DIETARY MYOINOSITOL SUPPLEMENTATION DOES NOT PREVENT RETINAL AND GLOMERULAR VASCULAR STRUCTURAL-CHANGES IN CHRONICALLY DIABETIC RATS

To assess effects of dietary myo-inositol supplementation on diabetes- induced vascular structural lesions, diabetes was induced in Sprague-D awley rats with streptozotocin; one-third of these rats was fed a 2% m yo-inositol diet for 9 months, one-third was left untreated for 5 mont hs then treated with myo-inositol for the last 4 months, and one-third was untreated for the entire 9 months. Controls included untreated an d myo-inositol-treated groups. Weight gain was impaired and plasma glu cose, glycosylated hemoglobin, food consumption, urine volume, and alb uminuria were increased significantly in diabetic versus age-matched c ontrol rats. Plasma myo-inositol levels were increased approximately f ivefold in controls and approximately six- to eightfold in diabetic ra ts treated with myo-inositol. In general, myo-inositol did not affect any of the above parameters in control or diabetic rats. Retinal capil lary basement membrane width (CBMW) was increased significantly (appro ximately 50% versus controls) after 9 months of diabetes. In the contr ol group myo-inosito, increased CBMW to the level of untreated diabeti c rats; myo-inositol had no effect on CBMW in each diabetic group. The number of retinal capillaries containing pericyte nuclei and pericyte capillary coverage were increased in untreated as well as myo-inosito l-treated diabetic rats and in the myo-inositol-treated control group. Glomerular CBMW was increased after 5 and 9 months of diabetes versus age-matched controls, and was increased even more by myo-inositol. Me sangial fractional volume of the glomerulus was increased 36% by diabe tes and was decreased slightly but significantly by myo-inositol. Thes e results indicate that diets supplemented with 2% myo-inositol (1) ca use capillary basement membrane (CBM) thickening and pericyte changes in retinal capillaries of normal rats, (2) are ineffective in preventi ng or reversing diabetes-induced retinal CBM thickening, and (3) cause further thickening of glomerular CBM in diabetic rats.