ArticleAlcoholism, clinical and experimental research2014
Alcohol alters insulin-like growth factor-1-induced transforming growth factor β1 synthesis in the medial basal hypothalamus of the prepubertal female rat.
Article in Alcoholism, clinical and experimental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The expression of IGFBP-5 in the reproductive axis and effect on the onset of puberty in female rats.Reproductive biology and endocrinology : RB&E · 2022Article
- RNA-seq analysis of lncRNA-controlled developmental gene expression during puberty in goat & rat.BMC genetics · 2018Article
- Screening and evaluating of long noncoding RNAs in the puberty of goats.BMC genomics · 2017Article
- Alcohol and Puberty: Mechanisms of Delayed DevelopmentAlcohol research : current reviews · 2017Review
- Manganese protects against the effects of alcohol on hypothalamic puberty-related hormones.Life sciences · 2016Article
- Alcohol alters hypothalamic glial-neuronal communications involved in the neuroendocrine control of puberty: In vivo and in vitro assessments.Alcohol (Fayetteville, N.Y.) · 2015Review
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4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInsulin-like growth factor-1 (IGF-1) and transforming growth factor β1 (TGFβ1) are produced in hypothalamic astrocytes and facilitate luteinizing hormone-releasing hormone (LHRH) secretion. IGF-1 stimulates release by acting directly on the LHRH nerve terminals and both peptides act indirectly through specific plastic changes on glial/tanycyte processes that further support LHRH secretion. Because the relationship between these growth factors in the hypothalamus is not known, we assessed the ability of IGF-1 to induce TGFβ1 synthesis and release and the actions of alcohol (ALC) on this mechanism prior to the onset of puberty.
methodsHypothalamic astrocytes were exposed to medium only, medium plus IGF-1 (200 ng/ml), or medium plus IGF-1 with 50 mM ALC. After 18 hours, media were collected and assayed for TGFβ1. For the in vivo experiment, prepubertal female rats were administered either ALC (3 g/kg) or water via gastric gavage at 07:30 hours and at 11:30 hours. At 09:00 hours, saline or IGF-1 was administered into the third ventricle. Rats were killed at 15:00 hours and the medial basal hypothalamus (MBH) was collected for assessment of TGFβ1, IGF-1 receptor (IGF-1R), and Akt.
resultsIGF-1 induced TGFβ1 release (p < 0.01) from hypothalamic astrocytes in culture, an action blocked by ALC. In vivo, IGF-1 administration caused an increase in TGFβ1 protein compared with controls (p < 0.05), an action blocked by ALC as well as a phosphatidylinositol 3 kinase/Akt inhibitor. IGF-1 stimulation also increased both total (p< 0.01) and phosphorylated (p)-IGF-1R (p < 0.05) protein levels, and phosphorylated (p)-Akt levels (p < 0.01), which were also blocked by ALC.
conclusionsThis study shows that ALC blocks IGF-1 actions to stimulate synthesis and release of hypothalamic TGFβ1, total and p-IGF-1R, and p-Akt levels further demonstrating the inhibitory actions of ALC on puberty-related events associated with hypothalamic LHRH release.
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