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

Breast diseases in 792 women were studied by biopsy and histological evaluation. In all subjects glucose tolerance was examined by OGTT (100 g glucose). The diabetes frequency of 22% in 326 women with breast cancer was compared with the frequency in women with fibroadenoma (n = 101), papilloma (n = 80), fibrocystic disease (n = 107), lipoma, granuloma, fibrosis (n = 88), papilloma with proliferation (n = 32), mastopathy with proliferation (n = 33) and carcinoma in situ lobulare (n = 11). The statistical evaluation was done with an electronic data processing system. We used matched pairs according to age, height and weight. Diabetogenic factors like age and overweight were thus allowed for. These comparative statistics showed a frequency of diabetes twice or three times higher in women with breast cancer. This result cannot be regarded as a consequence of age, overweight and menopause. In groups with fibroadenoma, fibrocystic disease and lipoma, we found glucose tolerance in 1-3%, whereas the group with proliferation (including carcinoma in situ) showed an incidence of 7%. The remarkably high incidence rate of 14% in women with papilloma can be explained by the higher age and the more frequent obesity in this collective.
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PMID:Altered carbohydrate metabolism in breast cancer and benign breast affections. 98 70

A case-control study conducted within the Breast Cancer Detection Demonstration Project allowed comparison of epidemiologic factors for benign breast diseases (n = 1,404), in situ cancer (n = 199), small (less than or equal to 1 cm) invasive cancer (n = 210), and larger invasive cancer (n = 788). Control subjects consisted of program participants who were not recommended for breast biopsy. Relationships were similar for small and larger invasive tumors, both showing associations with family history of breast cancer, age at first live birth, history of bilateral oophorectomoy, and obesity. In situ cancer was affected by family history and age at first childbirth but not by oophorectomy or obesity. These findings support the notion that "minimal" breast cancer is indeed cancer. In addition, the results suggest that hormonal influences early in life may initiate the carcinogenic process, while those that operate later may enhance the progression from in situ to invasive disease.
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PMID:Epidemiology of minimal breast cancer. 684 48

This review of the connection between unopposed estrogen therapy for climacteric symptoms and the development of endometrial hyperplasia briefly outlines the history of the association, and then concentrates on clinical classification problems which muddy the attempts to come to a clear understanding of the relationship between estrogen replacement therapy (ERT) and endometrial cancer. Little agreement exists about the definition of endometrial pathology and of the malignant potentials of different types of hyperplasia. This paper classifies 4 types of hyperplasia: 1) cystic hyperplasia, which has the risk of malignant change of less than 2%; 2) adenomatous hyperplasia, which has a risk of malignant change from 12-25%; 3) atypical hyperplasia, which has a malignancy potential of 45%; and 4) carcinoma in situ, which is malignant. The following conditions are discussed as they are associated with endometrial hyperplasia and adenocarcinoma: 1) obesity; 2) anovulation; 3) late menopause; 4) Stein-Leventhal syndrome; 5) functioning ovarian tumors; and 6) diabetes history. In addition hypertension and cancers of the breast and ovary occur more often with endometrial cancer than would be expected by chance. The remainder of the paper discusses the administration of exogenous estrogens unopposed, exogenous progestins, and their concurrent use, especially in controlling menopausal symptoms. Prevention, diagnosis, and treatment of hyperplasia are discussed. In terms of prevention, a study showed that low-dose cyclical Premarin (.625 mg) resulted in an incidence of hyperplasia of 7% and with higher doses (1.25 mg) rose to 15%. The addition of d-norgestrel for 7 days to the high dose of Premarin reduced incidences to 3%, whereas estrogen plus low-dose norethindrone resulted in 0% incidence of cystic hyperplasia. It is recommended that the unopposed use of estrogens be avoided if possible, although short-term therapy up to 6 months is probably safe. Longer term therapy must have added progestogen, and endometrial sampling in the form of Vabra curettage should be performed every year in patients taking unopposed estrogens and every 3 years in patients taking combined estrogen therapy.
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PMID:Oestrogens and endometrial hyperplasia. 699 95

