The Lipid Content of the Leydig Cell and Sertoli Cell in the Human Testis as Related to Age, Benign Prostatic Hyperplasia, and Prostatic Cancer

Abstract
This study comprised 168 human males of ages from 2 mos. premature to 84 yrs. Testicular parenchyma was secured by surgical biopsy in 74 and at autopsy in 94, the majority of the latter being cases of accidental death. Of the total, 38 were from men with proved benign prostatic hyperplasia; 21, with proved prostatic cancer; and 18, from men more than 58 yrs. of age who had been demonstrated to have neither. Frozen sections cut from formalin-fixed, gelatin-embedded tissue were stained with oil-red O for estimation of the lipid content and distr. The estimation was made independently by both authors on slides identified only by number. +++++ was selected as indicating the maximum amount of lipid in the series. In the prepubertal group of 19 cases, no lipid was demonstrated in the Sertoli cells. Leydig-cell lipid was demonstrated to be absent in the premature specimen, appeared at birth, increased to a level of ++++ at 2 to 4 mos. whence it diminished to + or less at 18 mos., and was absent at 9 yrs. In the postpubertal group of 149 cases, the Sertoli-cell lipid appeared in small quantities at 15 yrs. and gradually increased to ++++ in old age. Leydig-cell lipid appeared at 12 yrs., increased to ++++ at 17 yrs. where it remained until 35 yrs., and then gradually diminished to + in old age. Estimated Sertoli- and Leydig-cell lipid were plotted against age and relatively smooth curves obtained on connecting an avg. of the estimated lipid in each 5-yr. period. Superimposition of these 2 curves demonstrated a preponderance of Leydig-cell lipid prior to the age of 47 and a preponderance of Sertoli-cell lipid beyond the age of 58 yrs. A comparison of the lipid pattern in the 38 cases with proved benign prostatic hyperplasia, 21 cases with proved prostatic cancer, and 18 cases past 58 yrs. of age who had neither, showed no variation between the 3 groups. The possible significance of this lipid pattern was discussed. It was concluded that the increase of Sertoli-cell lipid with age does not represent an increased production of the lipid as postulated by Teilum, but rather an increasing lack of utilization of the lipid.
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