ABSTRACT
This chapter will briefly discuss human diabetic neuropathy and retinopathy and address various abnormalities in animal models of these diabetic complications and how they may enter into the complex pathogenetic web of this disorder. It addresses structural, biochemical, and functional changes in diabetic retinopathy. Diabetes and its complications are problems of enormous proportion. Both diabetic and galactosemic animals have been used as models for diabetic retinopathy. Diabetic neuropathy can be broadly classfied as mononeuropathy or polyneuropathy. Mononeuropathies can involve isolated single nerves or may affect multiple nerves. Nonenzymatic modification of tissue proteins by physiological hexoses in vivo is an important secondary mechanism in the pathogenesis of diabetic retinopathy. Animal experiments have been important in understanding the pathology and pathogenesis of human diabetic retinopathy. Experiments in animal diabetes have demonstrated that hyperglycemia is the primary insult in the pathogenesis of diabetic retinopathy. Retinal structural lesions have been produced in both diabetic and galactosemic animals.
