title: Food deprivation stimulates the luteolytic capacity in the gilt.
abstract: The aims of this study were to study the effects of fasting on progesterone (P4) production in the pig and to verify whether fasting influences luteal expression of PGF(2alpha) receptor (FPr) and prostaglandin secretion. Superovulated prepubertal gilts were used; half of them were fasted for 72h starting on day 2 (F2) or 9 (F9) of the induced estrous cycle, respectively, while two groups (C2 and C9) served as respective controls. Plasma P4 and PGFM concentrations were determined by RIA while FPr mRNA expression in CLs collected at the end of fasting period was measured by real-time PCR. In experiment 1, plasma P4 concentrations in fasted gilts were significantly (P<0.01) higher than in controls starting from day 3 (F2; n=6) and 10 (F9; n=6). FPr mRNA expression was similar in F2 and C2 (n=6) CLs while it was significantly (P<0.05) higher in F9 than in C9 (n=6) CLs. In experiment 2, cloprostenol administered on day 12 significantly (P<0.05) increased FPr mRNA expression in CLs from both F9 (n=6) and C9 (n=6) gilts. At the time of cloprostenol injection PGFM levels were significantly higher (P<0.05) in the fasted group and cloprostenol-induced luteolysis in fasted but not in normally fed gilts. Results from this study indicate that fasting in prepubertal gilts induced to ovulate stimulates luteal P4 and PGFM production as well as FPr mRNA expression, thus increasing luteolytic susceptibility.
authors.affiliation: Dipartimento di Morfofisiologia Veterinaria e Produzioni Animali (DIMORFIPA), Università di Bologna, Via Tolara di Sopra 50, 40064 Ozzano Emilia (BO), Italy. ggaleati@vet.unibo.it
authors.forename: Giovanna
authors.initials: G
authors.lastname: Galeati
authors.forename: Monica
authors.initials: M
authors.lastname: Forni
authors.forename: Nadia
authors.initials: N
authors.lastname: Govoni
authors.forename: Marcella
authors.initials: M
authors.lastname: Spinaci
authors.forename: Augusta
authors.initials: A
authors.lastname: Zannoni
authors.forename: Marco
authors.initials: M
authors.lastname: De Ambrogi
authors.forename: Sara
authors.initials: S
authors.lastname: Volpe
authors.forename: Eraldo
authors.initials: E
authors.lastname: Seren
authors.forename: Carlo
authors.initials: C
authors.lastname: Tamanini
mesh_terms: D000818:Animals; D003008:Cloprostenol / Q000494:pharmacology; D003338:Corpus Luteum / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D030762:Estrous Cycle / Q000502:physiology; D005260:Female; D005508:Food Deprivation / Q000502:physiology*; D003341:Luteolysis / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D011374:Progesterone / Q000096:biosynthesis / Q000097:blood; D011461:Prostaglandins F, Synthetic / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011863:Radioimmunoassay; D011897:Random Allocation; D011982:Receptors, Prostaglandin / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary; D013552:Swine / Q000097:blood / Q000502:physiology*
chemical_list: D011461:Prostaglandins F, Synthetic; D012333:RNA, Messenger; D011982:Receptors, Prostaglandin; C034671:prostaglandin F2alpha receptor; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; D003008:Cloprostenol; D011374:Progesterone; D015237:Dinoprost