Sustained hyperglycemia results in testicular dysfunction and reduced fertility potential in BBWOR diabetic rats

DOI Web Site 被引用文献1件
  • D. F. Cameron
    Department of Anatomy, University of South Florida, Tampa 33612.
  • J. Rountree
    Department of Anatomy, University of South Florida, Tampa 33612.
  • R. E. Schultz
    Department of Anatomy, University of South Florida, Tampa 33612.
  • D. Repetta
    Department of Anatomy, University of South Florida, Tampa 33612.
  • F. T. Murray
    Department of Anatomy, University of South Florida, Tampa 33612.

書誌事項

公開日
1990-12-01
DOI
  • 10.1152/ajpendo.1990.259.6.e881
公開者
American Physiological Society

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説明

<jats:p>Rats with short-term diabetes show a greater than 50% reduction of serum testosterone and increased lipid in Leydig cells but normal testicular structure. The purpose of this study was to determine the extent of testicular pathology (morphology index), integrity of the blood-testis barrier, daily sperm production (DSP), number of Leydig cells per testis (LC/T), and total trunk testosterone (TTT) in diabetic rats (BBWORdp) with long-term hyperglycemia (300-350 mg/dl for greater than 180 days) and to evaluate its effects on fertility potential. Results were compared with similarly aged normoglycemic rats (BBWORdr) and normal control Wistar rats. After 6 mo of diabetes, testis weights, DSPs, TTTs, and the morphology index were significantly reduced. The LC/T was not different from BBWORdr rats. The blood-testis barrier appeared intact, although structural abnormalities were noted in Sertoli-Sertoli junction complexes. There was a significant reduction in the number of pregnancies per rat and implantations per pregnancy in matings utilizing the diabetic BBWORdp rat and control Wistar female rats. Results indicate that long-term diabetes with sustained hyperglycemia leads to significant testicular dysfunction associated with decreased fertility potential.</jats:p>

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