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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity and its related diseases are the leading cause of death in western society, with associated risks of hypertension, coronary heart disease, stroke, diabetes, and breast, prostate and colon cancer. Recent epidemiologic data indicate an increased risk of Alzheimer's disease in association with adult obesity. There is now convincing evidence that, in both human and animal models, the in utero environment may impact on fetal developmental processes, altering offspring homeostatic regulatory mechanisms. "Gestational programming" may result in altered cell number, organ structure, hormonal set points or gene expression, with effects being permanent or expressed only at select offspring ages (e.g., newborn, adult). Our laboratory and others have demonstrated that low birth weight rats, induced by maternal food restriction or uterine artery ligation, paradoxically develop adult obesity with glucose intolerance and hypertension. Recent studies indicate alterations in peripheral (hepatic) and central (hippocampus) IGF-1 gene expression and epigenetic regulation among these offspring. These findings suggest that potential risk factors for the development of Alzheimer's disease may be present as early as newborn life.
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PMID:Gestational programming of offspring obesity: a potential contributor to Alzheimer's disease. 1743 Feb 49

Recent evidence indicates that obesity and related metabolic abnormalities are associated with increased incidence or mortality for a number of cancers, including those of the colon, prostate, and pancreas. Obesity, physical inactivity, visceral adiposity, hyperglycemia, and hyperinsulinemia are relatively consistent risk factors for colon cancer and adenoma. Also, patients with type 2 diabetes mellitus have a higher risk of colon cancer. For prostate cancer, the relationship to obesity appears more complex. Obesity seems to contribute to a greater risk of aggressive or fatal prostate cancer but perhaps to a lower risk of nonaggressive prostate cancer. Furthermore, men with type 2 diabetes mellitus are at lower risk of developing prostate cancer. Long-standing type 2 diabetes increases the risk of pancreatic cancer by approximately 50%. Furthermore, over the past 6 years, a large number of cohort studies have reported positive associations between obesity and pancreatic cancer. Together with data from prediagnostic blood specimens showing positive associations between glucose levels and pancreatic cancer up to 25 years later, sufficient evidence now supports a strong role for diabetes and obesity in pancreatic cancer etiology. The mechanisms for these associations, however, remain speculative and deserve further study. Hyperinsulinemia may be important, but the role of oxidative stress initiated by hyperglycemia also deserves further attention.
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PMID:The role of obesity and related metabolic disturbances in cancers of the colon, prostate, and pancreas. 1749 13

Obesity is a major public health problem associated with a wide range of health problems. This study estimates the prevalence of obesity, calculates the proportion (or population-attributable fraction [PAF]) of major chronic diseases which is attributable to obesity, estimates the deaths attributable to it and projects its future prevalence trends. In Canada, the overall age-standardized prevalence proportion of obesity has increased from 10 percent in 1970 to 23% in 2004 (8 percent to 23 percent in men and 13 percent to 22 percent in women). The increasing prevalence of obesity was observed for all five age groups examined: 20-34, 35-44, 45-54, 55-64 and 65+. On average, the PAF of prevalence of selected major chronic diseases which is attributable to obesity from 1970 to 2004 has increased by 138 percent for men and by 60 percent for women. Overall, in 2004, 45 percent of hypertension, 39 percent of type II diabetes, 35 percent of gallbladder disease, 23 percent of coronary artery diseases (CAD), 19 percent of osteoarthritis, 11 percent of stroke, 22 percent of endometrial cancer, 12 percent of postmenopausal breast cancer, and 10 percent of colon cancer could be attributed to obesity. In 2004, 8,414 (95 percent CI: 6,881-9,927) deaths were attributable to obesity. If current obesity prevalence trends remain unchanged, the prevalence proportion of obesity in Canada is projected to reach 27 percent in men and 24 percent in women by the year 2010. These increases will have a profound impact on the treatment needs and prevalence of a wide variety of chronic diseases, and also on the health care system in terms of capacity issues and resource allocation.
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PMID:The burden of adult obesity in Canada. 1762 59

