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

Epidemiologic studies of colorectal neoplasia have usually examined body mass index as a risk factor, but not other aspects of obesity. During 1991-1993, the authors obtained weight histories and comprehensive covariate data from men and women aged 50-75 years who underwent sigmoidoscopy at a health maintenance organization in southern California. Using 483 cases with adenomas and 483 controls, measures of obesity (body mass index), positive energy balance (net weight gain in the past 10 years), and weight variability (large weight changes) were each independently related to adenoma prevalence. Compared with subjects in the lowest quartile of body mass index, multivariate-adjusted odds ratios for subjects in increasingly higher quartiles were 2.1 (95% confidence interval (CI) 1.4-2.3), 1.8 (1.1-2.9), and 1.7 (1.0-2.8), respectively. Compared with subjects who reported a net weight loss during the 10 years before sigmoidoscopy, subjects with net weight gains of 1.5-4.5 kg or > or = 4.5 kg had adjusted odds ratios (95% CI) of 2.5 (1.2-5.6) and 1.8 (0.7-4.4), respectively. Compared with subjects who had no large weight changes during adulthood, subjects with 1-2, 3, or > or = 4 changes had adjusted odds ratios (95% CI) of 2.0 (1.0-3.9), 2.5 (1.2-5.5), and 1.5 (0.6-3.6), respectively. Obesity, weight gain, and unstable adult weight may be independently associated with colorectal carcinogenesis.
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PMID:Obesity, weight gain, large weight changes, and adenomatous polyps of the left colon and rectum. 955 6

A cross-sectional study was conducted to evaluate the relationship between body mass and serum level of female sex hormones among 153 adolescent girls, and 153 postmenopausal women in Korea. Information on lifestyles, and both menstrual and reproductive factors was collected by personal interview. Serum total estradiol (E2), progesterone (Pg), and sex hormone binding globulin (SHBG) concentrations were measured by radioimmunoassay. Multiple linear regression analysis was used to determine whether the hormonal levels would be affected by the obesity indices. Body weight and body mass index (BMI) were inversely related to SHBG level in both premenopausal (p<0.005) and postmenopausal women (p<0.005) after adjusting for age. E2 levels during any phase in premenopausal girls were not related to BMI, whereas heavier girls had significantly higher levels of late luteal-phase Pg (p<0.05). Taller postmenopausal women had lower E2 levels (p<0.05). Results on the association between SHBG and BMI are consistent with previous results in Caucasian women, and might suggest the potential role of bioavailable estradiol in breast carcinogenesis in pre- and post-menopausal women. The finding that progesterone might be related to body mass in premenopausal women should be pursued in further studies.
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PMID:Female sex hormones and body mass in adolescent and postmenopausal Korean women. 968 1

This review summarizes data on the occurrence, the trends, and the life-style, environmental, occupational and genetic determinants of pancreatic cancer. Epidemiologic evidence implicates tobacco smoking as one cause. The evidence regarding alcohol consumption is inconsistent. Although both positive and inconclusive findings are encountered, the bulk of the evidence on coffee consumption is negative. Fat intake is linked with obesity and diabetes mellitus, which are risk factors for pancreatic cancer. Fruit and vegetable consumption appears to be protective. No occupational or environmental agent has been confirmed to increase the risk, but epidemiologic evidence is inconsistent, Little is known about the role of genetic polymorphisms of metabolic enzymes in pancreas carcinogenesis. Pancreatic cancer shows high rates of mutations of Ki-ras and losses or mutations of tumor suppressor genes (p53, p16INK4A, and SMAD4/DPC-4). Ki-ras mutations have been associated with life-style factors in relation to pancreatic cancer, but the evidence is still scant and inconsistent.
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PMID:Occurrence, trends and environment etiology of pancreatic cancer. 971 Mar 67

