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

The female reproductive profile of a fertile genetically obese line of rats, named beta, is characterized. Hypophysis, ovaries, oviducts, and uteri weights do not differ from those of nonobese controls. Histological features in ovary, uterus, and vagina in beta line and alpha controls are similar, in agreement with classical descriptions in the subject. Vaginal opening, number of estrus, number of corpora lutea at ovulation time, and pregnancy patterns (i.e., ovary weight, number of corpora lutea, sites of implantation, and living fetuses, as well as productivity, fertility, litter size, and preweaning mortality) show no significant differences between obese and nonobese animals. From a reproductive standpoint, obese beta line would behave as nonobese. Up to now beta would represent the only fertile genetically obese line of rats, appearing as a profitable biological model to widen and deepen reproductive analysis on obesity.
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PMID:Female reproductive profile in a fertile, genetically obese line of rats. 799 24

A 38 year old patient with multiple known risk factors for endometrial carcinoma (monophasic cycles, obesity, familial prediabetes, nulliparity, polycystic ovaries with diffuse thecal hyperplasia) presented with metrorrhagia caused by an endometrial lesion for which the diagnosis hesitated between atypical endometrial hyperplasia and carcinoma. Hysterectomy was performed because of the presence of a bicornuate uterus, obesity of 130 kg and the patient's lack of desire to have children. Examination of the uterus did not reveal any myometrial invasion in contact with the hyperplastic endometrium. The discovery of an endometrioid carcinomatous metastasis in the lower third of the vagina one year later allowed the retrospective detection of a 3 mm endometrioid carcinoma in the isthmus. No other metastases or recurrence were observed with a follow-up of 5 years.
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PMID:[Endometrioid adenocarcinoma of the uterine isthmus associated with atypical endometrial hyperplasia and polycystic ovaries. Apropos of a case with bicornuate uterus in a 38 year old woman]. 827 61

Oral contraceptives (OCs) were first introduced more than 30 years ago. OC manufacturers have reduced the dosage of synthetic estrogens (e.g., ethinyl estradiol, 100-150 mcg to 20-35 mcg) and progestins to limit their metabolic effects on lipoproteins, carbohydrates, and hemostasis. In addition to protection from pregnancy, OC benefits include lower incidence of painful periods, excessive bleeding, and iron deficiency anemia; reduction of ovarian cysts, benign breast tumors, and pelvic inflammatory disease; and protection against endometrial and ovarian cancers. The risk of a cardiovascular event (myocardial infarction, cerebrovascular events, venous thromboembolism, and deep vein thrombophlebitis) in OC users is 1-2/100,000 women years. Cardiovascular risk factors include smoking, hypertension, lipid disorders, severe obesity, diabetes mellitus, and cardiovascular events in first degree relatives before age 40. Thus, women with any of these risk factors should not use OCs. OCs do not increase the risk of breast cancer in women less than 59 years old. They may increase this risk if used over a long duration before the first fullterm pregnancy. OCs may cause a modest increase in cervical neoplasia. Low-dose OCs have a small effect on lipid metabolism. OCs increase serum triglycerides 30-50%. OCs increase insulin secretion and hyperinsulinemia increases the cardiovascular risk. Practitioners should evaluate clients before prescribing OCs. They should not prescribe OCs to women with hypertension, diabetes mellitus, lipid disorders, gynecological cancers, and previous cardiovascular disorders. Practitioners should tell clients that smoking is a leading risk factor and about OC's side effects (e.g., menstrual disturbances). The physical exam should include a cervical PAP smear, gynecological exam of the uterus and the ovaries, and a breast exam. Practitioners should test cholesterol and triglycerides before and during OC use. Premenopausal healthy women with no risk factors can use low-dose OCs.
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PMID:Update on oral contraception. 836 2

