Biomedical subjects
Publications and source records attributed to G Verhoeven.
Gamma-glutamyltranspeptidase activity and fructose concentration have been measured in 100 semen samples, in 7 split ejaculates and in the seminal fluid of a patient with congenital absence of ductus deferens and seminal vesicles. Evidence is presented that the prostate is the major source of gamma-glutamyltranspeptidase in human semen.
Static measurements of immunoreactive inhibin have proven of little relevance in the diagnosis of testicular disorders. Dynamic evaluation of the inhibin secretory reserve might detect a specific Sertoli cell defect in a subgroup of infertile men. We compared the response of inhibin and steroids to an intravenous injection of pure FSH (Metrodin, Serono, 300 IU) in 13 infertile men with unilateral cryptorchidism to that in eight normal fertile men. Blood was aspirated before, 24, 48, and 72 h after the FSH injection. Two subgroups of patients with unilateral cryptorchidism were detected: those who responded by secreting inhibin in a pattern similar to normal men (seven patients), and those who responded poorly or not at all (six patients). The presumed cause of this difference is a defect of Sertoli cell reserve function due to a combination of insults to the testes, and not to cryptorchidism itself. The difference in response to FSH cannot be predicted from semen analysis nor from static hormone measurements. Overall, inhibin levels correlated significantly with the serum concentrations of FSH (r = -0.36, P < 0.05), testosterone (r = 0.37, P < 0.05), and 17-hydroxyprogesterone (r = 0.66, P < 0.001). It is concluded that, in infertile men with unilateral cryptorchidism, Stimulation of Sertoli cells by FSH can identify a subgroup of patients with Sertoli cell malfunction involving inhibin synthesis.
Treatment of male rats with hydrocortisone provoked a dose- and time-dependent decrease in plasma cholesterol concentration without a change in plasma triglyceride levels. In contrast, administration of triamcinolone and dexamethasone at equipotent glucocorticoid doses increased plasma cholesterol and triglyceride levels, respectively. Small effects on apolipoprotein E (apo E) and apo B mRNA levels were observed, but all corticosteroids increased apo A-I and apo A-IV mRNA and decreased apo A-II mRNA levels in the liver. Triamcinolone and dexamethasone, however, were three times more potent in stimulating hepatic apo A-IV gene expression than was hydrocortisone, whereas liver apo A-I and apo A-II mRNA levels were altered to a similar extent by all corticosteroids. Plasma apo A-I and apo B concentrations always varied in a similar fashion with their respective liver mRNA levels after administration of the distinct corticoids. For apo A-IV and apo E, discrepancies between plasma and liver mRNA levels after administration of the different steroids, however, point to additional regulatory effects on plasma apolipoprotein levels. We conclude that 1) in contrast to plasma apo A-I and apo B, alterations in plasma lipid, apo A-IV, and apo E levels depend on the type of corticosteroid used; and 2) glucocorticoids have a differential effect on hepatic mRNA levels of apo A-I and apo A-IV on the one hand and apo A-II on the other hand, an effect that may be of consequence in the process of reverse cholesterol transport.
Transplantable rat Leydig cell tumor H-540 was used to study the interactions between Leydig and Sertoli cells. These tumor cells maintain their steroidogenic capacity when cultured. Their responsiveness to a number of agonists that affect normal Leydig cells is markedly changed. Steroidogenesis can no longer be stimulated by luteinizing hormone (LH), but the cells remain responsive to dibutyrylcyclic adenosine monophosphate (dbcAMP) and cholera toxin. Cultured cells mainly produce C21-steroids, but the ability to produce androgens can be restored by pretreatment with dbcAMP. Coculture with Sertoli cells increases steroidogenesis in H-540 cells, and this effect is enhanced by follicle-stimulating hormone (FSH). Experiments with a two-chamber culture system show that these effects are mediated by one or more diffusible factors, some of which may be short-acting. SCF, a Sertoli cell-derived factor that stimulates normal Leydig cells, is not the mediator in this system since it is unable to stimulate steroidogenesis in Leydig tumor cells. Immunoneutralization experiments show that insulin-like growth factor I (IGF-I) is a permissive factor required to maintain steroidogenesis in Leydig tumor monocultures and in cocultures with Sertoli cells, but addition of IGF-I does not mimic the stimulatory effect of coculture. It was concluded that factors other than SCF and IGF-I must be involved in the stimulatory effects of coculture, and that H-540 cells may be a useful tool for the study of these factors.