Synergistic effects of insulin-like growth factor I and gonadotrophins on relaxin and progesterone secretion by ageing corpora lutea of pigs

Abstract

Summary. Insulin-like growth factor I (IGF-I) is involved in paracrine/autocrine regulation of gonadal steroidogenesis and peptide hormone biosynthesis. This study was designed to determine whether IGF-I alone, or an interaction of IGF-I, is involved in augmenting the actions of luteinizing hormone (LH) and prolactin in controlling relaxin and progesterone secretion from ageing corpora lutea of hysterectomized gilts at days 110, 113 and 116 after oestrus. Luteal tissue slices were incubated for 8 h with IGF-I (0, 50, 300 ng ml \ m=-\ 1) , LH (0, 100, 1000 ng ml \ m=-\ 1), and prolactin (0, 100, 1000 ng ml \ m=-\ 1) alone or in combination. Progesterone and relaxin concentrations were determined by radioimmunoassay of spent medium and of homogenates from luteal tissue slices before and after incubation. Porcine luteal tissue from day 110 had a net output of 25 ng progesterone and 26 ng relaxin in the control and of 65 ng progesterone and 2125 ng relaxin in the combined IGF-I, LH and prolactin treatment mg\m=-\1 of luteal tissue, respectively. IGF-I, LH and prolactin alone or in combination significantly increased (P<0\m=.\01) progesterone production by luteal tissue from day 110, but they were partially effective at day 113 and ineffective at day 116. By contrast, the same hormone treatments increased relaxin production by luteal tissue from days 110 and 113. Even at day 116, prolactin alone or with LH or IGF-I continued to stimulate relaxin production. In conclusion, IGF-I augments the ability of prolactin and LH to increase relaxin production by ageing corpora lutea; however, a decrease in progesterone secretion and an increase in relaxin secretion at day 113 indicate that different mechanisms control progesterone and relaxin secretion in pigs.

Stimulatory effect of luteinizing hormone, insulin-like growth factor-1, and epidermal growth factor on progesterone secretion and viability of cultured bubaline luteal cells

“…Agreeing with our findings, IGF-1 and IGF-2 stimulated progesterone production in bovine luteal cells in vitro [21,22,57]. IGF-1 treatment resulted in a dose-dependent rise in basal progesterone production by mid-cycle bovine luteal cells [58], and consistent results were obtained from cow [21], pig [59], rat [14], rabbit [60], and human [61] in which IGF-1 alone, and in combination with gonadotropins, enhanced progesterone production by cultured luteal cells. In bovine CL, IGFs were effective in releasing progesterone and its stimulation was greatest during late luteal phase (15-18 days) [22].…”

Growth hormone and insulin-like growth factor-I action on progesterone secretion by porcine corpora lutea isolated at various periods of the luteal phase

“…This is in agreement with the results of Nicholson et al (1999) who showed that IGF-I is produced within the porcine CL and suggested an autocrine/paracrine role in CL development/function during the early luteal phase. A stimulatory effect of IGF-I on luteal progesterone production in vitro was noted by Huang et al (1992) in the pig. Our results are in agreement with data reported by Gadsby et al (1996) who discovered that IGF-I mRNA expression in small luteal cells was significantly greater before day 12 (days 4-10) than after day 12 (day 12-16) and are in accordance with subsequent data of Schams et al (1999) and Ge et al (2000) who detected IGF-I receptor in the pig CL, especially during the early luteal phase.…”

Evidence for expression of relaxin hormone-receptor system in the boar testis

“…However, it is still unclear what factor(s) regulate the expression of RLN mRNA in the boar testis. Treatment of intact boars with hCG has been reported to have little effect on circulating levels of RLN detectable by RIA, although it induces testosterone secretion (Juang et al 1996), but there is evidence that LH and prolactin increase RLN production by porcine CL in vitro (Huang et al 1992), while prolactin maintains RLN secretion for 10 days in hypophysectomised-hysterectomised gilts (Li et al 1989). Thus, there may be marked differences in the factors regulating RLN gene expression between Leydig cells and CL cells.…”