title: Thymic, gonadal, and endocrine relationships in gilts and boars administered porcine somatotropin.
abstract: We hypothesized that much of the positive effect of porcine somatotropin (pST) on the immune system would be offset by the pST/IGF stimulation of gonadal function and that there would be negative effects on thymic weight and function from increased androgens in males. Male and female hogs (78 boars, 90 gilts) representing three genetic lines (lean, obese, and crossbred meat type) received 0, 2, or 4 mg of recombinant pST/d via implant for 42 d. Blood samples were collected on 0, 7, 14, 28, and 42 d of the trial for changes in pST, IGF-I, IGF-II, thymosin beta 4, dehydroepiandrosterone/dehydroepiandrosterone sulfate (DHEA/DHEASO4), and testosterone concentrations. Thymic, splenic, gonadal, and adrenal weights were collected at slaughter (d 42). Thymic weights increased with dose of pST in both sexes (P < .01), but splenic weights were unaltered. Adrenal weights increased with dose of pST (P < .01), but gonadal weights showed no response to pST in either sex or any line. Overall, concentrations of pST, IGF, and thymosin beta 4 increased with dose of pST. Serum testosterone concentrations in boars declined with dose of pST in lean and obese lines, and DHEA/ DHEASO4 declined in all lines with pST treatment. Testicular testosterone concentrations were not different among lines or doses of pST, indicating no stimulatory effect of increased pST/IGF-I on Leydig cell function. Although pST and its effects through increased circulating IGF are thought to be overall stimulants of growth and protein accretion, the actions on the tissues of the immune system (thymus/spleen) and steroidogenic tissues (adrenal/gonadal) can be selective. Increases in thymic weights and thymosin beta 4 concentrations from pST treatment in boars were partially due to the pST-induced decline in circulatory androgens, and the responses found in this in vivo model do not support pST/IGF effects documented in in vitro systems on Leydig cell function.
authors.affiliation: USDA-ARS, Roman L. Hruska U.S. Meat Animal Research Center, Clay Center, NE 68933-0166, USA.
authors.forename: T
authors.initials: T
authors.lastname: Wise
authors.forename: J
authors.initials: J
authors.lastname: Klindt
authors.forename: D D
authors.initials: DD
authors.lastname: Lunstra
authors.forename: F C
authors.initials: FC
authors.lastname: Buonomo
authors.forename: J T
authors.initials: JT
authors.lastname: Yen
mesh_terms: D000818:Animals; D003687:Dehydroepiandrosterone / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D004305:Dose-Response Relationship, Drug; D004702:Endocrine Glands / Q000033:anatomy & histology / Q000502:physiology*; D005260:Female; D013006:Growth Hormone / Q000097:blood / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D007335:Insulin-Like Growth Factor II / Q000032:analysis; D007985:Leydig Cells / Q000166:cytology; D008297:Male; D009929:Organ Size; D010053:Ovary / Q000033:anatomy & histology / Q000502:physiology*; D013154:Spleen / Q000033:anatomy & histology / Q000502:physiology; D013552:Swine / Q000097:blood / Q000235:genetics / Q000502:physiology*; D013737:Testis / Q000033:anatomy & histology / Q000502:physiology*; D013739:Testosterone / Q000097:blood; D013947:Thymosin / Q000097:blood; D013950:Thymus Gland / Q000033:anatomy & histology / Q000502:physiology*
chemical_list: D013739:Testosterone; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D013947:Thymosin; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II; D013006:Growth Hormone