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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity produces a variety of alterations in the reproductive system and, similarly, manipulations of the hypothalamic-pituitary-gonadal axis produce changes in food intake, body weight and fat distribution. In men, the primary effects of obesity are a weight related reduction in testosterone and, with massive overweight, a reduction in free testosterone. In females, the weight-related development of menarche leads to earlier menarche in obese girls than in normal weight girls. One explanation for the relationship of fatness to menarche may be the ob protein (leptin) which is defective in the obese (ob/ob) mouse. Leptin is secreted by adipose tissue in proportion to the quantity of fat and may serve as a signal to the hypothalamus that fat stores are adequate to nourish a conceptus to term. In women, parity affects obesity and obesity in turn affects the regularity of the menstrual cycle. In many experimental animals with obesity, particularly the genetic forms of obesity, there is complete infertility in the females and marked impairment of reproductive function in the males. In animals with hypothalamic lesions, there is a gender effect on the magnitude of weight gain associated with the sexually dimorphic regions in the medial preoptic area. Castration with removal of oestrogen is followed by obesity in female animals and this can be prevented, as can most forms of obesity, by adrenalectomy. The inhibitory effects of oestrogen on food intake may result from suppression of neuropeptide-Y or galanin peptidergic systems in the arcuate nucleus or medial preoptic area.
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PMID:Obesity and reproduction. 940 19

The adverse effects of obesity on reproductive function in women are well recognized, but women with polycystic ovary syndrome (PCOS), the most common cause of anovulatory infertility, seem particularly vulnerable to the effects of excessive intake of calories. Polycystic ovary syndrome is associated with hyperinsulinaemia and insulin resistance, the causes of which remain unclear. These metabolic abnormalities are, in turn, related to a disorder of energy expenditure, characterized by reduced post-prandial thermogenesis. It is proposed that these closely interlinked phenomena that, particularly in overweight subjects, are associated with anovulation, may confer a biological advantage for women with PCOS at times of food deprivation, when such women may reproduce more successfully than those without PCOS. A possible causal link between hyperinsulinaemia and ovulation is explored by reference to the interaction of insulin and LH in granulosa cells.
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PMID:Nutrition, insulin and polycystic ovary syndrome. 941 38

Polycystic ovary syndrome (PCOS), also known as Stein-Leventhal Syndrome, is a condition that afflicts many women during their childbearing years. It is one of the leading causes of female infertility. Symptoms of PCOS are related to androgen excess and are not associated with estrogen deficiency. Classic symptoms include amenorrhea, hirsutism, acne, and obesity. Management of PCOS is directed by the client's concerns regarding symptoms, desire for pregnancy, and degree of morbidity related to androgen excess. First-line management of PCOS includes diet modification, weight loss, and stress management. First-line treatment for androgen excess is estrogen therapy, the combination of estrogen and progesterone being the drugs of choice. Uncomplicated amenorrhea in PCOS is managed with monthly or bimonthly administration of medroxyprogesterone. The antiestrogen clomiphene citrate has been the drug of choice for inducing ovulation. The success of any treatment plan will depend largely on the client's ability to reduce body weight.
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PMID:Management of polycystic ovary syndrome. 943 70

Turner syndrome afflicts approximately 50 per 100,000 females and is characterized by retarded growth, gonadal dysgenesis, and infertility. Much attention has been focused on growth and growth promoting therapies, while less is known about the natural course of the syndrome, especially in adulthood. We undertook this study to assess the incidence of diseases relevant in the study of Turner syndrome. The study period was from January 1, 1984 to December 31, 1993, and the study base was all women living in Denmark during the study period. We used data from the Danish Cytogenetic Central Register and the Danish National Registry of Patients to assess morbidity. This study supports several earlier studies reporting increased morbidity and confirms results of a recent study on cancer in Turner syndrome. Women with Turner syndrome seem to have an increased incidence of fractures, osteoporotic fractures in adulthood, and non-osteoporotic fractures in childhood. Furthermore, diabetes mellitus, both NIDDM and IDDM, was found with a markedly increased incidence in Turner syndrome, as well as ischemic heart disease, hypertension, and stroke. The risk of cancer, except cancer of the large bowel, does not seem to be elevated in Turner syndrome. Our data suggest that patients with Turner syndrome are extraordinarily prone to abnormalities constituting the metabolic syndrome (e.g., hypertension, dyslipidaemia, NIDDM, obesity, hyperinsulinemia and hyperuricemia). The present data may help to explain the decreased life span found in patients with Turner syndrome.
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PMID:Morbidity in Turner syndrome. 947 75