The effect of the antidiabetic drug metformin on tumor growth was investigated using the paired isogenic colon cancer cell lines HCT116 p53(+/+) and HCT116 p53(-/-). Treatment with metformin selectively suppressed the tumor growth of HCT116 p53(-/-) xenografts. Following treatment with metformin, we detected increased apoptosis in p53(-/-) tumor sections and an enhanced susceptibility of p53(-/-) cells to undergo apoptosis in vitro when subject to nutrient deprivation. Metformin is proposed to function in diabetes treatment as an indirect activator of AMP-activated protein kinase (AMPK). Treatment with AICAR, another AMPK activator, also showed a selective ability to inhibit p53(-/-) tumor growth in vivo. In the presence of either of the two drugs, HCT116 p53(+/+) cells, but not HCT116 p53(-/-) cells, activated autophagy. A similar p53-dependent induction of autophagy was observed when nontransformed mouse embryo fibroblasts were treated. Treatment with either metformin or AICAR also led to enhanced fatty acid beta-oxidation in p53(+/+) MEFs, but not in p53(-/-) MEFs. However, the magnitude of induction was significantly lower in metformin-treated cells, as metformin treatment also suppressed mitochondrial electron transport. Metformin-treated cells compensated for this suppression of oxidative phosphorylation by increasing their rate of glycolysis in a p53-dependent manner. Together, these data suggest that metformin treatment forces a metabolic conversion that p53(-/-) cells are unable to execute. Thus, metformin is selectively toxic to p53-deficient cells and provides a potential mechanism for the reduced incidence of tumors observed in patients being treated with metformin.
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PMID:Systemic treatment with the antidiabetic drug metformin selectively impairs p53-deficient tumor cell growth. 1763 85

The non-cellulosic polysaccharides present in cereals (2-8%) are mostly arabinoxylans, (1 --> 3),(1 --> 4)-beta -glucans, pectins and arabinogalactans. Of these, the arabinoxylans are known to absorb large amounts of water and influence significantly the water balance, rheological properties of dough, and the retrogradation of starch and bread quality. (1 --> 3),(1 --> 4)-beta -glucans are known as biological response modifiers (BMS) as they are believed to modulate the immune response. Cereal Pectins and arabinogalactans form a very small amount and do not contribute substantially to the functionality of noncellulosic polysaccharides. Detailed structural investigations on cereal hetero xylans using modern techniques were initiated in the 1990s and still pose a challenge to carbohydrate chemists because of their structural complexity. Nutritionally, they are classified under "unavailable carbohydrates" (dietary fiber) along with lignin and cellulose and are known to have beneficial effects in alleviating disease symptoms such as diabetes, atherosclerosis, and colon cancer. In this review isolation, purification, characterization, structural elucidation, functional, and nutritional attributes of cereal heteroxylans are covered with particular emphasis on recently characterized finger millet arabinoxylans.
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PMID:Cereal non-cellulosic polysaccharides: structure and function relationship - an overview. 1765 83

Evidence is scarce about the influence of comorbidity on outcome of surgery, whereas this information is highly relevant for estimating the surgical risk of cancer patients, and for optimising pre-, peri- and postoperative care. In this paper, the prognostic role of increasing age and comorbid conditions in patients diagnosed with stage I-III colorectal, stage I-II NSCLC or stage I-III breast cancer between 1995 and 2004 in the southern part of the Netherlands is summarised. Almost all patients with stage I-III colon cancer or rectal cancer underwent surgery regardless of age or comorbidity. In contrast, the resection rate among elderly patients with stage I-II NSCLC was clearly lower than among younger patients and was significantly lower when COPD, cardiovascular diseases or diabetes were present. Among patients with stage I-III breast cancer, those aged 80 or older underwent less surgery, and the resection rate appeared to be lower when cardiovascular diseases or diabetes were present. Among patients with resected colorectal cancer, postoperative morbidity and mortality were higher among those undergoing emergency surgery, and also among those with reduced pulmonary function, cardiovascular disease or neurological comorbidity. Among those with resected NSCLC, postoperative morbidity and mortality were related to reduced pulmonary function or cardiovascular disease. Since surgery for breast cancer is low risk, elective surgery, morbidity and mortality were not higher for elderly or those with comorbidity. Among patients with colorectal or breast cancer, comorbidity in general, cardiovascular diseases, COPD, diabetes (only colon and breast cancer) and venous thromboembolism had a negative effect on overall survival, whereas the effect of comorbidity on survival of stage I-II NSCLC was less clear. Elderly and those with comorbidity (especially cardiovascular diseases and COPD) among colorectal cancer and NSCLC patients had more postoperative morbidity and mortality. Prospective randomised studies are needed for refining selection criteria for surgery in elderly cancer patients and for anticipation and prevention of complications.
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PMID:Comorbidity in older surgical cancer patients: influence on patient care and outcome. 1768 80