It is now possible to begin a difficult hysterectomy via laparoscopy with or without adnexal removal and then complete the operation vaginally. We report our successful experience with laparoscopically assisted vaginal hysterectomy in 62 of 68 patients. Techniques used for hemostatic separation of the uterus and adnexal pedicles included an automatic laparoscopic stapling device (49 cases), bipolar coagulation with sharp transection (11) and combined techniques (2). Minor complications occurred in four patients. Six patients had their operations converted from laparoscopy to laparotomy because of significant adhesions (three), large fibroids (two) and poor access due to obesity (one). The use of a stapling device required less anesthesia time (1 hour, 57 minutes, vs. 3 hours, 43 minutes), a smaller blood loss (145 vs. 247 mL) and shorter hospital stays (2.53 vs. 2.75 days) than did laparoscopic bipolar coagulation. However, the average hospital costs were greater for disposable automatic stapling devices and trocars when compared to bipolar coagulation techniques ($9,310 vs. $6,227). Postoperative patient satisfaction with the operation was high (98%), with a high rate of symptom resolution (95%). Laparoscopically assisted vaginal hysterectomy is a safe, effective operation in selected cases and may soon become a common alternative to abdominal hysterectomy in certain cases.
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PMID:Laparoscopically assisted vaginal hysterectomy. The initial Nashville, Tennessee, experience. 841 Aug 49

Endometrial carcinoma is the most frequent malignancy of the female reproductive tract, and irregular vaginal bleeding is its most common symptom. It is most common among postmenopausal women and is associated with obesity, nulliparity, and anovulation. Oral contraceptive (OC) use and tobacco smoking have been reported to protect against it. A 30-year-old nulligravida nulliparous woman presented with menometrorrhagia. She had had normal menses since age 11, she had smoked a pack of cigarettes a day for 15 years, and had been obese since age 15 (weighing 302 pounds). At age 26, she started taking a combination OC containing .1 mg ethynodiol diacetate and 35 mcg ethynyl estradiol (EE). 4 years later she gradually developed menorrhagia which improved upon changing the OC to .3 mg norgestrel and 30 mcg EE. Subsequently she developed early cycle metrorrhagia and was placed on .5 mg norgestrel and 50 mcg EE. She continued having early and midcycle breakthrough bleeding with clots. Physical examination and test results including a PAP smear were normal. She was taken to the emergency department because of continued bleeding. The uterus sounded to 14 cm. Curettings were consistent with grade 1-2, well-differentiated adenocarcinoma of the endometrium. 3 weeks later, she had total abdominal hysterectomy, bilateral salpingo-oophorectomy, and peritoneal biopsy for cytological examination. The pelvis and the abdomen were free of metastasis. Histological examination revealed a superficially invasive, well-differentiated adenocarcinoma consistent with stage IB, grade 1%. Ploidy analysis uncovered 12.5% tetraploid, with 0% aneuploid or hyperploid cells with 8.5% of the cells in S phase and 21% in the proliferative phase. Both estrogen and progesterone receptors were positive. The ploidy analysis and receptor status were consistent with the low-grade nature of the lesions. Postoperative radiation was not recommended, and the patient was well 6 months postoperatively.
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PMID:Menometrorrhagia in an oral contraceptive user. 842 44

Differing risk factors between men and women for a number of vascular and metabolic diseases have been linked to regional obesity. The differences in the distribution of adipose tissues between men (abdominal or upper-body obesity) and women (gluteal/femoral or lower body obesity) suggest a role for sex steroids in the regional distribution of fat. Previous work from this laboratory has shown the presence of oestrogen receptor (ER) in gluteal, perirenal and omental adipose tissues of ewes with similar physical characteristics to the ER in uterine tissue. The concentration profile for adipose ER was gluteal > perirenal > omental. In this report, we determined the physiological significance of adipose ERs by showing an up-regulation of the progesterone receptor (PR) in adipose tissues after oestrogen treatment in a fashion similar to that seen in a major responsive tissue such as uterus. Using PR antibodies (PR-6 and C-262), Western blot analysis of PR from oestrogen-treated sheep indicated that PR was induced in uterus >>> gluteal adipose > perirenal adipose consistent with the concentration of ER contained in these tissues. PR could not be detected by Western blotting in omental adipose tissue from oestrogen-treated animals or in gluteal, perirenal and omental adipose tissues from untreated animals. Sucrose gradient profiles of progestin (R-5020) binding from uterus and gluteal adipose tissues of oestrogen-treated ewes showed specific binding in both the 5S and 9S regions of the gradient, while perirenal and omental adipose tissue had only the 5S peak. The amount of specific binding was increased with oestrogen treatment in all the tissues. When gluteal adipose tissue cytosol was preincubated with PR antibody (C-262) to prevent binding of ligand and subjected to sucrose gradient analysis, both the 5S and 9S regions were diminished, suggesting that both peaks contained PR. Dilution of uterine cytosol resulted in an increase in the ratio of the 5S to the 9S peak, indicating that the 9S PR complex dissociates at low concentrations; this may be the reason why only the 5S peak was observed in perirenal and omental adipose tissues. These data offer further support for a direct role of sex steroids in regional adipose accretion and metabolism.
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PMID:Regional differences and up-regulation of progesterone receptors in adipose tissues from oestrogen-treated sheep. 856 67

