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

Current epidemiological data suggest that the number of preventive interventions aimed at controlling alcohol, drug, food abuse and smoking achieved only partial success, especially in young individuals. In order to improve preventive action efficacy, the literature suggests the adoption of contents and communication instruments specifically targeted to different groups of individuals. The Valentino Project is a comprehensive survey on the characteristics of abuse of a representative sample of 3000 young workers (aged 18-35 years)from the Abruzzo Region of Italy. This paper describes its main methodological issues and the complete version of the questionnaire HW-80 (Healthy-Worker 80), that will be administered. HW-80 questionnaire includes 80 items on demographic characteristics, self-reported health, job-related stress, work organization, pattern of abuse, physical activity and others, and several of these items have been taken or derived from repeatedly validated questionnaires (SF-12, CAGE, Job-Strain, Effort-Reward, EU-DAP, etc.). The aims of the Valentino Project are to quantify the prevalence of obesity, alcohol use, smoking and drug addiction in diverse typologies of workers, and to describe their pattern of use. The ultimate purpose is to provide the necessary knowledge for the development of preventive strategies targeted to different professions, in order to maximize their efficacy.
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PMID:[Drug, food, alcohol abuse and smoking in young workers. Methodology of a survey aimed at developing preventive interventions targeted to different type of workers: the Valentino Study]. 1765 11

Social stress resulting from dominant-subordinate relationships is associated with body weight loss and altered body composition in subordinate (SUB) male rats. Here, we extend these findings to determine whether stress-induced changes in energy homeostasis persist when the social stress is removed, and the animal is allowed to recover. We examined body weight (BW), body composition, and relevant endocrine measures after one or two cycles of 14 days of social stress, each followed by 21 days of recovery in each rat's individual home cage. SUB lost significantly more BW during social housing in a visible burrow system (VBS) compared with dominant (DOM) animals. Weight loss during social stress was attributable to a decrease in adipose tissue in DOM and SUB, with an additional loss of lean tissue in SUB. During both 21-day recovery periods, DOM and SUB regained lost BW, but only SUB were hyperphagic. Following recovery, SUB had a relatively larger increase in adipose tissue and plasma leptin compared with DOM, indicating that body composition changes were dependent on social status. Control animals that were weight matched to SUB or male rats exposed to the VBS environment without females, and that did not form a social hierarchy, did not exhibit changes in body composition like SUB in the VBS. Therefore, chronic social stress causes social status-dependent changes in BW, composition and endocrine measures that persist after repeated stress and recovery cycles and that may ultimately lead to metabolic disorders and obesity.
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PMID:Social stress and recovery: implications for body weight and body composition. 1785 91

Anorexia and weight loss are part of the wasting syndrome of late-stage cancer, are a major cause of morbidity and mortality in cancer, and are thought to be cytokine mediated. Macrophage inhibitory cytokine-1 (MIC-1) is produced by many cancers. Examination of sera from individuals with advanced prostate cancer showed a direct relationship between MIC-1 abundance and cancer-associated weight loss. In mice with xenografted prostate tumors, elevated MIC-1 levels were also associated with marked weight, fat and lean tissue loss that was mediated by decreased food intake and was reversed by administration of antibody to MIC-1. Additionally, normal mice given systemic MIC-1 and transgenic mice overexpressing MIC-1 showed hypophagia and reduced body weight. MIC-1 mediates its effects by central mechanisms that implicate the hypothalamic transforming growth factor-beta receptor II, extracellular signal-regulated kinases 1 and 2, signal transducer and activator of transcription-3, neuropeptide Y and pro-opiomelanocortin. Thus, MIC-1 is a newly defined central regulator of appetite and a potential target for the treatment of both cancer anorexia and weight loss, as well as of obesity.
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PMID:Tumor-induced anorexia and weight loss are mediated by the TGF-beta superfamily cytokine MIC-1. 1798 62