The paper deals with the contribution of risk factors to the spread of coronary heart disease (CHD) among males living in various cities and towns of Russia, CIS countries and Baltic states. The examination of random representative samples of male populations established that risk factors, such as age, arterial hypertension, obesity, hypercholesterolemia, dyslipoproteinemia, and smoking (p < 0.05), make a significant contribution to the spread of CHD, including acute CHD. Age, arterial hypertension, and body weight (p < 0.01) also make a substantial contribution to the development of CHD. The risk factors play a greater role in the spread of CHD in Tallinn, Alma-Ata, St. Petersburg, and Novosibirsk than in Moscow and Ufa, but in the spread of acute CHD in Tallinn, Kaunas, Ufa, and Alma-Ata than in Moscow and St. Petersburg.
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PMID:[Significance of risk factors in the prevalence of ischemic heart disease in men living in different climatic-geographic areas of Russia, the CIS countries and the Baltic states (a cooperative study)]. 812 Nov 33

Leptin affects food intake and body weight by actions on the hypothalamus. Although leptin resistance is common in obesity, mechanisms have not been identified. We examined the effect of leptin on expression of the suppressors-of-cytokine-signaling (SOCS) family of proteins. Peripheral leptin administration to ob/ob, but not db/db mice, rapidly induced SOCS-3 mRNA in hypothalamus, but had no effect on CIS, SOCS-1, or SOCS-2. A leptin-dependent increase of SOCS-3 mRNA was seen in areas of hypothalamus expressing high levels of the leptin receptor long form. In mammalian cell lines, SOCS-3, but not CIS or SOCS-2, blocked leptin-induced signal transduction. Expression of SOCS-3 mRNA in the arcuate and dorsomedial hypothalamic nuclei is increased in Ay/a mice, a model of leptin-resistant murine obesity. In conclusion, SOCS-3 is a leptin-inducible inhibitor of leptin signaling, and a potential mediator of leptin resistance in obesity.
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PMID:Identification of SOCS-3 as a potential mediator of central leptin resistance. 966 Sep 46

Leptin reflects the amount of energy stores, regulates energy balance and is associated with circulating levels of reproductive hormones and insulin-like growth factor-I (IGF-I). Breast cancer has also been associated with obesity, reproductive hormones and circulating IGF-I levels. To determine whether leptin is involved in the etiology of breast cancer, we compared serum leptin levels in 83 cases of pre-menopausal carcinoma in situ of the breast and 69 healthy controls recruited in Massachusetts. Serum leptin levels were 13.69 + 1.3 ng/ml in cases and 16.03 + 1.7 ng/ml in controls. Data were also analyzed using multiple logistic regression with adjustment for known risk factors for the development of breast cancer as well as anthropometric, demographic and hormonal variables, including estradiol, prolactin, IGF-I and IGF-binding protein-3. Odds ratios were 1.75 (95% CI, 0.73-4.21) for the second control-defined tertile and 1.54 (0.46-5.16) for the third control-defined tertile relative to the first. Thus, leptin does not appear to increase the risk of pre-menopausal breast cancer in situ substantially.
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PMID:Leptin in relation to carcinoma in situ of the breast: a study of pre-menopausal cases and controls. 993 51

Leptin concentrations are elevated in the majority of obese individuals raising the possibility that leptin resistance contributes to their obesity. Peripheral leptin administration for 48 h caused a several-fold increase in mRNA encoding the suppressors of cytokine signaling SOCS-3 and CIS in hypothalamus and peripheral tissues. Paradoxically, CIS and SOCS-3 mRNAs are also elevated in the leptin-deficient ob/ob mouse. Forced expression of CIS in insulinoma cells prevented transactivation mediated by leptin. Thus tissues continuously exposed to leptin and/or other factors associated with obesity accumulate excessive amounts of SOCS-3 and CIS which could provide a potential mechanism for leptin resistance.
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PMID:Leptin treatment increases suppressors of cytokine signaling in central and peripheral tissues. 1042 95