Carcinoma of the endometrium is the most common gynecologic malignancy, expected to account for 33,000 new cases and 6,000 deaths in 1995. Most endometrial cancers occur in postmenopausal women and produce abnormal vaginal bleeding. Some women exhibit the premalignant changes of atypical endometrial hyperplasia before developing an overt carcinoma. Identified epidemiologic risk factors include obesity, diabetes mellitus, use of unopposed exogenous estrogens, estrogen-secreting tumors, and a reproductive history characterized by prolonged estrogenic predominance. Diagnosis can be readily established by outpatient endometrial biopsy. Because clinical estimates of disease extent and spread are subject to substantial error, endometrial cancer is now a surgically staged neoplasm. A well-defined set of surgicopathologic risk factors have been incorporated into the staging scheme. Women with extrauterine disease comprise about 20% of cases and are at greatest risk for tumor recurrence and death from disease. Within the much larger group of women whose tumors are limited to the uterus, recurrence risk can be stratified by cytologic grade, cell type, depth of myometrial invasion, and extension to the cervix. About two-thirds of women have low-risk disease confined to the uterus when these criteria are employed, while the remaining one-third have high-risk subtypes. Recent areas of investigation have focused on molecular and genetic markers. Two clinical observations currently being examined are the poorer survival of Black women with uterine cancer and the apparent association of endometrial lesions with chronic tamoxifen suppression in women with breast carcinomas.
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PMID:Clinical aspects of risk in women with endometrial carcinoma. 874 87

Approximately 20% of all deaths in the United States are due to cancer. Cancers of the hormonal tissues such as breast, uterus, ovary in women and prostate in men account for about 8% and 5% of total mortality and 30% and 11% of cancer mortality in women and men, respectively. Diet is considered to be a major and important environmental factor contributing to cancers of hormonal tissues. Breast, uterus, and ovary cancers in women and prostate cancers in men were positively correlated with high fat consumption, high body weight (body mass), body fat, and obesity. A major mechanism for development of these cancers appears to be mediated through increased levels of hormones, especially estrogens. Adipose tissue is considered to be one of the major sources of extraglandular estrogen, produced by aromatization of androgen precursors. Weight reduction decreases the estrogen levels possibly due to a decrease in body fat, thus decreasing the risk for cancers of the hormonal tissues. Dietary fiber may modify the risk for these cancers by influencing estrogen metabolism, recirculation, and excretion. Vitamin A and its precursors may decrease the risk for prostate cancer. Iodine deficiency may increase the risk for thyroid neoplasms in humans and experimental animals. Tumors of the hormonal tissues are the most common tumors in laboratory rodents, especially rats and mice. Incidences of mammary and anterior pituitary tumors had significant and positive correlation with body weight in rats and mice. Lowering the body weight by either decreased caloric intake or other means (e.g., exercise, increased fiber consumption) markedly lowered the incidences of these tumors in laboratory rodents. Laboratory studies indicated that mammary tumor rates in rats may not depend on the amount of fat consumed per day. The mammary tumor-promoting effect of fat may be due to complex interactions involving energy intake and energy retention (body mass) mediated through paracrine, endocrine, and neurohormonal mechanisms. Dietary protein may influence chemically induced tumors by affecting the metabolism of chemicals through enzyme induction. Thus, environmental factors such as diet are considered to be major and important factors for tumors of the hormonal tissues such as breast, uterus, and ovary in women and prostate in men. Diet and associated body weight are considered to be the major factors for tumors of hormonal tissues such as mammary and pituitary glands in rodents, especially rats. Modification of diet and a decrease in caloric intake may markedly decrease the incidence or delay the development of tumors of hormonal tissues in humans and in experimental animals.
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PMID:Influence of diet on tumors of hormonal tissues. 877 7

