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  • Title: Influence of stage of the estrous cycle on insulin-like growth factor-I modulation of luteinizing hormone secretion in the gilt.
    Author: Whitley NC, Barb CR, Utley RV, Popwell JM, Kraeling RR, Rampacek GB.
    Journal: Biol Reprod; 1995 Dec; 53(6):1359-64. PubMed ID: 8562692.
    Abstract:
    Follicular phase (FOL; Days 17-19; n = 8), luteal phase (LUT; Days 7-9; n = 6), and ovariectomized (OVX; n = 5) crossbred gilts were used (Day 0 = onset of estrus). Blood samples were collected via jugular vein cannula every 15 min for 2 h the day before pituitary collection. Serum was assayed for insulin-like growth factor (IGF)-I, IGF-I binding proteins (IGFBP), LH, estradiol (E2), and progesterone (P4). Anterior pituitary cells were dispersed, cultured, and challenged on Day 4 of culture (Day 0 = day of seeding) with 10(-7) M GnRH or IGF-I (10(-11), 10(-10), 10(-9), 10(-8), or 3 x 10(-8) M) individually or in combination. Serum E2 and P4 concentrations indicated that the animals were in the appropriate stage of the estrous cycle. Mean serum LH concentrations were greater (p < 0.0004) for OVX animals compared to FOL and LUT animals. Mean serum IGF-I concentrations were lower (p < 0.05) for OVX compared to FOL and LUT animals, while serum IGFBP were not different among animals. Basal LH secretion (control) was greater (p < 0.04) in OVX than in FOL or LUT cultures. Relative to control, 10(-11) M IGF-I increased (p < 0.02) LH secretion in FOL, LUT, and OVX cultures, and this response was greater (p < 0.05) in FOL and OVX than in LUT cultures. Only the 10(-11) M IGF-I enhanced basal LH secretion in LUT cultures. In addition, 10(-10) M IGF-I increased (p < 0.05) LH secretion in OVX cultures, and 10(-10) and 10(-9) M IGF-I stimulated (p < 0.05) LH secretion in FOL cultures, whereas basal LH secretion in all groups was unaffected (p > 0.05) by 10(-8) or 3 x 10(-8) M IGF-I. The GnRH-induced LH secretion was unaltered by IGF-I treatment. Results indicate that in vitro IGF-I treatment increased basal LH secretion, with reproductive status modulating LH response to IGF-I.
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