Recent studies have provided evidence that mitochondrial dysfunction and endoplasmic reticulum (ER) stress are major pathogenic factors for diabetes and its complications. Mitochondria are the most important source of the chemical energy required by cells. Regulation of mitochondrial metabolism of glucose and fatty acids, the primary fuels used by cells to produce ATP, has been the subject of intensive research for several decades. In spite of this, much remains to be learned about tissue-specific fuel selection and the pathogenesis of diabetes and its complications. Cellular homeostasis also clearly depends upon the functional relationship between mitochondria and the ER. Propagation of calcium signaling from ER to mitochondria is involved in both ATP production and cell death. On the other hand, the ER requires ATP to function properly, which may make it the best site for sensing metabolic stress.

The goal of this special issue will be to clearly document the roles of mitochondrial dysfunction and ER stress in the pathogenesis of diabetes and its complications. The genesis of skeletal muscle insulin resistance, impaired hepatic glucose and lipid metabolism, beta-cell failure, and vascular dysfunction will be covered. Priority would be given to the regulation of mitochondrial metabolism of glucose and fatty acid, interaction between mitochondria and ER, and newer aspects of mitochondrial biology including mitochondrial biogenesis, mitochondrial dynamics (fission and fusion), and mitochondrial autophagy. Potential topics include, but are not limited to:

• Roles of mitochondrial dysfunction and ER stress in the pathogenesis of diabetes, microvascular complications of diabetes, atherosclerosis, and nonalcoholic fatty liver disease
• Tissue-specific fuel selection
• Interaction between mitochondria and ER
• Mitochondrial biogenesis, fission, fusion, or autophagy in diabetes
• Metabolomics analysis

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/jdr/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable: