The Significance of Weight Loss in the Evaluation of Pituitary Response to LH-RH in Women with Secondary Amenorrhea1

Warren, Michelle P.; Jewelewicz, Raphael; Dyrenfurth, Inge; R, Ans; Khalaf, S.; Wiele, Raymond L. Vande

doi:10.1210/jcem-40-4-601

Cited by 126 publications

(33 citation statements)

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“…Changes in food intake during growth in the rat are closely correlated with changes in the size of the adipose tissue (2,14). In the human female, loss of body weight in the range of 10-15%, which corresponds to a loss of body fat of 35-40%, is associated with loss of menstrual function (10,15), and the ability to respond to luteinizing-hormone-releasing factor (16).…”

Section: Resultsmentioning

confidence: 99%

Body weight and food intake at early estrus of rats on a high-fat diet.

Frisch¹,

Hegsted²,

Yoshinaga³

1975

Proc. Natl. Acad. Sci. U.S.A.

109

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Body weight, food intake, and age at vaginal opening and estrus were studied for two groups of weanling rats (age 21 days), fed on high-fat (24.6% by weight) and lowfat (5.0%) diets. Fat was substituted isocalorically for carbohydrate in the high-fat diet. The high-fat rats had estrus at 33.3 4 0.8 days, significantly earlier (P < 0.001) than the age at estrus, 37.4 4 0.7 days, of the low-fat rats. Estrus was simultaneous with vaginal opening in 81% of the high-fat rats, in comparison to 48% of the low-fat rats. The caloric intake per 100 g of body weight of the high-fat and low-fat rats did not differ at vaginal opening or at estrus, whereas the two groups differed significantly at both events in age, body weight, absolute food intake (g/day), and relative food intake (g/100 g of body weight per day) and absolute caloric intake (calories/day). Caloric intake/100 g of body weight as a function of chronological age first increased and then decreased steadily before estrus for both high-fat and low-fat rats. The findings support Kennedy's hypothesis that a food intake signal, now further defined as caloric intake/100 g of body weight, is a signal for puberty, and are in accord with the hypothesis that a critical body composition of fatness is essential for estrus in the rat, as in the human female. Puberty in the rat (defined by vaginal opening and estrus) is more closely related to body weight than to age (1, 2). Food intake "appropriate for body weight" of well grown, retarded, and chronically underfed rats has a constant relation to the onset of ovarian activity, independent of age (1). Kennedy concluded that "food intake, or its correlate metabolic rate may act as the normal signal to initiate puberty" (1).Weight growth in the rat has been reported to be more rapid on high-fat diets than on normal or low-fat diets (3-5). Female rats on high-fat diets, therefore, should have vaginal opening and estrus earlier than on a low-fat diet. Diets differing in the calories contributed by fat may also provide information on the finding of a constant food intake per unit of body weight at puberty in the rat (1, 2), since food intakes would differ between the two diets if rats were "eating to calories" in relation to body weight.A positive relation between rate of sexual development in the rat and the amount of fat contained in the diet up to 20-40% has been reported (4, 6). However, detailed observation of weight, food intake, vaginal opening, and estrus were not made in these or other (5) studies. This paper reports the age, body weight, food intake, and caloric intake at vaginal opening and at estrus of two groups of weanling rats fed on high-and low-fat diets. These relations between weight, fat and puberty in the rat are of special interest now because of the findings in the human female that a critical weight (7), representing a critical level of fatness (8,9), is closely related to menarche and to the continued maintenance of regular ovulatory cycles (10). Amenorrhea follows weight loss below a minimal level...

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Section: Resultsmentioning

confidence: 99%

Body weight and food intake at early estrus of rats on a high-fat diet.

Frisch¹,

Hegsted²,

Yoshinaga³

1975

Proc. Natl. Acad. Sci. U.S.A.