The adipocyte-specific hormone leptin, the product of the obese (ob) gene, regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure. Leptin acts through the leptin receptor, a single-transmembrane-domain receptor of the cytokine-receptor family. In rodents, homozygous mutations in genes encoding leptin or the leptin receptor cause early-onset morbid obesity, hyperphagia and reduced energy expenditure. These rodents also show hypercortisolaemia, alterations in glucose homeostasis, dyslipidaemia, and infertility due to hypogonadotropic hypogonadisms. In humans, leptin deficiency due to a mutation in the leptin gene is associated with early-onset obesity. Here we describe a homozygous mutation in the human leptin receptor gene that results in a truncated leptin receptor lacking both the transmembrane and the intracellular domains. In addition to their early-onset morbid obesity, patients homozygous for this mutation have no pubertal development and their secretion of growth hormone and thyrotropin is reduced. These results indicate that leptin is an important physiological regulator of several endocrine functions in humans.
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PMID:A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. 953 16

Obese women are associated with clinical symptoms suggestive of abnormal reproductive functions including irregular menses and infertility. Previous studies of gonadotropin release in obese women, basal or after luteal hormone releasing hormone (LHRH) stimulation, are controversial. Obese women are also often characterized by glucose intolerance and hyperinsulinemia which might relate to their excessive body fat. To understand the link between abnormal gonadotropin release, carbohydrate metabolism and percent body fat, we examined 17 premenopausal morbid obese women with body mass index (BMI) 38.7 +/- 1.6 Kg/m2 (mean +/- SEM) and 16 age-matched lean controls with BMI 19.7 +/- 0.6 Kg/m2. Plasma glucose, insulin and C-peptide values were measured before and 30, 60, 90 and 120 min after a 75 gm oral glucose tolerant test (OGTT). Each individual also received LHRH test which involved determinations of serum LH and FSH values at basal, 15, 30 and 60 min after injection of LHRH for 0.1 mg intravenously. Women with morbid obesity had significantly greater responses of glucose, insulin and C-peptide values as compared with lean women (all p < 0.001, two-way ANOVA). Despite that basal concentrations were not different, serum LH, FSH and ratio of LH to FSH values in response to LHRH test showed significantly lesser increase in obese women than lean controls. Percent body fat, determined by bioelectrical impedance analysis, correlated positively with plasma glucose, insulin and C-peptide responses to OGTT while negatively with ratio of LH to FSH responses (r = -0.418, p < 0.01) to LHRH test. Body mass index also correlated inversely with ratio of LH to FSH responses (r = -0.472, p < 0.01). In conclusion, morbid obese women had glucose intolerance, hyperinsulinemia and lower responses of serum LH and FSH values as compared with lean women. Excessive body fat play an important role in mediating these carbohydrate and gonadotropin abnormalities.
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PMID:Abnormal gonadotropin release and carbohydrate metabolism in morbid obese women. 955 Dec 49

Obesity is the number one public health concern in the United States, affecting over one-third of women. Minorities are at highest risk, with nearly 50% of African-American and Mexican-American women obese. Obesity significantly increases risk for mortality and morbidity in women, including several gynecological and reproductive disorders and infertility. Obesity, with the resultant hyperinsulinemia and hyperandrogenemia, negatively affects normal menstrual function and fertility. In addition, maternal adiposity may increase risk in offspring through perinatal mechanisms, resulting in a never-ending cycle of obesity. Data suggest that modest weight losses of about 10% of initial weight are effective in improving hormonal profiles, menstrual regularity, ovulation, and pregnancy rates. Available treatments include life-style modification programs, with a focus on eating a healthful diet and increasing physical activity, plus adjunctive pharmacotherapies.
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PMID:Obesity: a never-ending cycle? 960 11

The aetiology of the polycystic ovarian syndrome together with new advances in the molecular genetics and possible candidate genes for the inheritance of the syndrome is discussed. The possible role of leptin in the obesity of polycystic ovarian syndrome is reviewed. Hyperinsulinaemia acts not only as the trigger for hyperandrogenaemia and infertility, but also by stimulating plasminogen activator inhibitor type 1; hyperinsulinaemia may also promote atherogenesis in polycystic ovarian syndrome. The long-term effects of the metabolic derangements accompanying hyperinsulinaemia are reviewed. Special emphasis is placed on the use of novel insulin sensitizers such as troglitazone which promise new treatment opportunities in polycystic ovarian syndrome for both fertility and long-term disease prevention.
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PMID:New approaches to insulin resistance in polycystic ovarian syndrome. 961 41

