifying the framework of the mechanisms behind short-term adiponectin secretion from white adipocytes. The result of the model work upholds the role of adrenergic signaling as a central regulatory mechanism for adiponectin release. The constructed model could be used as a fundament for creating a model describing adiponectin release under diabetic conditions.