Ethanol Blocks the Central Action of Igf-1 to Induce Luteinizing Hormone Secretion in the Prepubertal Female Rat

Hiney, Jill K.; Srivastava, Vinod K.; Lara, Tirso M.; Dees, W. Les

doi:10.1016/s0024-3205(97)01111-9

Cited by 33 publications

(38 citation statements)

References 26 publications

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“…In several previous studies in male rats, EtOH has been shown to decrease IGF-1 (Lang et al, 1998;Sonntag and Boyd, 1988), but this work is the first to show the same effect of EtOH in adult female rats, to our knowledge. We acknowledge, however, the report that EtOH feeding may decrease IGF-1 in prepubertal female rats (Hiney et al, 1998). Thus, a second mechanism of EtOH disruption of reproductive cyclicity, suggested by our work and that of others, is by diminished IGF-1 neuroendocrine stimulation.…”

Section: Discussionsupporting

confidence: 58%

“…This was elegantly demonstrated by Hiney et al (1991Hiney et al ( , 1996, both in vivo and in vitro. Additionally, in acute studies, the ability of IGF-1 to increase luteinizing hormone was blocked by EtOH (Hiney et al, 1998). In several previous studies in male rats, EtOH has been shown to decrease IGF-1 (Lang et al, 1998;Sonntag and Boyd, 1988), but this work is the first to show the same effect of EtOH in adult female rats, to our knowledge.…”

Section: Discussionmentioning

confidence: 43%

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Effect of Chronic Ethanol Exposure on Female Rat Reproductive Cyclicity and Hormone Secretion

Emanuele

LaPaglia

Steiner

et al. 2001

Alcoholism Clin & Exp Res

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 43%

Effect of Chronic Ethanol Exposure on Female Rat Reproductive Cyclicity and Hormone Secretion

Emanuele

LaPaglia

Steiner

et al. 2001

Alcoholism Clin & Exp Res

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“…Ethanol suppresses hepatic IGF-I mRNA levels in vivo, with a subsequent and concomitant decrease in the circulating concentrations of IGF-I and LH (17,18), indicating a possible linkage between IGF-I and LH secretion. The findings of recent studies suggest a correlation between serum concentrations of IGF-I and estradiol: estradiol treatment leads to an increase in serum IGF-I concentration in mature cows (19), gilts (20) and ewes (21), whereas it suppresses serum IGF-I concentration in the rat (22).…”

Section: Introductionmentioning

confidence: 99%

Interactions of insulin-like growth factor-I, insulin and estradiol with GnRH-stimulated luteinizing hormone release from female rat gonadotrophs

Xia¹,

Weiss²,

Polack³

et al. 2001

European Journal of Endocrinology

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Background: It is well established that ovarian steroids modulate gonadotropin secretion from anterior pituitary cells. It has been speculated that insulin and IGF-I might influence gonadotropin secretion. Objective: To investigate the effects of IGF-I and estradiol alone, or combinations of IGF-I with insulin and estradiol on GnRH-stimulated LH release from female rat pituitary cells in serum-supplemented and serum-free culture conditions. Methods: Pituitary cells were incubated for 24 h or 48 h with a series of increasing concentrations of IGF-I or estradiol and stimulated with 1 nmol/l GnRH for 3 h. To determine the interaction of IGF-I and estradiol on GnRH-stimulated LH secretion, cells were exposed to increasing concentrations of IGF-I and 100 pmol/l estradiol for 24 h. We also investigated the effects of combined treatment with IGF-I and insulin on GnRH-stimulated LH secretion. Results: Our findings indicate that long-term IGF-I treatment (24 h) alone has a significant augmenting effect on GnRH-stimulated LH release in serum-free medium only, with a maximum at low concentrations (10 and 100 pmol/l). Estradiol significantly increased GnRH-induced LH release in a dose-dependent manner. The extent of GnRH-stimulated LH secretion by long-term estradiol treatment (24 h) was significantly greater in serum-supplemented (+42%) medium than in serumfree medium. Estradiol facilitated IGF-I-primed LH responses to GnRH in serum-free medium. In contrast, in serum-supplemented medium, the facilitating potential of estradiol was lower. We also found that, in GnRH-stimulated cells, LH release was augmented by insulin treatment, in contrast to quiescent cells that had been pretreated with 100 pmol/l IGF-I alone and 1 nmol/l insulin alone. Conclusions: IGF-I and to a lesser extent insulin stimulate GnRH-induced LH secretion from pituitary gonadotrophs. This action is enhanced by estradiol treatment of the cells. However, the well known stimulatory action of estradiol on LH secretion is dependent on the presence of growth factors.

