The role of insulin-like growth factor-1 in the initiation of female puberty /
In several species, including humans, peripheral insulin-like growth factor-1 (IGF-1) levels increase during puberty; hence, suggesting this peptide plays an important role in events leading to sexual maturation. Because IGF71 elicits LHRH release from the median eminence (ME) of immature female ra...
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| Format: | Thesis Book |
| Language: | English |
| Published: |
[Place of publication not identified] :
[publisher not identified] ;
1996.
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| Subjects: | |
| Online Access: | http://proxy.library.tamu.edu/login?url=http://proquest.umi.com/pqdweb?did=743273541&sid=1&Fmt=2&clientId=2945&RQT=309&VName=PQD |
| Summary: | In several species, including humans, peripheral insulin-like growth factor-1 (IGF-1) levels increase during puberty; hence, suggesting this peptide plays an important role in events leading to sexual maturation. Because IGF71 elicits LHRH release from the median eminence (ME) of immature female rat in vitro, it was thought to represent one of the peripheral signals suspected to link somatic development to the activation of the LHRH/LH releasing system at puberty. This study asseses the specific action(s) of IGF-1 during female sexual maturation, and uses ethanol (ETOH), a drug known to delay puberty, to further define the importance of IGF-1 during pubertal development. Results showed that during pubertal development no changes in IGF-1 MRNA levels were detected in brain. However, in liver, IGF-I MRNA levels were significantly elevated during early proestrus, which was followed by an significant increase in serum IGF-1 during late proestrus. This increase in IGF-1 was accompanied by increased IGF-1 receptor (IGF-lR) MRNA levels in the ME. Additionally, third ventricular administration of IGF-1 was capable of inducing LH release during juvenile and peripubertal development, an effect shown to be centrally diated. Importantly, in vivo exposure of juvenile animals to IGF-I advanced the onset of puberty. Also, we showed that ETOH significantly decreased the prepubertal expression of hepatic IGF-1 MRNA; hence, resulting in significant depressions in both serum IGF-1 and LH. These results suggest that this is the mechanism by which ETOH delays the onset of female puberty. conclusion, this study presents molecular and physiological evidence that IGF-I of peripheral origin contributes to the initiation of female puberty by stimulating hypothalamic LHRH release. This effect appears to be amplified centrally by the increased synthesis of IGF-IRs in the ME during first proestrus. Additionally, this study shows ETOHs' detrimental effects on growth rates and the pubertal process are due to the drugs' effects on IGF-I synthesis and release, and lends further evidence to the importance of IGF-1 during puberty. Collectively, these results support the hypothesis that IGF-1 is a metabolic signal capable of activating the LHRH/LH releasing system at the time of puberty. |
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| Item Description: | Vita. "Major Subject: Veterinary Anatomy". In title, numerals are used. |
| Physical Description: | xi, 97 leaves : illustrations ; 28 cm. Issued also on microfiche from University Microfilms Inc. |
| Bibliography: | Includes bibliographical references. |