The prevalence of obesity, insulin resistance and type II diabetes (T2DM) continue to rise worldwide. The liver is a central insulin responsive metabolic organ that governs whole-body metabolic homeostasis. Therefore, defining the mechanisms underlying insulin action in the liver is essential to our understanding of the pathogenesis of insulin resistance. My thesis aims to identify the role of the insulin pathway in which the mammalian target of rapamycin complex 1 (mTORC1) controls hepatic phospholipid and glycogen synthesis to maintain metabolic homeostasis, and how these pathways are dysregulated in NAFLD and type 2 diabetes. I explore the hypothesis that mTORC1 has a role in the regulation of phosphatidylcholine and VLDL-TG secretion, and that disruption of these pathways have a key role in the progression of NAFLD. Using transgenic mouse models, our data support literature that suggest that PC deficiency correlates to onset of hepatic fibrosis. Furthermore, I evaluate the role of mTORC1 signaling in glycogen synthesis in the liver to maintain systemic glucose homeostasis. Using unbiased metabolomics and stable isotope tracing, I identify an essential role for mTORC1 in the regulation of postprandial glycogen storage. Taken together, my thesis provides insight to the fundamental pathways downstream of insulin signaling regulating liver metabolism.