The New York Diabetes Association's 48th Annual Scientific Meeting, the American Diabetes Association's 48th Annual Advanced Postgraduate Course, and the meeting of the Naomi Berry Diabetes Center of Columbia University.

Abstract

This report covers the New York Diabetes Association’s 48th Annual Scientific Meeting, October 2000; the Meeting of the Naomi Berry Diabetes Center of Columbia University, December 2000; and the American Diabetes Association’s 48th Annual Advanced Postgraduate Course, January 2001, New York, New York. Topics include diabetic retinopathy, diabetic nephropathy, the cell biology of insulin action, and islet cell transplantation. At the 48th Annual Scientific Meeting of the Gerald J. Friedman Symposium on October 28, 2000, in New York, NY, Lloyd P. Aiello, Boston, MA, discussed potential pharmacologic treatments of diabetic retinopathy. Diabetic retinopathy is a major cause of blindness and visual loss, acting via two complications, proliferative retinopathy, which leads to retinal hemorrhage and scarring with the inevitable development of traction detachment, and that of macular edema, which is caused by abnormalities of retinal vessels. Panretinal photocoagulation, the existing treatment, is less effective for macular edema and can be expected to lead to some degree of visual loss; it may also lead to severe complications when performed incorrectly. The original hypothesis that diabetic retinopathy is caused by abnormal production of growth factors stimulated by retinal hypoxia was made more than 50 years ago by I.C. Michaelson. Growth hormone and IGFs play a permissive role, fibroblast growth factor may act synergistically, and vascular endothelial growth factor (VEGF) appears to be the major mediator. The expression of this glycoprotein is increased by hypoxia, and its levels are particularly high in patients with active proliferative retinopathy. VEGF increases retinal permeability in a dose-related fashion at levels encountered clinically in patients with retinopathy. These considerations suggest a number of potential approaches to treatment. Prevention of hypoxia with glycemic control, antioxidants, and AGE inhibitors might directly protect the retinal vessels. Angiotensin II (A2) is an important signal for VEGF secretion, with ACE inhibitors and A2 …