The prevalence of pediatric obesity is increasing in the United States. Sequelae from pediatric obesity are increasingly being seen, and long-term complications can be anticipated. Obesity is the most common cause of abnormal growth acceleration in childhood. Obesity in females is associated with an early onset of puberty and early menarche. Puberty is now occurring earlier in females than in the past, and this is probably related either directly or indirectly to the population increase in body weight. The effect of obesity on male pubertal maturation is more variable, and obesity can lead to both early and delayed puberty. Pubertal gynecomastia is a common problem in the obese male. Many of the complications of obesity seen in adults appear to be related to increased accumulation of visceral fat. It has been proposed that subcutaneous fat may be protective against the adverse effects of visceral fat. Males typically accumulate fat in the upper segment of the body, both subcutaneously and intraabdominally. In females, adiposity is usually subcutaneous and is found particularly over the thighs, although visceral fat deposition also occurs. Gender-related patterns of fat deposition become established during puberty and show significant familial associations. There are no reliable means for assessing childhood and adolescent visceral fat other than radiologically. Noninsulin-dependent diabetes is being seen more commonly in the pediatric population. Diabetes and impaired glucose tolerance are noted particularly in obese children with a family history of diabetes. In this situation, a glucose tolerance test may be indicated, even in the presence of fasting normoglycemia. Hypertriglyceridemia and low high-density lipoprotein-cholesterol levels are the primary lipid abnormalities of obesity and are related primarily to the amount of visceral fat. Low-density lipoprotein-cholesterol levels are not typically elevated in simple obesity. The offspring of parents with early coronary disease tend to be obese. Very low-density lipoprotein and intermediate-density lipoprotein particles, which are small in size, may be important in atherogenesis but they cannot be identified in a fasting lipid panel. The propensity to atherogenesis cannot be interpreted readily from a fasting lipid panel, which therefore should be interpreted in conjunction with a family history for coronary risk factors. Hypertriglyceridemia may be indicative of increased visceral fat, familial combined hyperlipidemia, familial dyslipidemic hypertension, impaired glucose tolerance, or diabetes. Almost half of adult females with polycystic ovary syndrome are obese and many have a central distribution of body fat. This condition frequently has its origins in adolescence. It is associated with increased androgen secretion, hirsutism, menstrual abnormalities, and infertility, although these may not be present in every case. Adults with polycystic ovary syndrome adults are hyperlipidemic, have a high incidence of impaired glucose tolerance and noninsulin-dependent diabetes, and are at increased risk for coronary artery disease. Weight reduction and lipid lowering therefore are an important part of therapy. Obstructive sleep apnea with daytime somnolence is a common problem in obese adults. Pediatric studies suggest that obstructive sleep apnea occurs in approximately 17% of obese children and adolescents. Sleep disorders in the obese may be a major cause of learning disability and school failure, although this remains to be confirmed. Symptoms suggestive of a sleep disorder include snoring, restlessness at night with difficulty breathing, arousals and sweating, nocturnal enuresis, and daytime somnolence. Questions to exclude obstructive sleep apnea should be part of the history of all obese children, particularly for the morbidly obese. For many children and adolescents with mild obesity, and particularly for females, one can speculate that obesity may not be a great health risk
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PMID:Childhood obesity, adipose tissue distribution, and the pediatric practitioner. 965 56

Polycystic ovary syndrome is a common endocrine disorder, presenting with menstrual irregularities, hirsutism, obesity, infertility and abnormal ovarian morphology. In addition, polycystic ovary syndrome is associated with a self-perpetuating imbalance involving the endocrine system and metabolic pathways, in which carbohydrates, lipids and growth factors are involved. Because of its chronicity, it is considered to be a substantial risk factor for atherogenesis and hormone-dependent neoplasia. The etiology and pathophysiology of the syndrome remain elusive. However, during the last decade, several clues have emerged from human and animal studies that may have significant repercussions in the treatment of polycystic ovary syndrome. Therapeutic maneuvers should be directed towards the dominant abnormalities present in individual patients with polycystic ovary syndrome. Gonadotropin releasing hormone (GnRH) agonists can directly affect the gonadotropin generator and secondary downstream derangements, whereas combined oral contraceptives (COCs) can modify hypothalamic as well as peripheral abnormalities. In view of the fact that GnRH agonistic analogs (GnRH-a) will induce hypoestrogenemia and its sequelae, the add-back strategy of estrogenic supplementation is recommended for preventive reasons and, as it transpires from some studies, for enhancement of GnRH-a effectiveness.
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PMID:Combined oral contraceptives and gonadotropin releasing hormone agonistic analogs in polycystic ovary syndrome: clinical and experimental studies. 967 76


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