109

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“…In patient 2 FSH was undetectable throughout and the small FSH increase seen during the initial study did not occur. In contrast, plasma LH responses were reduced to a lesser degree by estrogen treatment and were not significantly lower on days 4 Effects of pulsatile GnRH injections in anorexia nervosa patients after weight regain Previous studies (16)(17)(18)(19) have shown that LH is secreted in a pulsatile manner, responsiveness to GnRH matures, and plasma estradiol concentrations increase, following weight regain in patients with anorexia nervosa. We therefore administered GnRH to five patients who had regained weight, but who remained amenorrhic, in an effort to determine the effects of increased endogenous estrogen concentrations on gonadotropin responses.…”

Section: Ighdmentioning

confidence: 98%

“…The individual hormone concentrations are shown for patient 14 in Fig. 5, and mean data for patients [14][15][16][17][18] are shown in Fig. 6.…”

Section: Ighdmentioning

confidence: 99%

Selective inhibition of follicle-stimulating hormone secretion by estradiol. Mechanism for modulation of gonadotropin responses to low dose pulses of gonadotropin-releasing hormone.

Marshall¹,

Case²,

Valk³

et al. 1983

J. Clin. Invest.

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“…Reduced food intake is known to be associated with reproductive dysfunction in humans (1,2), and rats (3)(4)(5). Several kinds of endogenous sugar acids found in rat blood have been reported to be involved in control of food intake (6,7).…”

Section: Introductionmentioning

confidence: 99%

The endogenous feeding suppressant, 2-buten-4-olide, impairs the pulsatile secretion of luteinizing hormone through endogenous opioid peptides

Kaji

Saito

Shitsukawa

et al. 1998

European Journal of Endocrinology

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Objective: To clarify the mechanism of the suppressive effect of 2-buten-4-olide (2-B4O), an endogenous feeding suppressant, on the pulsatile secretion of luteinizing hormone (LH), by studying whether endogenous opioid peptides are involved in this suppressive effect. Methods: Using ovariectomized (ovx) rats, blood samples were taken every 6 min for 2 h after administration of 2-B4O or saline into the third cerebroventricle (3V) and sequential i.v. injection of naloxone (0.5 mg/kg per h) or saline. Rats were divided into three experimental groups: group 1: 3V saline þ i.v. saline (control); group 2: 3V 2-B4O þ i.v. saline; group 3: 3V 2-B4O+i.v. naloxone. Serum LH concentrations were determined by double-antibody RIA. To determine whether 2-B4O affected the biosynthetic activity of the opioidergic neurons within the ovx rat arcuate nucleus, we measured the concentrations of pro-opiomelanocortin (POMC) mRNA, a precursor of b-endorphin, in the rostral arcuate nucleus using non-radioactive in situ hybridization and a computerized image-analysis system. Results: 2-B4O significantly suppressed the pulse frequency of LH (group 2: 1.5 Ϯ 0.33 pulses/2 h, group 1: 2.43 Ϯ 0.2 pulses/2 h; P < 0.05), but naloxone blocked its suppressive effect and restored the pulse frequency (group 3: 3.29 Ϯ 0.36 pulses/2 h, group 2: 1.5 Ϯ 0.33 pulses/2 h; P < 0.01). There were no significant changes in the mean LH concentrations and amplitude. Furthermore, 2-B4O significantly stimulated the expression of POMC mRNA in the rostral arcuate nucleus. Conclusion: These results suggest that 2-B4O may impair the pulsatile secretion of LH by activating the opioid pathway within the hypothalamus.

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The Significance of Weight Loss in the Evaluation of Pituitary Response to LH-RH in Women with Secondary Amenorrhea1

Cited by 126 publications

References 0 publications

Body weight and food intake at early estrus of rats on a high-fat diet.

Body weight and food intake at early estrus of rats on a high-fat diet.

Selective inhibition of follicle-stimulating hormone secretion by estradiol. Mechanism for modulation of gonadotropin responses to low dose pulses of gonadotropin-releasing hormone.

The endogenous feeding suppressant, 2-buten-4-olide, impairs the pulsatile secretion of luteinizing hormone through endogenous opioid peptides

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