Organisms have developed a wide range of sophisticated stress response mechanisms, which act at the cellular or organelle-specific level to restore homeostasis when they experience noxious stimuli. Compromised stress responses contribute to the onset of many human diseases including obesity. Our research aims to identify the molecular components of integration between organelle stress responses that are in play in obesity and diabetes at the cellular and organismic levels. Autophagy is a ubiquitous process in eukaryotic cells that results in the breakdown of damaged or superfluous proteins and organelles within the lysosome to allow cells to adapt to environmental stress. We recently identified that autophagy is an important regulator of hepatic glucose metabolism and insulin signaling, and that loss of autophagy is a critical contributor to the defective ER function characteristic of obesity. We are specifically interested in identifying the physiological causes of defective hepatic autophagy in obesity, and defining the molecular mechanisms underlying how autophagy, as a catabolic pathway, controls energy homeostasis in obesity-associated metabolic disorders.