While most studies show a higher body mass in Western women to be positively associated with an increased breast cancer risk in postmenopausal women, they show a negative association in the case of premenopausal women. A review of case-control and cohort studies suggest that such protection applies mainly to obesity in teenage girls, whereas obesity appearing after the teenage years is more likely to be associated with a higher risk of postmenopausal breast cancer. The mechanisms are uncertain. There is evidence that obesity and the components of the Western diet can independently provoke hyperinsulinaemic insulin resistance at puberty, and in adolescent girls this has been related to evidence of abnormal ovarian steroidogenesis and anovulation. This may decrease promotion of mammary carcinogenesis. If however, obesity continues after the teenage years, the higher concentration of insulin-like growth factor 1 (IGF1) associated with hyperinsulinaemia can interact with oestrogen receptors in mammary epithelium to lead to increased proliferative activity. This review postulates that the observed protective effect of early obesity against premenopausal breast cancer is likely to be replaced by an increased risk of postmenopausal breast cancer if obesity continues after the teenage years. The manifestation of breast cancer is merely postponed to an older age. Recent prospective and case-control studies suggest that increased bioavailability of IGF1 is a marker of increased breast cancer risk in premenopausal women. Nutritional intake in early life may programme later activity in the growth hormone-IGF1 axis and influence the progression of transformed cells in mammary tissue. The question remains whether deliberate weight loss can reverse the effects of weight gain.
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PMID:Teenage obesity in relation to breast cancer risk. 982 39

Macrophage migration inhibitory factor (MIF) was the first T-cell-derived soluble lymphokine to be identified. It was originally found to inhibit the migration of macrophages and activate them at inflammatory loci. During the past few years, however, previously unrecognized properties of MIF have been discovered. It also functions, for example, as a pituitary hormone, glucocorticoid-induced immunomodulator and isomerase. We cloned rat MIF cDNA and reported that the nucleotide sequence of the cDNA predicts a protein consisting of 114 amino acids. Northern blot analysis indicated that the MIF mRNA was expressed in a wide variety of organs, including the brain, kidney, and liver. Following this, we demonstrated definitively that MIF was expressed in a variety of cells, suggesting its involvement in various biological events such as wound healing, atopic dermatitis, and, possibly, diabetes/obesity. Furthermore, we elucidated its physicochemical properties, including the tertiary structures of both human and rat MIF. These tertiary structures showed that this protein forms a homotrimer with each monomer consisting of two beta/alpha/beta motifs, thus resembling 5-carboxymethyl-2-hydroxymuconate isomerase and d-dopachrome tautomerase. From the available data on MIF, including ours, it is considered that the protein is associated not only with immune responses but also with cell growth and differentiation during wound repair and carcinogenesis. Thus, MIF could become a major target protein in a variety of pathophysiological states and anti-MIF antibodies and antagonists could be applied therapeutically in the clinical situation for treatment of various diseases. Bearing this in mind, this review discusses the role of MIF, considering its gene and protein structures as well as its pathophysiological functions in various organs and disease states, finally considering perspectives for the future.
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PMID:Novel pathophysiological aspects of macrophage migration inhibitory factor (review). 985 38

Numerous lifestyle factors have been implicated in colorectal carcinogenesis. These include diet, inadequate physical activity, obesity, alcohol consumption, and smoking. Epidemiologic studies, animal experiments, and randomized clinical trials have shown that dietary factors can influence all stages of colorectal carcinogenesis, from cell proliferation to transformation to cancer. Defining the precise role of diet and other lifestyle factors in colorectal carcinogenesis may require the elucidation of genetic susceptibility and genetic-environmental interactions. Despite the preoccupation with nutrition by the public and the media in the United States, trends in food consumption have not been favorable. The average U.S. diet is still too high in calories and fat and too low in fiber, cereals, fruits, and vegetables. Dietary modifications along with secondary prevention measures may have a major impact on reducing the mortality from colorectal cancer.
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PMID:Diet and lifestyle in the prevention of colorectal cancer: an overview. 1008 8

