Diabetes mellitus (DM) is one of the most common diseases in the world population, associated with obesity, pancreatic endocrine changes, cardiovascular disease, renal glomerular disease, cerebrovascular disease, peripheral neuropathy, neurodegenerative disease, retinal disease, sleep apnea, some of which are bundled into the metabolic syndrome. The main characteristic of this disease is hyperglycemia, and often with albuminuria. Nevertheless, the classic features, with ketoacidosis in the extreme, are only a first layer of description of this condition. The description of the islet cells of the endocrine pancreas was first described by Opie, and the discovery of insulin by tying off the exocrine pancreatic ducts followed. We later find that the β-cells secrete insulin and glucagon, which synchronously stimulate or suppress glycogenolysis, and that insulin is essential for glucose intake into the cell. There are yet two other layers for our understanding of diabetes and the effects of its dysfunction, which is the basis for understanding the system-wide expression of the disease. We describe the molecular basis for the central nervous system neuropathic diseases that are associated with both Type 1 DM (T1DM) and Type 2 DM (T2DM), but more so with T2DM. T2DM is an autoimmune disease that destroys the insulin secreting islet cells. T2DM is the diabetes that is associated with an imbalance in the glucagon/insulin homeostasis that leads to the formation of amyloid deposits in the brain, pancreatic islet cells, and possibly the kidney glomerulus.
Keywords: Diabetes mellitus; endoplasmic reticulum; mitochondria; neurodegeneration; stress.
© 2017 Wiley Periodicals, Inc.