Objectives were to test the hypothesis that pre and postnatal nutrition in the bovine female, independently or interactively, affect age at puberty and functional characteristics of the estrous cycle of sexually mature offspring. Brangus and Braford (n = 97) beef cows bearing a female fetus were fed to achieve body condition scores of 7.5–8 (H, obese), 5.5–6 (M, moderate) or 3–3.5 (L, thin) by the start of the third trimester and maintained until parturition. Heifer offspring were weaned and fed to gain weight at either a high (H; 1 kg/d) or low (L; 0.5 kg/d) rate between 4 and 8 months of age, then fed the same diet during a common feeding period until puberty which resulted in compensatory growth of heifers in the L group. Heifers (n = 95) from the H postnatal diet reached puberty two months earlier (12 ± 0.4 months; P = 0.0002) than those from the L postnatal diet (14 ± 0.4 months). Estrous cycles of a subgroup of postpubertal heifers (n = 53) were synchronized to evaluate antral follicle count (AFC), rate of growth and size of the pre-ovulatory follicle, size of corpus luteum and ovary, endometrial thickness, and plasma concentrations of progesterone and estradiol-17β (E2). Although there was a trend for postnatal H heifers to have greater AFC and plasma concentrations of E2 compared to L heifers, neither pre nor postnatal nutrition affected any other physiological or hormonal variables, including short-term fertility. Postnatal nutritional effects on pubertal age remained the dominant observed feature.
Objectives were to test the hypotheses that nutritional extremes during prenatal development interact with postnatal nutrition during the juvenile period of heifers to impact 1) tonic secretion of gonadotropins, and 2) estradiol-17β (E2) negative and positive feedback responsiveness in adulthood. Heifers were selected from a larger population programmed nutritionally using a 3 x 2 factorial arrangement of pre- and postnatal diets. Beginning at 90 days of pregnancy, Bos indicus-influenced cows (n = 95) were fed to achieve body condition scores (BCS; 1–9 scale) of 3–3.5 (L; thin), 5.5–6 (M; moderate), or 7.5–8 (H; obese) by onset of the third trimester and maintained thereafter. Heifer offspring were weaned at 3–3.5 months of age and assigned to either a low- (L; 0.5 kg/day) or high-gain (H; 1.0 kg/day) diet until 8 mo. of age, then fed a common diet until puberty. Heifers (n = 18; 6/grp) representing HH, MH and LL combinations were ovariectomized postpubertally (17.1 mo. of age) and received E2 replacement. In Exp. 1, blood samples were collected at 10-min intervals to evaluate pulsatile secretion of LH and FSH for 5.5 hours. In Exp. 2, heifers received E2 (2.4 ug/kg I.M.), with blood sampling at 30-min to 1-h intervals for 30 h. Heifers in the MH (1.25 ± 0.11 ng/mL) group tended (P < 0.09) to have greater LH pulse amplitude compared to HH (0.91 ± 0.14 ng/mL) and LL (0.96 ± 0.09 ng/mL); otherwise, frequency, amplitude, and mean concentrations of LH and FSH did not differ among groups. Exogenous E2 (Exp. 2) suppressed (P < 0.0001) mean plasma concentrations of LH and FSH equally among groups, then stimulated equivalent surges of LH beginning at 14 ± 0.02 h, with only two FSH surges detected. Neither pre- nor postnatal nutrition affected E2 negative or positive feedback in this study.
Prenatal testosterone excess causes reproductive perturbations in sheep that recapitulate those seen in women with polycystic ovary syndrome (PCOS). Obesity has a significant role in the development and severity of the PCOS phenotype. Our objective was to investigate the effects of testosterone excess from gestational days (GD) 60-90 (unlike the GD 30-90 model, these animals are not virilized) and postnatal body weight (BW) gain on puberty in first-generation ewe lambs. Pregnant Suffolk ewes received testosterone propionate (T; 100 mg) or corn oil (C) i.m. twice weekly from GD 60-90 (term=147d). Ewe lambs were weaned ~3 mo of age. Control and T lambs were assigned to gain either 0.3 kg/d (C and T-maintenance) or 0.4 kg/d (T-overfed). Maintenance diet was designed to promote optimal growth without excess fat deposition. Overfed ration was designed to achieve a BW ~30% above that of maintenance. Progesterone concentrations were measured via radioimmunoassay in blood samples collected twice weekly from ewe lambs (n=15/group) during the first breeding season. Puberty was defined as when progesterone concentrations were < 0.5 ng/mL for four consecutive samples followed by three consecutive samples ≥0.5 ng/mL. Six animals (C, n=1; T-maintenance, n=3; T-overfed, n=2) did not attain puberty during the study and puberty was assigned as last day of sampling. Average daily gain was not different among treatments (C, 0.23±0.02kg; T-maintenance, 0.25±0.01kg; T-overfed, 0.27±0.02kg). Age at puberty did not differ between groups (C, 274.6±9.9d; T-maintenance, 270.0±11.3d; T-overfed, 266.0±10.2d). Similarly, BW at puberty did not differ across treatments (C, 50.44±2.2kg; T-maintenance, 52.5±2.4kg; T-overfed, 57.3±2.5kg). In conclusion, unlike GD 30-90 exposure which advanced puberty, GD 60-90 exposure did not affect age and BW at puberty in ewe lambs. Collectively, these studies suggest that GD 30-60 is a critical developmental window in which prenatal testosterone excess advances puberty in female sheep. Research support: NIH-NICHD (R01HD099096).
Objectives were to test the hypothesis that nutritional extremes during prenatal development interact with postnatal nutrition during the juvenile period of heifers to impact KNDy neuron responsiveness to a neurokinin B (NKB) agonist (Senktide) during progesterone dominance. Heifers were selected from a larger population programmed nutritionally using a 3x2 factorial arrangement of pre- and post-natal diets. Bos indicus-influenced cows (n = 95) were fed to achieve body condition scores (BCS; 1-9 scale) of 3-3.5 (L; thin), 5.5-6 (M; moderate), or 7.5-8 (H; obese) by the onset of the third trimester and maintained thereafter. Heifer offspring were weaned at 3-3.5 mo of age and assigned to either a low- (L; 0.5 kg/day) or high-gain (H; 1 kg/day) diet until 8 mo of age, then fed a common diet until puberty. For the current experiment, heifers (n = 18; 6/group) representing LL, MH, and HH combinations were ovariectomized postpubertally (17.1 mo of age) and received estradiol (E2) replacement to maintain basal E2 concentrations at 2-4 pg/mL. To achieve progesterone dominance, 3 CIDR devices were placed intravaginally 6 days prior to the initiation of Senktide challenge. Heifers were sampled for a 4.5-h period and received intravenous injections of saline or Senktide (14.8 ug/kg I.V.) at 0, 90, and 180 min. Jugular blood samples were collected at 10-min intervals for radioimmunoassay of LH. Irrespective of Senktide treatment, heifers in the MH group had greater pulse amplitudes (P = 0.016) and mean concentrations (P < 0.0001) of LH compared with both the HH and LL groups. Senktide treatment increased (P = 0.003) concentrations of LH compared with saline in all groups; however, the response to Senktide was greatest in the MH group compared with HH and LL. Pre- and postnatal nutritional extremes appear to interact to impact KNDy neuron responsiveness to NKB receptor signaling in heifers.
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