Obesity is the most common nutritional disorder in the developed world and represents a major risk factor for associated diseases like type 2 diabetes mellitus, cardiovascular diseases and hypertension. The condition affects the whole body homeostasis but mainly the adipose tissue and is characterised by low grade inflammation, insulin resistance and hyperlipidemia. In adipocytes, it has been associated with endoplasmic reticulum stress (ER stress) induction and activation of the unfolded protein response (UPR). ER stress has been shown to play a central role in the molecular events leading to inflammation and insulin resistance in obese adipocytes, but the physiological triggers of ER stress are still unknown. The aim of my thesis was to investigate the role of obesity-related factors such as high concentrations of saturated fatty acids, cholesterol, proinflammatory cytokines or tissue remodelling-induced hypoxia and glucose starvation in ER stress induction My results indicate for the first time that glucose starvation and hypoxia, two markers of adipose tissue remodelling in obesity, represent physiological triggers of ER stress in in vitro differentiated 3T3-F442A and 3T3-L1 adipocytes. High concentrations of saturated fatty acid palmitic acid, cholesterol or proinflammatory cytokines (TNFα, IL-6 and IL-1β), although shown to be potent inducers in other cell lines, do not induce ER stress in my model of in vitro differentiated adipocytes. In conclusion, my results suggest that the adipose tissue remodelling process in obesity could play a central role in ER stress induction in adipocytes.