Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have indicated dysfunction of the hypothalamic-hypophyseal axis in obesity. We have studied 12 obese males to further characterize the extent of this dysfunction. The hypothalamic-hypophyseal-gonadal axis is normal as determined by the testicular response to human chorionic gonadotropin (hCG), the pituitary response to 200 micrograms gonadotropin-releasing hormone (GnRH), and the hypothalamic-pituitary-testicular response to clomiphene. Although L-dopa suppresses prolactin normally, the ability of thyrotropin releasing hormone (TRH) to stimulate the release of prolactin and thyroid stimulating hormone (TSH) is blunted. These latter responses are inversely related to the degree of obesity. The response to chlorpromazine, a hypothalamic stimulus for prolactin secretion, is also blunted, and to a greater extent than the prolactin response to TRH. These data indicate that exogenous obesity in males is associated with more extensive hypothalamic and pituitary dysfunction than previously realized. The abnormalities with regard to prolactin and TSH release become progressively worse when body weight exceeds 200 percent of ideal. In addition, when evaluating pituitary function with regard to gonadotropin release, obese males may have an abnormal response to 100 micrograms GnRH but respond normally to 200 micrograms.
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PMID:Hypothalamic and pituitary dysfunction in obese males. 680 59

Prader-Willi syndrome (PWS) is characterized by hypotonia at birth, hypogonadism, early childhood obesity, and mental deficiency. Hypogonadotropic hypogonadism is a major characteristic of patients with PWS, and it is speculated to be due to hypothalamic insufficiency. Two adult female patients with PWS and no prior history of menses are presented. Both of these patients were treated with fluoxetine for psychopharmacologic management of obsessive features in the form of food preoccupation and hyperphagia or for compulsive behaviors in the form of severe self-injurious behaviors. The two female patients with PWS who had primary amenorrhea developed vaginal bleeding believed to be menses following at least 6 months of treatment with fluoxetine. Mature hypothalamic function is characterized by pulsatile release of gonadotropin-releasing hormone (GnRH) in a critical range of frequency and amplitude. Central nervous system neurotransmitters may modify GnRH secretion. Fluoxetine specifically inhibits the reuptake of serotonin which may impact the hypothalamic-pituitary-ovarian system in female patients with PWS.
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PMID:Onset of menses in two adult patients with Prader-Willi syndrome treated with fluoxetine. 749 74

Exaggerated adrenal response (ExAR), i.e. hypersecretion of both 17-hydroxypregnenolone (170HPreg) and 17-hydroxyprogesterone(17OHP) in response to adrenocorticotropic hormone (ACTH) stimulation, is frequently found in women with polycystic ovary (PCO) syndrome who had precocious adrenarche. In an earlier study we found an abnormal adrenal response in girls with idiopathic true central precocious puberty (CPP) at early stages of puberty. On follow-up it was noted that a significant number of girls with CPP develop PCO-like syndrome at a relatively young age. The aim of the present study was to determine if there is an association between ExAR and early PCO in girls with a history of CPP. Included were 49 girls with a history of CPP, 34 of whom were treated with gonadotropin-releasing hormone (GnRH) analog. All 49 were evaluated at full maturity, at ages 12.5-14 years, 0.5-4 years after menarche or resumption of menses. Of the 49 girls, 20 had at least 3/4 clinical signs of PCO (irregular menses, hirsutism, acne and obesity) and were defined as PCO-like+, whereas 29 did not fulfil the criteria and were considered PCO-like-. Girls with a definite enzyme deficiency were excluded from the study. All participants underwent a combined iv ACTH-GnRH test at early follicular phase. The PCO-like+ girls all revealed ExAR, i.e. an elevated stimulated 17OHPreg of 63.4 +/- 9.6 nmol/l (normal 28.6 +/- 9.2 nmol/l) and a normal stimulated 17OHPreg/17OHP ratio of 7.1 +/- 1.8 (normal 6.2 +/- 2.7), whereas all the PCO-like- had a normal adrenal response (30.0 +/- 8.7 and 5.3 +/- 2.0 nmol/l, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early polycystic ovary-like syndrome in girls with central precocious puberty and exaggerated adrenal response. 758 60

The male adolescent may present several endocrinological problems, the most frequent of which is the retardation or absence of puberty due to constitutional delay of growth and development. This form does not require therapy and must be distinguished from other forms of hypogonadism (primitive or secondary) by endocrine tests (LHRH test, nightly pulses LH secretion, plasmatic basal level of testosterone and after HCG, cerebral NMR). Hypogonadism treatment consists of replacement therapy with testosterone or testes stimulation with HCG or LHRH. Another frequent disease is gynecomastia, usually due to physiological enlargement of mammary gland during pubertal development, sometimes it may be secondary to hypogonadism, tumors, liver function abnormalities. Severe or psychologically disturbing gynecomastia can be corrected by reductive mammoplasty. Very often, adolescents may present diseases related to incorrect food habits. Obesity is common and anorexia is becoming an important problem also in males.
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PMID:[Endocrinological problems in male adolescents]. 770 35

