Insulin, secreted by pancreatic beta cells, is the main regulator of blood glucose levels. It inhibits glucose production in the liver, stimulates glucose uptake in muscle and fat, promotes glycogen and lipid synthesis, and inhibits lipolysis. Insulin signaling promotes glucose uptake by activating intracellular signaling pathways that promote translocation of the GLUT4 glucose transporter to the plasma membrane. Additionally, insulin signaling inactivates GSK-3, which keeps Glycogen Synthase active, thereby promoting storage of glucose as glycogen. Insulin signaling can be enhanced or inhibited by adipocytokines secreted by the adipose tissue. The ability of these cytokines to influence insulin signaling suggests that changes in their levels may contribute to the development of insulin-related metabolic disorders such as Type II diabetes. In support of this hypothesis, one of the leading risk factors for Type II diabetes is obesity, a condition characterized by an increase in adipose tissue mass, altered adipocytokine secretion, and chronic inflammation. Obesity is associated with reduced Leptin sensitivity and decreased Adiponectin production, two adipocytokines that normally enhance insulin sensitivity. These changes are coupled with an increase in the production of pro-inflammatory cytokines such as TNF-alpha and IL-6, which can negatively affect adipose tissue functions and promote insulin resistance. Characterizing the mechanisms by which adipocytokines enhance or interfere with insulin signaling pathways is critical to our understanding of how these factors may contribute to the pathogenesis of metabolic disorders.