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Cow body condition affects the hormonal release of ovarian cells and their responses to gonadotropic and metabolic hormones
AV. Sirotkin, AV. Makarevich, E. Kubovicova, J. Laurincik, S. Alwasel, AH. Harrath,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
- MeSH
- estradiol farmakologie MeSH
- folikulární buňky účinky léků sekrece MeSH
- ghrelin farmakologie MeSH
- insulinu podobný růstový faktor I farmakologie MeSH
- kultivované buňky MeSH
- leptin farmakologie MeSH
- ovarium cytologie účinky léků sekrece MeSH
- pohlavní steroidní hormony farmakologie MeSH
- primární buněčná kultura MeSH
- progesteron farmakologie MeSH
- proliferace buněk účinky léků MeSH
- skot * MeSH
- tělesná konstituce fyziologie MeSH
- testosteron farmakologie MeSH
- zvířata MeSH
- Check Tag
- skot * MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
The body condition score (BCS) of cows affects their reproductive efficiency, but the underlying mechanism is unclear. We examined the effect of BCS on the basic ovarian cell functions and their responses to gonadotropic and metabolic hormones. We isolated ovarian cells from cows with a tendency toward emaciation (BCS2) and those with an average body condition (BCS3), and we compared their hormonal release and responses to FSH, leptin, ghrelin, and neuropeptide Y (NPY) added at doses of 0, 1, 10, or 100 ng/mL. Progesterone, testosterone, estradiol, and insulin-like growth factor I (IGF-I) release were evaluated by RIA. No differences were found in progesterone or testosterone release between BCS2 and BCS3 cells; however, ovarian cells from BCS2 cows released more estradiol and IGF-I than cells from BCS3 cows. FSH, ghrelin, and NPY promoted progesterone release in BCS2 cells but had no stimulatory or inhibitory effect on BCS3 cells. In contrast, leptin promoted progesterone release in BCS3 cells and inhibited progesterone release in BCS2 cells. FSH also promoted testosterone release in both BCS2 and BCS3 cells but inhibited progesterone at a low dose in BCS3 cells. Leptin inhibited testosterone release in BCS3 cells but not in BCS2 cells. Estradiol release was promoted by leptin and ghrelin in BCS3 cells; however, it was unaffected by leptin and inhibited by ghrelin in BCS2 cells. IGF-I production was promoted by FSH and inhibited by leptin in both groups. Ghrelin suppressed IGF-I release in BCS2 cells and increased IGF-I release in BCS3 cells. NPY promoted IGF-I release in BCS2 cells but not in BCS3 cells. Our results demonstrate the effects of BCS on ovarian cell estradiol and IGF-I (but not progesterone or testosterone) release, as well as on the responses of ovarian cells to FSH, leptin, ghrelin, and NPY.
Department of Zoology and Anthropology Constantine The Philosopher University 949 74 Nitra Slovakia
Institute of Animal Physiology and Genetics AS CR Liběchov Czech Republic
King Saud University Zoology Department College of Science Riyadh Saudi Arabia
Citace poskytuje Crossref.org
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- $a Sirotkin, A V $u Department of Zoology and Anthropology, Constantine The Philosopher University, 949 74 Nitra, Slovakia; Department of Genetics and Reproduction, Research Institute of Animal Production, 949 59 Lužianky, Slovakia. Electronic address: asirotkin@ukf.sk.
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- $a The body condition score (BCS) of cows affects their reproductive efficiency, but the underlying mechanism is unclear. We examined the effect of BCS on the basic ovarian cell functions and their responses to gonadotropic and metabolic hormones. We isolated ovarian cells from cows with a tendency toward emaciation (BCS2) and those with an average body condition (BCS3), and we compared their hormonal release and responses to FSH, leptin, ghrelin, and neuropeptide Y (NPY) added at doses of 0, 1, 10, or 100 ng/mL. Progesterone, testosterone, estradiol, and insulin-like growth factor I (IGF-I) release were evaluated by RIA. No differences were found in progesterone or testosterone release between BCS2 and BCS3 cells; however, ovarian cells from BCS2 cows released more estradiol and IGF-I than cells from BCS3 cows. FSH, ghrelin, and NPY promoted progesterone release in BCS2 cells but had no stimulatory or inhibitory effect on BCS3 cells. In contrast, leptin promoted progesterone release in BCS3 cells and inhibited progesterone release in BCS2 cells. FSH also promoted testosterone release in both BCS2 and BCS3 cells but inhibited progesterone at a low dose in BCS3 cells. Leptin inhibited testosterone release in BCS3 cells but not in BCS2 cells. Estradiol release was promoted by leptin and ghrelin in BCS3 cells; however, it was unaffected by leptin and inhibited by ghrelin in BCS2 cells. IGF-I production was promoted by FSH and inhibited by leptin in both groups. Ghrelin suppressed IGF-I release in BCS2 cells and increased IGF-I release in BCS3 cells. NPY promoted IGF-I release in BCS2 cells but not in BCS3 cells. Our results demonstrate the effects of BCS on ovarian cell estradiol and IGF-I (but not progesterone or testosterone) release, as well as on the responses of ovarian cells to FSH, leptin, ghrelin, and NPY.
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