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“…The fact that ALC causes suppressed serum LH at this critical time of development is important, but a question remains as to whether this effect is due to a hypothalamic or a pituitary site of action. In immature rodents there have been several reports suggesting an ALC-induced deficit at the hypothalamic level (12)(13)(14)(15), but this has not been tested in immature primates. This is an important question considering the major influence of E 2 directly at the pituitary level in primates (16).…”

mentioning

confidence: 99%

Alcohol Alters Luteinizing Hormone Secretion in Immature Female Rhesus Monkeys by a Hypothalamic Action

et al. 2004

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We determined whether the effect of alcohol (ALC) to suppress LH secretion in immature female monkeys is due to a hypothalamic or pituitary site of action. Beginning at 20 months of age, four monkeys received a single intragastric dose of ALC (2.4 g/kg), and four monkeys received an equal volume of a saline/sucrose solution daily until they were 36 months old. For the hypothalamic response test, two basal samples (3.5 ml) were collected at 15-min intervals via the saphenous vein, and then N-methyl-D-L-aspartic acid (NMA; 20 mg/kg) was given iv and four more blood samples collected. Three weeks later, this protocol was repeated except LH-releasing hormone (LHRH) (5 g/kg) was used to test pituitary responsiveness. NMA or LHRH was administered 3 h after the ALC. After the pituitary challenge, each monkey was ovariectomized and 6 wk later, implanted with an indwelling subclavian vein catheter. Blood samples were drawn every 10 min for 8 h to assess effects of ALC on post-ovariectomy LH levels and the profile of LH pulsatile secretion. The hypothalamic challenge showed NMA stimulated LH release in control monkeys, an action that was blocked by ALC. The pituitary challenge revealed that LHRH stimulated LH release equally well in control and ALC-treated monkeys. A post-ovariectomy rise in LH was observed in both groups, but levels were 45% lower in ALC-treated monkeys. This reduction was attributed to an ALC-induced suppression of both baseline and amplitude of pulses. Results demonstrate that the ALC-induced suppression of LH in immature female rhesus monkeys is due to an inhibitory action of the drug at the hypothalamic level. (Endocrinology 145: 4558 -4564, 2004)I N RECENT YEARS, there has been an increase in alcohol (ALC) use and abuse during adolescence, especially by females (1). The adolescent period is a potentially vulnerable time for developing individuals who may be more sensitive to the drug and less tolerant to its detrimental effects than adults. This concept has been supported by work using the rat as an animal model (2, 3). The possibility that ALC could alter neuroendocrine development has been suspected for years because a history of any drug ingestion is routinely conducted to identify potential causes of altered endocrine function or pubertal development. Any detrimental effect of ALC on puberty-related hormones at this critical time of growth and development could elevate the risk for developmental deficits.Research with experimental animals and case reports from humans further suggest that determining the effects of ALC on endocrine development warrants serious consideration. Studies using rats have shown that ALC suppresses the levels of LH and estradiol (E 2 ) and causes delayed female puberty (4 -6). Even though case studies involving ALC use and abuse by adolescent and teenage humans are limited in number and scope, they have suggested that the drug can disrupt endocrine function, stature, and weight distribution in young people (7-9), as well as place them at risk for nutritional deficiencies ...

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Ethanol Blocks the Central Action of Igf-1 to Induce Luteinizing Hormone Secretion in the Prepubertal Female Rat

Cited by 33 publications

References 26 publications

Effect of Chronic Ethanol Exposure on Female Rat Reproductive Cyclicity and Hormone Secretion

Effect of Chronic Ethanol Exposure on Female Rat Reproductive Cyclicity and Hormone Secretion

Interactions of insulin-like growth factor-I, insulin and estradiol with GnRH-stimulated luteinizing hormone release from female rat gonadotrophs

Alcohol Alters Luteinizing Hormone Secretion in Immature Female Rhesus Monkeys by a Hypothalamic Action

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