scholarly journals Effects of Intermittent Pulsatile Infusion of Luteinizing Hormonereleasing Hormone on Dihydrotestosterone-suppressed Gonadotropin Secretion in Castrate Rams

1985 ◽  
Vol 33 (3) ◽  
pp. 603-611 ◽  
Author(s):  
Bruce D. Schanbacher
Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 5115-5120 ◽  
Author(s):  
David R. Simorangkir ◽  
Suresh Ramaswamy ◽  
Gary R. Marshall ◽  
Tony M. Plant

Abstract This study examined, in adult monkeys, the role that gonadotropin-independent mechanisms play in compensation of testosterone (T) secretion by the testis that remains after unilateral orchidectomy (UO). We employed a model (testicular clamp), in which endogenous gonadotropin secretion was abolished with a GnRH receptor antagonist, and the gonadotropin drive to the testes was concomitantly replaced with an invariant iv pulsatile infusion of recombinant human LH and FSH (1-min pulse every 2.5 h: LH, 0.08–0.12 IU/kg·pulse; FSH, 0.12–0.32 IU/kg·pulse) that provided the Leydig cells with a physiological stimulus. Within 5 h of UO (n = 5), circulating T concentrations had declined to 43% of pre-UO levels. By d 4, however, loss of the first testis was partially compensated, as reflected by the finding that circulating T had reached a plateau of 67% of the pre-UO level, where it remained for the duration of the study (39 d). That the recovery in circulating T was the result of increased T secretion by the remaining testis was suggested by the finding that the pulsatile pattern and decay of T during the intergonadotropin pulse interval before and after UO were indistinguishable. Interestingly, inhibin B production by the remaining testis also showed a delayed, albeit, minor, compensation (13% on d 10–11; P > 0.05) after loss of the first testis. These results suggest that compensation in T production by the remaining testis after UO in adult monkeys may be achieved in part by a gonadotropin-independent mechanism that probably involves direct neural inputs to the primate testis.


1998 ◽  
Vol 5 (1) ◽  
pp. 93A-93A
Author(s):  
E CHEN ◽  
M LUTHER ◽  
A MORENO ◽  
T KING ◽  
R SCHENKEN

1987 ◽  
Vol 116 (3_Suppl) ◽  
pp. S187-S188 ◽  
Author(s):  
O. ORTMANN ◽  
G. EMONS ◽  
R. KNUPPEN ◽  
K.J. CATT

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S93-S94
Author(s):  
M. BETTENDORF ◽  
F. DE ZEGHER ◽  
N. ALBERS ◽  
S. L. KAPLAN ◽  
M. M. GRUMBACH

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Vengala Rao Yenuganti ◽  
Dirk Koczan ◽  
Jens Vanselow

Abstract Background Metabolic stress, as negative energy balance on one hand or obesity on the other hand can lead to increased levels of free fatty acids in the plasma and follicular fluid of animals and humans. In an earlier study, we showed that increased oleic acid (OA) concentrations affected the function of cultured bovine granulosa cells (GCs). Here, we focus on genome wide effects of increased OA concentrations. Results Our data showed that 413 genes were affected, of which 197 were down- and 216 up-regulated. Specifically, the expression of FSH-regulated functional key genes, CCND2, LHCGR, INHA and CYP19A1 and 17-β-estradiol (E2) production were reduced by OA treatment, whereas the expression of the fatty acid transporter CD36 was increased and the morphology of the cells was changed due to lipid droplet accumulation. Bioinformatic analysis revealed that associated pathways of the putative upstream regulators “FSH” and “Cg (choriogonadotropin)” were inhibited and activated, respectively. Down-regulated genes are over-represented in GO terms “reproductive structure/system development”, “ovulation cycle process”, and “(positive) regulation of gonadotropin secretion”, whereas up-regulated genes are involved in “circulatory system development”, “vasculature development”, “angiogenesis” or “extracellular matrix/structure organization”. Conclusions From these data we conclude that besides inhibiting GC functionality, increased OA levels seemingly promote angiogenesis and tissue remodelling, thus suggestively initiating a premature fulliculo-luteal transition. In vivo this may lead to impeded folliculogenesis and ovulation, and cause sub-fertility.


1989 ◽  
Vol 264 (19) ◽  
pp. 10939-10942
Author(s):  
S S Stojilković ◽  
E Rojas ◽  
A Stutzin ◽  
S Izumi ◽  
K J Catt

1985 ◽  
Vol 40 (4) ◽  
pp. 297-302 ◽  
Author(s):  
David R. Mann ◽  
Diane Evans ◽  
Festus Edoimioya ◽  
Freja Kamel ◽  
George M. Butterstein

1991 ◽  
Vol 40 (1-3) ◽  
pp. 417-420 ◽  
Author(s):  
G. Schaison ◽  
B. Couzinet

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