Anti-Müllerian hormone in queens: Serum concentrations and total ovarian follicle population.

The objectives of this study were: a) To report anti-Müllerian hormone (AMH) serum concentrations in neonatal, pre and postpubertal female cats. b) To establish the relationship between serum AMH with either age and estrous cycle c) To correlate the total number of different ovarian follicle types with AMH in adult queens. A single blood sample was collected from 10 neonates (including 5 male), 15 prepubertal and 48 postpubertal female cats to measure AMH. Eight, 10, and 18 of this latter group were in follicular (FP), luteal phase (LP), and anestrus (AN), respectively. The total number of each follicle type was histologically counted using the Gougeon and Chainy (1987) formula in a subgroup of 10 adult queens. Overall AMH mean of these the female cats was 6.31 ± 0.54 ng/mL. The neonatal females had lower AMH serum concentrations than their male littermates (2.56 ± 0.49 vs. >23 ng/mL; P < 0.01). Concentrations were also higher in prepubertal than in neonatal and postpubertal cats (11.79 ± 1.36 vs. 2.56 ± 0.49 vs. 4.87 ± 0.38 ng/mL; P < 0.01). Queens below 12 mo of age had the highest AMH levels (10.41 ± 1.16; P < 0.01). Age was inversely correlated with AMH (r = -0.5; P < 0.01). Animals in FP had lower AMH concentrations than AN females (2.51 ± 0.33 vs. 5.46 ± 0.76 ng/mL; P < 0.05). No difference in the total number of each follicle type were found between either ovary (P > 0.05). A high correlation was only found between small antral follicles and AMH concentrations (r = 0.85; P < 0.01). It was concluded, that AMH can provide an indirect, reliable marker for the assessment of ovarian follicle size and functionality. Age as well as pubertal state should be considered when evaluating AMH concentrations in this species.

Physical, histological, endocrinological and steroidogenical evaluation of male cats postnatally exposed to sexual steroids.

To test the hypothesis that postnatal sexual steroids induce an impairment of domestic male cat reproductive function, this study describes the physical, endocrine, steroidogenical and histological effects of a single, high dose of a postnatal sexual steroid in this species. Twenty male kittens were randomly assigned within the first 24 h of birth to: Testosterone enanthate 12.5 mg sc (TE; n = 8), medroxyprogesterone acetate 10 mg sc (MA; n = 6), or Placebo sc (PL; n = 6). The cats were followed until puberty when they were castrated. Kittens achieved puberty without age differences among groups (P > 0.05). Two MA cats presented abnormal testicular descent. Histological evaluation of the MA (P < 0.01), but not of TE testes revealed decreased diameter (P < 0.01) and epithelial height (P < 0.01) of the seminiferous tubules. Leydig cell nuclear area was also reduced in this group. Conversely, tubular/intertubular ratio was increased in TE animals (P < 0.01). Quantitative real-time PCR analysis of mRNA expression of testicular tissue revealed no significant differences among groups for StAR, CYP17A1 and androgen receptors. TE animals showed decreased CYP19A1 mRNA expression (P < 0.05). In the first 4 postnatal weeks, fecal testosterone (T) values were high, basal and intermediate in TE, MA and PL (P < 0.05), respectively. These differences progressively diminished and the three groups presented basal T concentrations from the 7th week on (P > 0.05). It was concluded that the postnatal progestagen initially suppressed the gonadal axis and caused an impairment of spermatogenesis and testicular descent at puberty. Androgen treatment caused downregulation of the final steroidogenic cascade.

Postponement of canine puberty by neonatal administration of a long term release GnRH superagonist.

The objective of this study was to assess the efficiency and clinical safety of postnatal administration of a GnRH agonist on canine puberty postponement. Sexual steroids and histological gonadal changes were also described. Twenty-four littermate puppies were randomly assigned to: Deslorelin acetate 18.8 mg sc (DESLO; n = 12) or Placebo: sc (PLACE; n = 12) postnatally. The dogs were clinically and endocrinologically followed up until puberty when they were gonadectomized and their gonads histomorphometrically studied. Deslorelin postponed the age of puberty (72.7 ±â€¯4.8 vs. 35.8 ±â€¯1.9 weeks; P < 0.01) in these dogs. At the time of this submission, 3 DESLO dogs (108 weeks old) remain non-pubertal. All dogs concluded growing at a similar age (29.75 ±â€¯2.44 vs. 29.25 ±â€¯0.90 weeks; P > 0.1) independently of their group and pubertal status. None of the females had side effects while the 2 non pubertal DESLO males presented bilateral cryptorchydism. All the bitches ovulated at puberty (P > 0.1) and the 2 DESLO that were mated became pregnant. Deslorelin postponed basal serum sexual steroids up to puberty in both genders (P < 0.01). The histomorphometrical study of the testes revealed that the tubular diameter (P < 0.05), germinal epithelium height and composition (P < 0.01) were decreased in DESLO group. Ovarian structures did not differ between treatments (P > 0.05). It was concluded that postnatal deslorelin decreased sexual steroids reversibly postponing puberty in both genders without side effects in bitches and causing 2/6 of cryptorchydism and impairment of testicular histomorphometry in male dogs.