Dietary myo-inositol 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-Dawley rats with streptozotocin; one-third of these rats was fed a 2% myo-inositol diet for 9 months, one-third was left untreated for 5 months then treated with myo-inositol for the last 4 months, and one-third was untreated for the entire 9 months. Controls included untreated and myo-inositol-treated groups. Weight gain was impaired and plasma glucose, glycosylated hemoglobin, food consumption, urine volume, and albuminuria were increased significantly in diabetic versus age-matched control rats. Plasma myo-inositol levels were increased approximately fivefold in controls and approximately six- to eightfold in diabetic rats treated with myo-inositol. In general, myo-inositol did not affect any of the above parameters in control or diabetic rats. Retinal capillary basement membrane width (CBMW) was increased significantly (approximately 50% versus controls) after 9 months of diabetes. In the control group myo-inositol increased CBMW to the level of untreated diabetic 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-inositol-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. Mesangial fractional volume of the glomerulus was increased 36% by diabetes and was decreased slightly but significantly by myo-inositol. These results indicate that diets supplemented with 2% myo-inositol (1) cause capillary basement membrane (CBM) thickening and pericyte changes in retinal capillaries of normal rats, (2) are ineffective in preventing or reversing diabetes-induced retinal CBM thickening, and (3) cause further thickening of glomerular CBM in diabetic rats.
Tilton
R G
RG
Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110.
Faller
A M
AM
LaRose
L S
LS
Burgan
J
J
Williamson
J R
JR
D000419:Albuminuria; D000818:Animals; D001485:Basement Membrane / Q000473:pathology; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D002196:Capillaries / Q000473:pathology*; D003921:Diabetes Mellitus, Experimental / Q000473:pathology* / Q000503:physiopathology*; D005527:Food, Fortified; D006442:Glycated Hemoglobin / Q000032:analysis; D007294:Inositol / Q000008:administration & dosage / Q000627:therapeutic use*; D007672:Kidney Cortex / Q000098:blood supply / Q000473:pathology / Q000648:ultrastructure; D007678:Kidney Glomerulus / Q000098:blood supply* / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values; D012160:Retina / Q000473:pathology* / Q000648:ultrastructure; D012171:Retinal Vessels / Q000473:pathology* / Q000648:ultrastructure
D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007294:Inositol