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

The metabolic mechanism for increased circulating free fatty acids in post-menopausal women with metastatic breast cancer was investigated. Hormone and metabolic response to glucose and growth hormone were compared to cancer patients and control subjects; thyroid, adrenal and pituitary function were evaluated. The results of these studies indicated that breast cancer patients had glucose intolerance and delayed and prolonged insulin secretion, increased basal growth hormone levels and insensitivity of adipose tissue to growth hormone. Cortisol and protein-bound iodine levels were normal and there was no lipolytic factor in the sera of breast cancer patients. The changes observed in breast cancer patients were not attributable to age, obesity, inanition or stress. These metabolic abnormalities may characterize host susceptibility to breast cancer or be effects of tumor.
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PMID:Metabolic parameters in women with metastatic breast cancer. 4 95

Studies on the relationship of urinary excretion of androgen metabolites and estrogens to the natural history of breast cancer are reviewed. The importance of distinguishing between "within-population" studies (i.e., cancer patients versus normal controls) and "between populations" studies (i.e., low-risk versus high-risk populations) is emphasized, and it is pointed out that "qualitative" agreement (i.e. the same direction of differences) between the two types of studies must be present in order to implicate a hormonal parameter as a determinant of the natural history of breast cancer. For reasons detailed in this paper, it is concluded that the reported relationship of low urinary androgen metabolite excretion to increased risk of developing breast cancer and poor response to adrenalectomy or hypophysectomy and the validity of the "estriol hypothesis," namely, that a high urinary ratio of estriol to estrone-plus-estradiol in early life is protective against subsequent development of breast cancer, are both dubious. A new hypothesis concerning the relationship of estrogens to breast cancer risk is presented: "A period of of time, prior to age 30, during which the amount of biological availability of active estrogens' (i.e., estrone and estradiol) is diminished, protects against subsequent development of cancer." This hypothesis is shown to be compatible with the epidemiological and biochemical data. Reports concerning the influence of nutrition on endocrine parameters are reviewed. Inanition and obesity have been shown to alter steroid metabolism but it is not known whether nutritional "microdifferences" (i.e., differences between populations or individuals that are due to cultural, geographic, or socioeconomic factors, but that fall within the range of "normal" or adequate nutrition) can also alter steroid metabolism.
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PMID:Hormone profiles in hormone-dependent cancers. 110 49

Suicide in anorexia nervosa and bulimia nervosa is a major cause of death. Meta-analyses have shown that individuals suffering from anorexia nervosa and bulimia nervosa commit suicide more often than their counterparts in the general population; also a few studies have suggested that suicide is the major cause of death among patients with anorexia nervosa, refuting the assumption that inanition generally threatens the life of these patients. Data concerning suicide in bulimia nervosa, on the other hand, are still scarce but suicide attempts are easily found among cohorts of patients with bulimia nervosa, which constitutes a risk factor for completed suicide. Suicidality in obesity and individuals with disturbed weight status has been reported. Both in the case of bulimia nervosa and obesity more long-term follow-up studies need to be completed before the risk of suicide for such disorders may be compared with that for anorexia nervosa.
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PMID:Suicide and attempted suicide in eating disorders, obesity and weight-image concern. 1705 16

Prader-Willi syndrome (PWS), with a prevalence of 60:1.000.000, results from the loss of paternal chromosome 15, being 56% due to deletion, 24% due to uniparental maternal disomy, and 18% from methylation, an epigenetic phenomenon. The clinical picture begins with extreme muscular hypotonia, which makes it difficult to feed the child in the first year. As the hypotonia improves, usually in the first two years, around the 4th year of life, an insatiable appetite leads these children to an extreme obesity, with alveolar hypoventilation which endangers their lives. So, paradoxically, PWS threatens the lives of the patients, through inanition in a first phase and, afterwards, through excessive weight gain. The use of growth hormone (hrGH) in these children has a primary goal to change the body composition and improve the physical activity and the quality of life. On the other hand, many PWS patients are indeed GH deficient, and an improvement in the height SDS occurs with treatment. We have to be careful, however. When starting a PWS treatment with a patient on hrGH, a careful evaluation of sleep apnoea (polysomnography) as well as a careful examination of the airways is extremely mandatory, since the treatment may compromise the respiratory pattern of some patients.
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PMID:[Growth hormone usage in Prader-Willi syndrome]. 1879 90