· Type I diabetes (results from beta cell destruction, usually leading to absolute insulin deficiency).

· Type II diabetes (results from a progressive insulin secretory defect on the background of insulin resistance).

· Gestational diabetes mellitus (GDM) usually temporary condition during pregnancy.

· Other types are due to causes ranging from:

a. generic defects in beta cell function

b. genetic defects in insulin action

c. diseases of the exocrine pancreas

For the purposes of this report, the concentration will be on type II diabetes. Each type

obviously have its own complexities that are unique to it.

Type II diabetes, which is also sometimes known as non-insulin dependent diabetes mellitus (NIDDM) is a “heterogeneous disorder characterized by impaired insulin secretion and reduced tissue sensitivity to insulin” [Rubin]. Within the pancreas, specifically the islets o

Another major adverse effect of hyperglycemia is the production of sorbitol. Increased glucose uptake by insulin independent cells is characterized by the polyol pathway. Glucose + NADH + H+ aldose reductase sorbitol + NAD+.

and consequently can be subject to complex chemical rearrangements forming advanced glycosylation products. These products are responsible for inactivating functional proteins to which the latter proteins are bound and cross-linking of other proteins, contributing to the characteristic thickening of vascular basement membranes in patients with diabetes.

Essential Pathology 3rd Edition: by Emanuel Rubin. Lippincott Williams & Wilkins.

Some topics in this essay:
Type II, NAD+ Sorbitol, Islands Pacific, Antithrombin III, Diabetes Diabetes, Health Organization, Treatment DA, Laura Randal, beta cell, type ii, type ii diabetes, ii diabetes, hyperglycemic condition, cells �, beta cells, skeletal muscle, diabetes mellitus, atp production, Reference List, Wilkins Physiology, � source, cells � source, insulin receptors plasma, mg/dl glucose tolerance, receptors plasma membrane,