The objective was to determine whether exogenous insulin and dietary energy interact to affect follicular development in gilts. In a 2 x 2 x 2 completely randomized design, main effects were level of dietary energy (5771 or 9960 kcal metabolizable energy/day beginning on Day 12 of the estrous cycle), insulin dosage (0 or 0.4 IU/kg twice daily beginning on Day 15 of the cycle), and day of cycle at ovary removal (Day 17 or Day 19). Percentage of follicles designated small (less than or equal to 3 mm diameter) decreased from Day 17 to Day 19 of the cycle, and the percentage of large follicles (greater than or equal to 7 mm) increased (p less than 0.05). Insulin interacted with day of the cycle (p less than 0.05) to affect distribution of medium (4-6 mm) and macroscopically atretic follicles. Percentage of atretic follicles increased from Day 17 to Day 19 in saline-treated (from 15.5% to 38.2%) but not in insulin-treated animals (6.3% to 10.7%). Percentage of medium (4-6 mm) follicles decreased from Day 17 to Day 19 in saline-treated gilts (from 41.7 to 16.6%) but not in insulin-treated gilts (39.8% to 35.1%). Intrafollicular testosterone and progesterone concentrations were not affected by treatments. In medium follicles, the ratio of estradiol to progesterone was greater (p less than 0.05) for insulin-treated gilts on Day 17 than for the other treatment combinations.(ABSTRACT TRUNCATED AT 250 WORDS)

Uterine infections (i.e., endometritis) can have a major economic impact on dairy production. Identifying cows that are susceptible to endometritis and improving the diagnosis of endometritis could lead to a reduction in the impact of such infections. Thus, we used Holstein cows to determine whether postpartum changes in 13, 14-dihydro-15-keto-PGF2alpha (PGFM), a metabolite of PGF2alpha, could be used to identify cows that are susceptible to endometritis and to improve the diagnosis of endometritis. Cows were assigned to three treatments. 1) Control (n = 10) had no clinical or bacteriological signs of endometritis during the study. 2) Treated (n = 11) developed endometritis spontaneously and were treated i.m. with 25 mg of PGF2alpha immediately after clinical diagnosis (d 17.6 +/- 0.8 postpartum; mean +/- SEM). 3) Untreated (n = 10) developed endometritis spontaneously and were not treated after diagnosis (d 20.0 +/- 0.5). Examinations of external and internal genitalia and bacteriological data were used to diagnose endometritis. From d 0 (calving) until approximately d 63 postpartum, jugular blood was collected three times weekly. Progesterone and PGFM were quantified in plasma. For PGFM, the treatment x day interaction was significant (P < 0.01). Overall PGFM profiles for Control and Treated differed (P < 0.05), but the Untreated profile did not differ from either Control or Treated. To better understand the interaction, PGFM data from d 0 to 35 postpartum were partitioned into consecutive 7-d periods, and d-36 and greater data were partitioned into one period. Effects of treatment, day, and the treatment x day interaction were then evaluated within period. Except for the d-15 to -21 period, PGFM was greater (P < 0.03) in Control than in Treated and Untreated. In Treated and Untreated, PGFM increased during the d-15 to -21 period. For progesterone, treatment did not affect the profiles, but day was significant (P < 0.001). Progesterone concentrations were basal from d 0 until approximately d 12, and they generally increased after d 12. Onset of endometritis was associated with increased progesterone concentrations. Treatment did not affect the interval from calving to first detected estrus (29.5 +/- 4.9 d) or from calving to AI (73.3 +/- 8.7 d). We conclude that PGFM measures have the potential to be used to identify cows that are more likely to develop endometritis and that PGFM may aid in the diagnosis of endometritis.

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To determine influences of insulin and body condition on follicular growth, prepuberal gilts (n = 16) treated with pregnant mare's serum gonadotropin (PMSG) were used in a 2 X 2 factorial experiment with main effects of insulin (0 or .4 IU/kg every 12 h beginning at 1800 on the day before PMSG) and backfat depth (moderate, 25 +/- .8; high, 32 +/- .7 mm; P less than .0001). Body weights were similar. Blood sampling was at 6-h intervals for analyses of LH, FSH, growth hormone (GH), glucagon, cortisol, insulin, insulin-like growth factor-I (IGF-I), plasma urea nitrogen (PUN), nonesterified fatty acids (NEFA), testosterone, estradiol-17 beta, and progesterone. Ovaries were removed 75 h after PMSG treatment, and visible small (less than or equal to 3 mm), medium (4 to 6 mm), large (greater than or equal to 7 mm), and macroscopically atretic follicles were counted. Administration of insulin increased IGF-I in fluid of medium follicles (108.8 vs 60.7 ng/ml; SEM = 13.3; P less than .05). Neither insulin nor fatness affected hCG binding by granulosa cells (12.5 +/- 1.6 ng/10(6) cells) or numbers of large (16.7 +/- 2.6) and medium (10.4 +/- 2.3) follicles. However, insulin increased the number of small follicles (58.9 vs 29.9; SEM = 9.7; P less than .05) and reduced the number of atretic follicles (3.8 vs 11.3; SEM = 1.1; P less than .05). The predominant effect of insulin on reducing number of atretic follicles was in the small size class (.6 vs 6.9; SEM = .6, P less than .01). Follicular fluid estradiol and progesterone were not affected by treatments; however, testosterone concentrations in large follicles were lower in gilts with higher backfat (32.5 vs 59.9 ng/ml; SEM = 4.0; P less than .05). Systemic LH, FSH, glucagon, cortisol, PUN, NEFA, estradiol, and testosterone were not affected by insulin or level of feeding. However, GH was lower in gilts that had higher backfat (overall average of 3.2 vs 2.8 ng/ml; SEM = .1; P less than .05). Insulin reduced atresia and altered intrafollicular IGF-I independently of body condition and without sustained effects on other hormones.

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