Fasting influences steroidogenesis, vascular endothelial growth factor (VEGF) levels and mRNAs expression for VEGF, VEGF receptor type 2 (VEGFR-2), endothelin-1 (ET-1), endothelin receptor type A (ET-A) and endothelin converting enzyme-1 (ECE-1) in newly formed pig corpora lutea.
This study was designed to verify whether fasting influences vascular endothelial growth factor (VEGF) production and VEGF, VEGF receptor-2 (VEGFR-2) as well as endothelin (ET) system members (endothelin converting enzyme-1, ECE-1; ET-1; endothelin receptor type A, ET-A) mRNA expression in pig corpora lutea; furthermore, we wanted to assess whether fasting affects steroidogenesis in luteal cells. Eight prepubertal gilts were induced to ovulate and were randomly assigned to two groups: (A) n = 4, normally fed; and (B) n = 4, fasted for 72 h starting 3 days after ovulation. At the end of fasting, ovaries were removed from all the animals and corpora lutea (CLs) were collected. VEGF and steroid levels in luteal tissue were determined by ELISA and RIA, respectively; VEGF, VEGFR-2, ET-1, ET-A and ECE-1 mRNAs expression was measured by real-time PCR. VEGF protein levels were similar in the two groups, while all steroid (progesterone, testosterone, estradiol 17beta) concentrations were significantly (P < 0.001) higher in CLs collected from fasted animals compared with those from normally fed gilts. VEGF, VEGFR-2, ET-1 and ECE-1 (but not ET-A) mRNA expression was significantly lower (P < 0.05) in fasted versus normally fed animals. The overall conclusion is that all the parameters studied are affected by feed restriction, but the mechanisms activated at luteal level are possibly not fully adequate to compensate for nutrient shortage.
Galeati
Giovanna
G
Dipartimento di Morfofisiologia Veterinaria e Produzioni Animali, University of Bologna, Via Tolara di Sopra 50, 40064 Ozzano Emilia, BO, Italy.
Forni
Monica
M
Spinaci
Marcella
M
Zannoni
Augusta
A
Govoni
Nadia
N
Ribeiro
Luciana A
LA
Seren
Eraldo
E
Tamanini
Carlo
C
D000818:Animals; D016282:Aspartic Acid Endopeptidases / Q000235:genetics; D019332:Endothelin-1 / Q000235:genetics; D000072396:Endothelin-Converting Enzymes; D016232:Endothelins / Q000502:physiology*; D004958:Estradiol / Q000096:biosynthesis; D005215:Fasting / Q000502:physiology*; D005260:Female; D015870:Gene Expression; D008666:Metalloendopeptidases / Q000235:genetics; D018919:Neovascularization, Physiologic / Q000502:physiology*; D016133:Polymerase Chain Reaction; D011374:Progesterone / Q000096:biosynthesis; D012333:RNA, Messenger / Q000032:analysis; D044022:Receptor, Endothelin A / Q000235:genetics; D013256:Steroids / Q000096:biosynthesis*; D013552:Swine / Q000502:physiology*; D013739:Testosterone / Q000096:biosynthesis; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000235:genetics
D019332:Endothelin-1; D016232:Endothelins; D012333:RNA, Messenger; D044022:Receptor, Endothelin A; D013256:Steroids; D042461:Vascular Endothelial Growth Factor A; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D040301:Vascular Endothelial Growth Factor Receptor-2; D016282:Aspartic Acid Endopeptidases; D008666:Metalloendopeptidases; D000072396:Endothelin-Converting Enzymes