Testicular Luteinizing Hormone Receptor Content and in Vitro Stimulation of Cyclic Adenosine 3‚, 5‚- Monophosphate and Steroid Production: A Comparison between Man and Rat*

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Abstract
LH recepto rs, cAMP production and steroidogenesiswere compared in the human and rat testis in vitro,using whole tissue preparations and interstitial cell suspensions.Human testis tissue was obtained from prostatic cancer patientsundergoing orchiectomy (mean age, 71.6 yr); rat testis tissue wasfrom 80- to 90-day-old animals. The amount of [125I]iodohCGbinding in human testis homogenates averaged 0.57 ± 0.14 nmol⁄g wet wt (SE; n = 13), and the number of binding sites per Leydigcell was 1630 ± 220 (n = 5). In the rat, a similar calculation gave23,500 ± 2,500 (n = 4) binding sites per Leydig cell. The equilibriumassociation constants (Kas) of hCG binding to the humanand rat Leydig cell suspensions were 1.4 and 2.9 X 1010 M-1,respectively. Basal cAMP production in the human testis tissuewas 729 ± 225 pmol⁄g 4 h (n= 4), and maximal hCG stimulation(2 X 10-9 M) increased it on average by 590%. The basal rate ofcAMP production in the rat testis tissue was 59 ± 4.0 pmol⁄g 4h (n = 5), and hCG stimulated this rate by 1,030%. Basaltestosterone (T) production in the human testis tissue was 4.4± 0.7 nmol⁄g. 4 h (n = 15), but the hCG stimulation was only 44± 11% (P < 0.02). Similar rates of hCG stimulation were seen inthe production of pregnenolone, progesterone, and 17-hydroxyprogesterone(P < 0.01–0.05). In the rat testis, the basal Tproduction was 0.54 ± 0.10 nmol⁄g 4 h, and gonadotropinstimulation of T production was as high as 5- to 6-fold. TheED50s of hCG-induced production of T and cAMP, measured inLeydig cell suspensions, were similar in both species, on theorder of 1 pM for T and 100 pM for cAMP. In interstitial cellsuspensions, the rates of stimulation of cAMP production in therat and of T production in both species were comparable withthose observed in whole tissue preparations. However, the hCGstimulation of human Leydig cell cAMP production was only 2-fold. It is concluded that human Leydig cells, in comparison withthose of the rat, have a low amount of LH receptors (less than10%). When corrected for the differences in Leydig cell proportionof the tissue, the basal rates of T and cAMP productionwere similar in the tissue pieces of both species. Gonadotropinstimulation increased human testicular steroidogenesis onlymarginally (less than 50%), in contrast to a 5- to 17-fold increasein the rat. The cAMP production was stimulated by hCG 7- to10-fold in both species studied. The low level of acute stimulationof human testicular steroidogenesis was localized to a metabolicstep beyond LH receptors and cAMP formation but beforefurther metabolism of pregnenolone, being most likely due to aninsufficient supply or further metabolism of mitochondrial cholesterol.(Clin Endocrinol Metab55: 882, 1982)