Insulin resistance is a major characteristic of obesity and type 2 diabetes and develops in multiple organs, including the heart. Compared to other organs, the physiological role of cardiac insulin resistance is not well understood. The heart uses lipid as a primary fuel, but glucose becomes an important source of energy in ischemia. The impaired ability to utilize glucose may contribute to cell death and abnormal function in the diabetic heart. Recent discoveries on the role of inflammation, mitochondrial dysfunction, and ER stress in obesity have advanced our understanding of how insulin resistance develops in peripheral organs. This review will apply these findings to the diabetic heart to provide new insights into the mechanism of cardiac insulin resistance.