Although turmeric (Curcuma longa; an Indian spice) has been described in Ayurveda, as a treatment for inflammatory diseases and is referred by different names in different cultures, the active principle called curcumin or diferuloylmethane, a yellow pigment present in turmeric (curry powder) has been shown to exhibit numerous activities. Extensive research over the last half century has revealed several important functions of curcumin. It binds to a variety of proteins and inhibits the activity of various kinases. By modulating the activation of various transcription factors, curcumin regulates the expression of inflammatory enzymes, cytokines, adhesion molecules, and cell survival proteins. Curcumin also downregulates cyclin D1, cyclin E and MDM2; and upregulates p21, p27, and p53. Various preclinical cell culture and animal studies suggest that curcumin has potential as an antiproliferative, anti-invasive, and antiangiogenic agent; as a mediator of chemoresistance and radioresistance; as a chemopreventive agent; and as a therapeutic agent in wound healing, diabetes, Alzheimer disease, Parkinson disease, cardiovascular disease, pulmonary disease, and arthritis. Pilot phase I clinical trials have shown curcumin to be safe even when consumed at a daily dose of 12g for 3 months. Other clinical trials suggest a potential therapeutic role for curcumin in diseases such as familial adenomatous polyposis, inflammatory bowel disease, ulcerative colitis, colon cancer, pancreatic cancer, hypercholesteremia, atherosclerosis, pancreatitis, psoriasis, chronic anterior uveitis and arthritis. Thus, curcumin, a spice once relegated to the kitchen shelf, has moved into the clinic and may prove to be "Curecumin".
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PMID:Curcumin as "Curecumin": from kitchen to clinic. 1790 May 36

Clinically relevant family history information is frequently missing or not readily available in electronic health records. Improving the availability of family history information is important for optimum care of many patients. Family history information on five conditions was collected in a survey from 163 primary care patients. Overall, 53% of patients had no family history information in the electronic health record (EHR) either on the patient's problem list or within a templated family history note. New information provided by patients resulted in an increase in the patient's risk level for 32% of patients with a positive family history of breast cancer, 40% for coronary artery disease, 50% for colon cancer, 74% for diabetes, and 95% each for osteoporosis and glaucoma. Informing physicians of new family history information outside of a clinic visit through an electronic clinical message and note in the EHR was not sufficient to achieve recommended follow-up care. Better tools need to be developed to facilitate the collection of family history information and to support clinical decision-making and action.
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PMID:Do physicians take action on high risk family history information provided by patients outside of a clinic visit? 1791 69

Resistin was initially identified as a protein, secreted by adipocytes, which inhibits insulin action and adipose differentiation. The three proteins homologous to resistin were identified and given the names resistin-like molecules (RELM) alpha, beta and gamma. Resistin and RELMalpha are abundantly expressed in adipose, but RELMbeta and RELMgamma are secreted mainly from the gut. Since nutrient composition greatly affects insulin sensitivity, we investigated the regulatory effects of various nutritional factors in food on the expressions of resistin family proteins. First, mice were given diets with different nutritional compositions (high-carbohydrate, high-protein and high-fat) for 2 weeks. RELMbeta mRNA expression in the intestines was markedly suppressed by the high-protein and high-carbohydrate diets, while slightly but not significantly upregulated by the high-fat diet. In the epididymal fat, resistin expression was unchanged, while RELMalpha expression was markedly decreased by the high-carbohydrate diet. Taking into consideration that humans have neither RELMalpha nor RELMgamma, our subsequent studies focused on RELMbeta expression. We used the human colon cancer cell line LS174T. Treatments with insulin and TNFalpha as well as stearic acid, a saturated free fatty acid, upregulated RELMbeta expression, while d-glucose downregulated RELMbeta. These results suggest RELMbeta expression to be regulated directly by nutrients such as glucose and saturated free fatty acids including stearic acid, as well as by hormones including insulin and TNFalpha. These regulations may play an important role in the nutrient-associated induction of insulin resistance.
Diabetes Res Clin Pract 2008 Jan
PMID:Regulation of gut-derived resistin-like molecule beta expression by nutrients. 1793 98

Peroxisome proliferator-activated receptor-gamma (PPARgamma) is expressed at very high levels in the gastrointestinal epithelium. Many of the functions of PPARgamma in gastrointestinal epithelial cells have been elucidated in recent years, and a pattern is emerging which suggests that this receptor plays an important role in gastrointestinal physiology. There is also strong evidence that PPARgamma is a colon cancer suppressor in pre-clinical rodent models of sporadic colon cancer, and there is considerable interest in exploitation of PPARgamma agonists as prophylactic or chemopreventive agents in colon cancer. Studies in mice and in human colon cancer cell lines suggest several mechanisms that might account for the tumor suppressive effects of PPARgamma agonists, although it is not in all cases clear whether these effects are altogether mediated by PPARgamma. Conversely, several reports suggest that PPARgamma agonists may promote colon cancer under certain circumstances. This possibility warrants considerable attention since several million individuals with type II diabetes are currently taking PPARgamma agonists. This review will focus on recent data related to four critical questions: what is the physiological function of PPARgamma in gastrointestinal epithelial cells; how does PPARgamma suppress colon carcinogenesis; is PPARgamma a tumor promoter; and what is the future of PPARgamma in colon cancer prevention?
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PMID:PPARgamma physiology and pathology in gastrointestinal epithelial cells. 1797 68


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