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Query: UMLS:C0848255 (female puberty)
 121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study assessed the effect of a dietary deficiency in the essential fatty acids (EFA) linoleic and linolenic acids on the onset of female puberty. EFA deficiency was produced in female rats by means of a semipurified diet and was biochemically documented by analyzing serum and erythrocyte fatty acid levels of more than 30 fatty acids, including all members of the n-6 and n-3 series. Levels of linoleic acid (18:2 n-6) and all n-6 derivatives, particularly arachidonic acid, were strikingly reduced. A less pronounced but clear-cut decrease in n-3 fatty acids, including docosahexaenoic acid (22:6 n-3) was also found. The times of puberty and first ovulation, as assessed by the ages at vaginal opening and first diestrus, were significantly delayed in EFA-deficient rats. The mechanisms underlying this delay appear to reside at both hypothalamic and ovarian sites. Simulation of preovulatory plasma estradiol (E2) levels via implantation of E2-containing Silastic capsules evoked a LH surge 30 h later in control juvenile rats, but not in EFA-deficient animals, indicating a delay in the development of the hypothalamic component of E2-positive feedback in the latter group. This delay appears to be due at least in part to reduced prostaglandin E2 (PGE2) synthesis, as the ability of the neurotransmitter norepinephrine to induce PGE2 release from median eminence nerve terminals was markedly reduced in EFA-deficient rats compared with that in controls. The decrease in hypothalamic PGE2 release was related to the EFA deficiency and not to reduced PG synthase activity, as determined by HPLC analysis of PG synthase products derived from exogenous [14C]arachidonic acid. Basal and hCG-stimulated PGE2 synthesis was also compromised in ovaries from EFA-deficient rats. Depressed gonadal function resulting from the EFA deficiency was further evidenced by a reduced gonadotropin receptor content, a blunted E2 response to hCG in vitro, and an increase in mean serum FSH levels. These results suggest that the delay in puberty resulting from EFA deficiency is due to a reduced availability of arachidonic acid for synthesis of bioactive metabolites. This results in delayed development of both the hypothalamic and ovarian components of the reproductive axis.
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PMID:Essential fatty acid deficiency delays the onset of puberty in the female rat. 275 37

Biological factors which influence the progression through female puberty stages are delineated, and an increase in the proportion of the body's fat content is identified as a critical prerequisite for the onset and maintenance of regular ovulatory cycles. Excessive exercise or malnutrition may interfere with the normal increase in the proportion of body fat and retard the onset of menarche. Pubic hair growth and breast development begins in most American females between the ages of 8-13. Menarche follows 4.2 years later for 50% of the females, but of others, the time period ranges from 18 months to 6 mor years. Both males and females experience hormonal changes before the 1st physical signs of puberty are manifested. As sex hormones increase, changes in the body's proportion of lean, fat, and skeletal mass occur. For females an increase in body fat begins at 7 years and continues through ages 16-18 years. Studies indicate that the body's fat content must account for 17% of the body's weight before menarche can occur and that, at age 18 years, the fat content must be at least 22% for the maintenance of regular menstrual cycles. Apparently, hypothalamic sensitivity to estrogens is decreased when the critical ratio of lean mass to body fat is reached, and changes in the hypothalamic and pituitary hormones promote pubertal progression and the establishment of reproductive functions. Poor nutrition alters the ratio of lean mass to body fat and delays the onset of menarche. In the US, the age at menarche decreased by 3 years since 1840 due to improvements in the population's nutritional status. Underweight females generally experience menarche at later ages than normal weight females. In contrast overweight females often experience menarche earlier than the average weight female. Athletic females and ballet dancers frequently experience late menarche, and these delays may be due to the disruption in fat accumulation which results from excessive exercise. Physically, inactive adolescents, on the other hand, tend to experience menarche at an earlier age than normally active females. In conclusion, the body's fat content along with a variety of environmental and psychosocial factors are responsible for the development and maintenance of female reproductive functions.
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PMID:Body weight and the initiation of puberty. 405 51

The possibility of an alteration in the age at which pubertal onset occurs has shown that we still lack knowledge on the molecular and physiological mechanisms of normal female puberty. In this study, the adjustment effects of different suckling and prepuberty nutrition on puberty onset and the expression of hypothalamic Kiss1/kisspeptin and gonadotrophin-releasing hormone (GnRH) were examined in 1-day-old female Sprague-Dawley rats. Animals were randomly assigned according to different suckling nutritional challenges (different milk intake before weaning) and prepuberty nutritional challenges (different food supply after weaning) into four groups: overnutrition group 1, overnutrition group 2 (O2), normal group (N, control group), and malnutrition group (M). In situ hybridization, Western blot analysis, and immunohistochemistry were used to analyze the expression of hypothalamic Kiss1/kisspeptin and GnRH. In the O1 group, GnRH and Kiss1/kisspeptin levels in the hypothalamus peaked at an early age, while malnutrition resulted in a delay in the GnRH and Kiss1/kisspeptin peaks. This study indicated that nutrition greatly affected the sexual development of female rats and that the effects of suckling nutrition were much greater than those of prepuberty nutrition.
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PMID:The effect of different nutritional states on puberty onset and the expression of hypothalamic Kiss1/kisspepetin. 2345 11