In distinction to the course of reproductive ageing in women, men do not experience a rapid decline of Leydig cell function or irreversible arrest of reproductive capacity in old age. Hence, strictu sensu, the andropause does not exist. Nevertheless, both spermatogenesis and fertility as well as Leydig cell function do decline with age, as shown by a decrease of +/- 35% of total and of 50% of free testosterone levels between the age of 20 and 80 years. The origin of this decline of Leydig cell function resides on the one hand in the testes, and is essentially characterized by a decreased number of Leydig (and Sertoli) cells and on the other hand in the hypothalamo-pituitary complex characterized by a decreased luteinzing hormone (LH) pulse amplitude, LH pulse frequency being maintained. As the responsiveness of the gonadotrophs to gonadotropin-releasing hormone (GnRH) remains unimpaired, one may assume that the amount of GnRH released at each pulse is also reduced, possibly as the consequence of a reduction of the cellular mass of GnRH neurones. Plasma levels of testosterone below the lower normal limit occur, however, only in a minority of elderly men from 7% in the age group 40-60, to 20% in the age group 60-80 and 35% in the age group over 80 years old. Factors influencing testosterone levels in elderly men are multiple: hereditary, environmental (obesity, stress), psychosocial (depression, smoking, drugs) or socioeconomical (diet, hygiene). Whether these elderly men should be substituted with androgens remains controversial.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ageing of the hypothalamo-pituitary-testicular axis in men. 772 Dec 58

Massively obese males often show symptoms of hypogonadism, but the mechanism for this is unclear. Increased endogenous opioid inhibition of the hypothalamic GnRH pulse generator resulting in insufficient stimulation of the pituitary gonadotroph has been proposed as a possible mechanism. If this hypothesis is correct, obese males should be more sensitive to the LH-elevating effects of the opiate antagonist, naloxone, than men of normal weight and gonadal status. This study investigated the etiology of obesity-related hypogonadism by examining luteinizing hormone (LH) and follicle stimulating hormone (FSH) responses to gonadotropin-releasing hormone (GnRH) and to infusions of saline or naloxone. Subjects were five obese (201 +/- 14% IBW) and five normal weight (control) (97 +/- 4% IBW) males. Before treatment, obese males had significantly (p < 0.05) lower testosterone levels than control subjects (307 +/- 72 vs. 597 +/- 49 ng/dl), whereas estradiol, androstenedione, and dehydroepiandrosterone levels were not different between the two groups. Both groups showed equivalent elevations in LH (fourfold to sixfold) in response to GnRH stimulation, but obese patients had significantly lower basal (p < 0.05) and GnRH-stimulated (p < 0.01) FSH levels. Infusions of naloxone (but not saline) led to significant (p < 0.01) increases in LH above preinfusion baseline levels (20.5 +/- 2.8% in obese and 28.6 +/- 6.3% in controls). In control subjects, integrated LH levels during naloxone infusion were not significantly elevated above those found during saline infusion, while obese subjects exhibited a 43% augmentation of integrated LH (31.0 +/- 5.3 ng/ml during naloxone vs. 21.7 +/- 1.8 ng/ml during saline, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endogenous opioids and hypogonadism in human obesity. 792

As the hypothalamic gonadotropin-releasing hormone (GnRH) pulse generator is an integrator of hormonal, metabolic, and neural signals, it is not surprising that the function of the hypothalamogonadal axis is subject to the influence of a large array of environmental factors. Before puberty, the central nervous system (CNS) restrains the GnRH pulse generator. Undernutrition, low socioeconomic status, stress, and emotional deprivation, all delay puberty. During reproductive life, among peripheral factors that effect the reproductive system, stress plays an important role. Stress, via the release of corticotropin-releasing factor (CRF), eventually triggered by interleukin 1, inhibits GnRH release, resulting in hypogonadism. Effects of CRF are probably mediated by the opioid system. Food restriction and underweight (anorexia nervosa), obesity, smoking, and alcohol all have negative effects on the GnRH pulse generator and gonadal function. Age and diet are important determinants of fertility in both men and women. The age-associated decrease in fertility in women has as a major determinant chromosomal abnormalities of the oocyte, with uterine factors playing a subsidiary role. Age at menopause, determined by ovarian oocyte depletion, is influenced by occupation, age at menarche, parity, age at last pregnancy, altitude, smoking, and use of oral contraceptives. Smoking, however, appears to be the major determinant. Premature menopause is most frequently attributable to mosaicism for Turner Syndrome, mumps ovaritis, and, above all, total hysterectomy, which has a prevalence of about 12-15% in women 50 years old. Premature ovarian failure with presence of immature follicles is most frequently caused by autoimmune diseases or is the consequence of irradiation or chemotherapy with alkylating cytostatics. Plasma estrogens have a physiological role in the prevention of osteoporosis. Obese women have osteoporosis less frequently than women who are not overweight. Early menopause, suppression of adrenal function (corticoids), and thyroid hormone treatment all increase the frequency of osteoporosis. Aging in men is accompanied by decreased Leydig cell and Sertoli cell function, which has a predominantly primary testicular origin, although changes also occur at the hypothalamopituitary level. Plasma testosterone levels, sperm production, and sperm quality decrease, but fertility, although declining, is preserved until senescence. Stress and disease states accelerate the decline on Leydig cell function. Many occupational noxious agents have a negative effect on fertility.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Environment, human reproduction, menopause, and andropause. 824 11

