Morphometry and cytochemistry of Leydig cells in experimental diabetes.
Leydig cell ultrastructure and function in diabetic rats were studied by concurrent cytochemistry, morphometry, and testosterone assay. The streptozotocin (Stz) model was modified to include nondiabetic Stz-injected rats, an insulin-treated diabetic group, and semistarved animals in addition to controls and untreated diabetic rats. The separation of the effects of diabetes, Stz, semistarvation, and insulin treatments was achieved by application of orthogonal contrast statistics. After 3 months of treatments, testes were perfusion-fixed, incubated for delta 5,3 beta-hydroxysteroid dehydrogenase (HSD) activity, and processed for electron microscopy. Diabetes increased Leydig cell smooth endoplasmic reticulum (SER), increased mitochondrial and lipid content, decreased HSD staining, and decreased serum testosterone levels. Insulin treatment reduced SER and increased testosterone concentrations. Semistarvation also increased SER and reduced testosterone levels but did not alter HSD staining. Stz had no significant effect on these variables. The results suggested that the hypoandrogen state was due to a primary Leydig cell compromise and not solely to malnutrition and that it was correctable by insulin treatment.
Anderson
J E
JE
Department of Anatomy, University of British Columbia, Vancouver, Canada.
Thliveris
J A
JA
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000473:pathology* / Q000503:physiopathology; D006651:Histocytochemistry; D006913:Hydroxysteroid Dehydrogenases / Q000032:analysis*; D007328:Insulin / Q000494:pharmacology; D007985:Leydig Cells / Q000648:ultrastructure*; D008297:Male; D051381:Rats; D013217:Starvation; D013739:Testosterone / Q000097:blood*
D007328:Insulin; D013739:Testosterone; D006913:Hydroxysteroid Dehydrogenases