The brain utilizing mechanisms of glucose for neuronal functions are still poorly understood. To identify a unified model of blood-brain glucose metabolism, we developed a model that incorporates the pancreatic β-cell and the fishbone models of glucose metabolism and called it the CoBBGluM Model (or the Convergence model of Blood-Brain Glucose Metabolism) and examined the role of addictive substances (alcohol, cocaine etc) on the functions of the model.

The databases of Pubmed, Elsevier were searched for peer reviewed literatures (from 1950-2009yy) on the mechanisms and models of blood-brain glucose metabolism.

The major concept of the unified model is based on the fact that the major regulators (leptin and insulin) of blood-brain glucose metabolism work synergistically, rather than individually. Addictive substances adversely affect the blood-brain glucose transport system by their stimulating and toxic action on the control mechanisms of leptin and insulin. The metabolic byproducts of addictive substances might acquire electron-transmitter properties across mitochondrial membranes. All these processes subsequently lead to total equilibrium disorder of the CoBBGluM Model, and is the etiopathogenetic basis of most addiction-associated neurodegenerative disorders. Adequate therapies for addiction might lie on the full understanding of the CoBBGluM Model, since it serves a classical tool for explaining the role of addictive substances in the nervous system.