The secondary sequelae of diabetes are believed to result from insulin deficiency and hyperglycemia and may be diminished by good control of blood glucose. One of several mechanisms by which hyperglycemia can produce secondary complications is a direct, non-enzymatic glycosylation of proteins. Glucose can directly modify some proteins and thereby alter their function. The proposed study will examine the diabetic lens and the peripheral nerve to determine how an increased incidence of modified proteins is related to hyperglycemia. The modifying sugar and/or metabolite will be identified. The modified proteins will be studied for their relation to the impairment of normal tissue function. Proteins in the lens which have an increased incidence of glycosylation will be studied for their role in cataract formation. Those in the nerve, particularly in the myelin portion, will be studied for their relation to conduction velocity and cell membrane metabolism. Electrophoresis, gradient centrifugation and amino acid analysis will be employed to test whether protein glycosylation can relate some complications of diabetes to hyperglycemia. A positive correlation of protein glycosylation to hyperglycemia and to functional impairment of the lens or nerve would reinforce the importance of good control and provide a basis for the study of the reversal of diabetic sequelae.