Primary malignant tumours of the body of the uterus are less common in India compared to carcinoma of the cervix. This study analyzed 86 primary malignant tumours of the body of the uterus over a 5 year period with regard to incidence of the various tumours, age group, gravidity, any predisposing factor, and the incidence of carcinoma of the cervix in the same period. Adeno-carcinomas were found to be the most common type of tumour. Tropho-blastic malignancies and mixed mullerian tumours also formed a significant number of cases. Compared to Western studies our patients with adenocarcinoma, adenosquamous carcinoma, squamous cell carcinoma and mixed mullerian tumour, were younger. Patients with adeno-carcinomas had a higher parity and patients with choriocarcinoma had a lower parity. Diabetes, hypertension and obesity were not as common as in the West. Carcinoma of the cervix was found to be commoner than primary malignant tumours of the body of the uterus.
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PMID:Primary malignancies of the corpus uteri retrospective five year analysis. 891 71

The pesticide residues 1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2,2-trichloroethane (o,p'-DDT) and beta-hexachlorocyclohexane (beta-HCH) act as weak estrogens, producing uterotrophic responses in ovariectomized rodents and stimulating human breast cancer cells in culture. Such activity suggests that these compounds may act as tumor promoters in estrogen-responsive tissues. Organochlorine compounds such as o,p'-DDT and beta-HCH are concentrated in body fat. The present report tests whether sufficient compound can be released from fat depots to produce estrogenic effects in uteri of ovariectomized mice. Adult animals were "loaded" with test compound by three daily injections of vehicle (DMSO), 17beta-estradiol (E2), beta-HCH, or o,p'-DDT. Uterotrophic effects were assessed at 24 h after the last loading dose of test compound and at 2 weeks after the loading regimen, with or without a prior 2-day period of fasting. The initial 3-day treatment with either beta-HCH or o,p'-DDT doubled the relative dry weight of the uterus: 102 +/- 8.6 mg/kg body weight (BW) and 104 +/- 4.4 mg/kg BW for beta-HCH and o,p'-DDT, respectively, compared to 49 +/- 1.9 mg/kg BW for vehicle-treated animals. E2-treated animals had uterine dry weights of 228 +/- 11 mg/kg BW. After 2 weeks without further treatment, a 2-day fast produced a decrease in body mass of 4.1 g/animal (fasted, 25.9 +/- 1.89 g versus fed, 30.0 +/- 2.82 g). Animals that had been loaded with beta-HCH and fasted had uterine weights (88 +/- 12 mg/kg BW) significantly greater (P < 0.05) than those of vehicle-loaded, fasted animals (51 +/- 2.9 mg/kg BW) or of beta-HCH-loaded, fed animals (59 +/- 4.6 mg/kg BW). The uterine weights of the fasted and fed o,p'-DDT-loaded or E2-loaded animals were not different from those of control weights. The difference between wet and dry weights showed that fasting of beta-HCH-loaded animals also increased water imbibition in the uterus; there was no effect from fasting in the other groups. Generally, epithelial cell height reflected the same responses as uterine weight with the exception that cell heights of beta-HCH-loaded, fed animals were slightly higher (P < 0.05) than corresponding controls, indicating that there may have been some active compound available to the tissues even without fasting. The effects of fasting show that during periods of lipolysis beta-HCH can be released in quantities sufficient to stimulate estrogen target tissues, suggesting a novel mechanism linking obesity and the progression of estrogen-responsive tumors. The lack of effect from fasting in o,p'-DDT-loaded animals indicates that these compounds are differentially mobilized from fat depots.
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PMID:Xenobiotics released from fat during fasting produce estrogenic effects in ovariectomized mice. 904 Nov 87


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