We earlier demonstrated that leptin induces expression of SOCS-3 mRNA in the hypothalamus. Furthermore, transfection data suggest that SOCS-3 is an inhibitor of leptin signaling. However, little is known about the regulation of SOCS-3 expression by leptin and the mechanism by which SOCS-3 inhibits leptin action. We here show that in CHO cells stably expressing the long form of the leptin receptor (CHO-OBRl), leptin induces transient expression of endogenous SOCS-3 mRNA but not of CIS, SOCS-1, or SOCS-2 mRNA. SOCS-3 protein levels were maximal after 2-3 h of leptin treatment and remained elevated at 20 h. Furthermore, in leptin-pretreated CHO-OBRl cells, proximal leptin signaling was blocked for more than 20 h after pretreatment, thus correlating with increased SOCS-3 expression. Leptin pretreatment did not affect cell surface expression of leptin receptors as measured by (125)I-leptin binding assays. In transfected COS cells, forced expression of SOCS-3 results in inhibition of leptin-induced tyrosine phosphorylation of JAK2. Finally, JAK2 co-immunoprecipitates with SOCS-3 in lysates from leptin-treated COS cells. These results suggest that SOCS-3 is a leptin-regulated inhibitor of proximal leptin signaling in vivo. Excessive SOCS-3 activity in leptin-responsive cells is therefore a potential mechanism for leptin resistance, a characteristic feature in human obesity.
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PMID:The role of SOCS-3 in leptin signaling and leptin resistance. 1051 92

The question is whether the administration of estrogenic substances to the human female causes cancer of the endometrium. Current data seems to indicate that in predisposed individuals the unopposed action of estrogenic substances for a considerable period of time will result in endometrial adenomatous hyperplasia, carcinoma in situ (atypical adenomatous hyperplasia), and eventually carcinoma. The relationship of estrogenic substances to the development of endometrial hyperplasia of all degrees is clear, but the relationship of these substances to invasive endometrial cancer is blurred by assumptions based on individual case reports, retrospective reasoning, and uncontrolled experimentation. 4 published reports reviewed here have compared the use of exogenous estrogen by patients with endometrial cancer to that by controls. These studies have not been comprehensive and they raise more questions than they answer. If a physician chooses to use estrogen for the treatment of symptoms or signs of estrogen insufficiency, the selection of patients is crucial. Obesity, hypertension, diabetes, and infertility associated with oligo-ovulation are predisposing factors in the development of endometrial cancer, and patients with these conditions should have endometrial biopsy or uterine aspiration before the institution of therapy. There are 2 therapeutic regimens which can be used to prevent or even reverse the endometrial hyperplasia that may otherwise result from excessive and continuous estrogen administration.
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PMID:Estrogen controversy updated. 1233 9

Risk factors for breast carcinoma in situ and invasive breast cancer were compared using data from 61,844 women (61% post-menopausal) with no prior breast cancer and at least one screening mammogram between April 1, 1996 and June 30, 2001. The women were followed until a subsequent mammogram before July 1, 2001, or a benign biopsy or breast cancer diagnosis before June 30, 2002. A total of 1,191 breast cancers (300 in situ and 891 invasive) were diagnosed during an average follow-up of 3.1 years. Multivariate Cox regression models were used to estimate the relative risks (RR) of in situ and invasive cancer associated with family history of breast cancer, age at first childbirth or nulliparity, post-menopausal hormone use, body mass index (BMI), and mammographic breast density. Separate analyses were done for pre- and post-menopausal women. BMI was unrelated to risk of in situ cancer regardless of menopausal status, but was associated with an increased risk of invasive cancer in post-menopausal women (RR = 1.9 for BMI > or = 30 vs. BMI < 22, 95% confidence interval 1.4-2.5). Later childbearing and nulliparity were more strongly associated with in situ than invasive cancer in pre-menopausal women. Post-menopausal hormone use was more strongly associated with invasive disease. RR associated with family history and breast density were similar for in situ cancer and invasive cancer. Results indicating that BMI is related to post-menopausal invasive cancers but unrelated to in situ cancers are consistent with the hypothesis that concomitants of obesity activate proliferation.
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PMID:Risk factors for breast carcinoma in situ versus invasive breast cancer in a prospective study of pre- and post-menopausal women. 1706 72


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