The prevalence of obesity is increasing in the developed as well as underdeveloped countries. Obesity in women is associated with reproductive disorders. The levels of estrone and androgens are higher in obese women along with a reduction in the levels of sex hormone binding globulin ( SHBG ). The pituitary secretion of hormones is altered either due to a deficient peripheral feedback regulation or a concomitant central defect in the obese. Luteinizing hormone ( LH ) level may increase in some of the obese subjects. The secretion of LH in response to luteinizing hormone releasing hormone ( LHRH or GnRH ), clonidine and naloxone may be altered in obese women. The levels of circulating prolactin may fall along with a delay in the nocturnal surge of the hormone. The secretion of prolactin in response to thyrotropin releasing hormone ( TRH ), insulin-induced hypoglycemia, arginine and chlorpromazine is altered. Similarly growth hormone secretion in response to growth hormone releasing hormone ( GHRH ), clonidine, naloxone and arginine is also altered in obesity. The literature suggests an alteration in the autonomic nervous system activity and the metabolism of carbohydrates and fats in the obese. Steroid hormones could affect the distribution of fat in the various regions of the body, and the distribution of body fat is linked with the severity of hyperandrogenism and metabolic disorders in obese subjects. However, it is heartening to note that many of the endocrinological and reproductive disorders are reversible with weight reduction in the obese subjects.
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PMID:Reproductive functions in obese women. 837 28

In female mammals, reproduction is extremely sensitive to the availability of oxidizable metabolic fuels. When food intake is limited or when an inordinate fraction of the available energy is diverted to other uses such as exercise or fattening, reproductive attempts are suspended in favor of processes necessary for individual survival. Both reproductive physiology and sexual behaviors are influenced by food availability. Nutritional effects on reproductive physiology are mediated by changes in the activity of gonadotropin-releasing hormone (GnRH) neurons in the forebrain, whereas the suppression of sexual behaviors appears to be due, at least in part, to decreases in estrogen receptor in the ventromedial hypothalamus. Work using pharmacological inhibitors of glucose and fatty acid oxidation indicates that reproductive physiology and behavior respond to short-term (minute-to-minute or hour-to-hour) changes in metabolic fuel oxidation, rather than to any aspect of body size or composition (e.g., body fat content or fat-to-lean ratio). These metabolic cues seem to be detected in the viscera (most likely in the liver) and in the caudal hindbrain (probably in the area postrema). This metabolic information is then transmitted to the GnRH-secreting or estradiol-binding effector neurons in the forebrain. There is no evidence to date for direct detection of metabolic cues by these forebrain effector neurons. This metabolic fuels hypothesis is consistent with a large body of evidence and seems to account for the infertility that is seen in a number of situations, including famine, eating disorders, excessive exercise, cold exposure, lactation, some types of obesity, and poorly controlled diabetes mellitus.
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PMID:Control of fertility by metabolic cues. 925 2

The male adolescent may present several endocrinological problems, the most frequent of which is the retardation or absence of puberty due to constitutional delay of growth and development. This form does not require therapy and must be distinguished from other forms of hypogonadism (primitive or secondary) by endocrine tests (LHRH test, nightly pulses LH secretion, plasmatic basal level of testosterone and after HCG, cerebral NMR). Hypogonadism treatment consists of replacement therapy with testosterone or testes stimulation with HCG or LHRH. Another frequent disease is gynecomastia, usually due to physiological enlargement of mammary gland during pubertal development, sometimes it may be secondary to hypogonadism, tumors, liver function abnormalities. Severe or psychologically disturbing gynecomastia can be corrected by reductive mammoplasty. Very often, adolescents may present diseases related to incorrect food habits. Obesity is common and anorexia is becoming an important problem also in males.
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PMID:[Endocrinologic problems of the male adolescent]. 904 25


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