Recent advances in biosciences support the hypothesis that diet modulates various body functions. Diet may maintain well-being and reduce the risk of some diseases. Such discoveries have led to the concept of "functional food" and the development of the new discipline, i.e., "functional food science." A practical and simple definition of a "functional food" is a food for which a claim has been authorized. The food components to be discussed as potential "functional food ingredients" are the inulin-type fructans, i.e., chicory inulin and oligofuctose. The targets for their effects are the colonic microflora, the gastrointestinal physiology, the immune functions, the bioavailability of minerals, the metabolism of lipids and colonic carcinogenesis. Potential health benefits include reduction of risk of colonic diseases, noninsulin-dependent diabetes, obesity, osteoporosis and cancer. The documentation of such benefits requires scientific evidence that must be evaluated in terms of "health claims." Previous assessments have concluded that, in terms of "functional claims," strong evidence exists for a prebiotic effect and improved bowel habit. The evidence for calcium bioavailability is promising, and positive modulation of triglyceride metabolism is undergoing preliminary evaluation. Scientific research still must be done to support any "disease risk reduction claim," but sound hypotheses do already exist for designing the relevant human nutrition trials.
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PMID:Concepts in functional foods: the case of inulin and oligofructose. 1039 6

The peroxisome proliferator-activated receptor gamma (PPARgamma) quickly evolved over the last decade from a new orphan receptor to one of the best characterized nuclear receptors. This fast pace in PPARgamma research was triggered by two main discoveries. Firstly, that PPARgamma was shown to have a key role in adipogenesis and be a master controller of the "thrifty gene response" leading to efficient energy storage. Secondly, the discovery that its synthetic ligands, the thiazolidinediones, are promising insulin sensitizing drugs, which are currently being developed for the treatment of Type II (non-insulin-dependent) diabetes mellitus. More recently this nuclear receptor emerged from a role limited to metabolism (diabetes and obesity) to a power player in general transcriptional control of numerous cellular processes, with implications in cell cycle control, carcinogenesis, inflammation, atherosclerosis and immunomodulation. This widened role of PPARgamma will certainly initiate a new flurry of research, which will not only refine our current often partial knowledge of PPARgamma but more importantly also establish that this receptor has a definite role as a primary link adapting cellular, tissue and whole body homeostasis to energy stores.
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PMID:PPARgamma, the ultimate thrifty gene. 1044 13

Biological markers associated with in situ carcinoma and atypical intraductal hyperplasia in the breast are examined to help in identifying a subgroup of premalignant lesions whose natural history may be influenced by epigenetic factors. The biomarkers may be used as indices in clinical trials aiming to assess the effect of weight reduction, dietary intervention or hormone replacement therapy on the risk of progression to invasive breast cancer. In the current state of knowledge, the expression of oestrogen receptors, p53, bcl-2 and HER-2 neu oncogenes and the Ki-67 index of proliferative activity, are the most useful biomarkers for this purpose. In situ carcinoma of the breast manifests a variety of morphological phenotypes with specific biological characteristics. There is evidence that only a proportion of premalignant lesions are committed to progression to invasive cancer while other lesions undergo spontaneous regression at the time of the menopause. Cross-cultural studies suggest that it is the late-stage epigenetic promoting factors which are responsible for the high incidence of postmenopausal breast cancer in Western women. Obesity in middle life and the Western diet favour the development of hyperinsulinaemic insulin resistance, and the metabolic-endocrine effects of its concomitants may promote mammary carcinogenesis around the time of the menopause and increase the incidence of invasive cancer after the menopause. Because biomarker changes in premalignant lesions are nearer in time to these promoting influences, they could provide intermediate endpoints for testing the hypothesis.
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PMID:Premalignant breast lesions: role for biological markers in predicting progression to cancer. 1050 26

The peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear receptor that controls the expression of a large array of genes involved in adipocyte differentiation, lipid storage and insulin sensitization. PPARgamma is bound and activated by prostaglandin J2 and fatty acid derivatives, which are its natural ligands. In addition, thiazolidinediones and nonsteroidal anti-inflammatory drugs are synthetic ligands and agonists of this receptor. Several studies have recently shown that this nuclear receptor has a role expanding beyond metabolism (diabetes and obesity) with functions in cell cycle control, carcinogenesis, inflammation and atherosclerosis. This review addresses the role of PPARgamma in these processes.
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PMID:Peroxisome proliferator-activated receptor-gamma: a versatile metabolic regulator. 1057 7


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