Obesity is an epidemic disease that may affect brain function. The present study examined the effect of high fat diet (HF) and physical exercise on peripheral tissue and hippocampal signaling. CF-1 mice (n = 4, per cage) were divided into groups receiving high fat (HF) or control (CD) diets for 5 months, with or without voluntary exercise. Serum triacylglycerol, total cholesterol, HDLc, liver triacylglycerol and glycogen concentrations were evaluated (n = 6). Also, the phosphorylation state of the AKT --> ERK 1/2 --> CREB pathway (AKT, pAKTser473, ERK 1/2, pERK 1/2, CREB and pCREB, n = 4-6) was analyzed in the hippocampus. HF diet caused an increase in AKT phosphorylation at ser473 (P < 0.05), while exercise increased the phosphorylation of ERK 1/2 (P < 0.05) and CREB (P < 0.05). As expected, exercise reversed some of the harmful effects of HF, i.e., increased liver deposition of fat (P < 0.05) and fat gain in the abdominal region (P < 0.05). In conclusion, the effects of exercise and HF diet on brain signaling appear to affect the hippocampal AKT --> ERK 1/2 --> CREB pathway in independent ways: HF intake caused increased phosphorylation of AKTser473, while exercise increased ERK 1/2 --> CREB signaling. The physiological relevance of these findings in brain function remains to be elucidated.
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PMID:Different effect of high fat diet and physical exercise in the hippocampal signaling. 1803 3

We determined whether altered physical activity levels might underlie the contrasting adiposity of a divergently selected polygenic murine model of metabolic syndrome (Fat; F) and leanness (Lean; L) mice. We measured physical activity with a long term running wheel experiment and performed an additional high fat diet intervention. Further, we measured posture allocation by visual monitoring within the home cage as a non-exercise correlate of 'normal' physical activity. Whilst initially similar, running wheel activity of the F line declined with age, while the activity of the L line increased. Food intake was higher in the L line and increased with wheel exposure. Vertical rearing measured by video quantification in the home cage, without the stimulus of a running wheel was also significantly higher in the L line. The two lines developed novel alternate strategies to defend their body weight when exposed to high fat diets with a running wheel. F mice increased their running wheel activity, and despite unaltered food intake, still gained weight. L mice reduced their food intake and maintained activity levels without a significant change in body weight. Phenotypic selection for divergence in body fat content has co-segregated with a genetic predisposition for divergent physical activity levels and different strategies for coping with exposure to high fat diets that will facilitate the discovery of the genes underlying these important obesity related traits.
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PMID:Divergent physical activity and novel alternative responses to high fat feeding in polygenic fat and lean mice. 1834 69

The Tub gene was originally identified as a spontaneous mutation in C57Bl/6J mice, and associated with adult-onset obesity (Tub MUT mice). Although the original Tub MUT mouse was identified over 15 years ago, there have been few reports on the animal's food intake, body fat percentage or energy expenditure. In this study, we report food intake, body weight from 5-20 weeks, body fat, body temperature and three different measures of physical activity behavior. Tub MUT mice display reduced food intake, uncharacteristic of many obese mouse models, and reduced voluntary wheel running with normal home cage ambulatory behavior. We conclude that motivation for food and exercise is an underlying defect in TUB MUT mice.
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PMID:Reduced activity without hyperphagia contributes to obesity in Tubby mutant mice. 1861 28

Obesity is associated with diverse health risks, but the role of body weight (BMI) as a risk factor for all and site-specific cancers remains controversial and risks for cancer associated with obesity have not been well-characterized in Asians. Body weight and risk for cancer were examined in a 14-year prospective cohort study of 1,213,829 Koreans aged 30-95 years insured by the National Health Insurance Corporation who had a biennial medical evaluation in 1992-1995. Incidence rates for all cancers and site-specific cancers were examined in relation to BMI. Age- and smoking-status adjusted hazard ratios (HR) with 95% confidence intervals (CI) were examined using the Cox proportional hazards model. For both sexes, the average baseline BMI was 23.2 kg/m(2), and the association of risk for all-cancers with BMI was positive. Obese men (BMI >or= 30 kg/m(2)) were at increased risk for developing the following cancers: stomach (1.31, 1.05-1.64), colon (1.42, 1.02-1.98), liver (1.63, 1.27-2.10) and gallbladder (1.65, 1.11-2.44). Obese women (BMI >or= 30 kg/m(2)) were at increased risk for developing liver cancer (1.39, 1.00-1.94), pancreatic cancer (1.80, 1.14-2.86) and breast cancer among women aged >or=50 years old (1.38, 1.00-1.90). The HRs were comparable in never and ever smokers for all cancers and all specific sites except for lung cancer. For all cancers common to both sexes, the association was significantly weaker (p < 0.01) in females. Our study provides further confirmation of the excess cancer risk associated with obesity. Rising obesity in Asian populations raises concern that increasing numbers of avoidable cancer cases will occur among Asians.
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PMID:Body mass index and cancer risk in Korean men and women. 1865 71

Sleep deprivation in humans has been related to weight gain and consequently, increased risk for insulin resistance. In contrast, there is a significant loss of weight in sleep deprived rats suggesting a state of insulin resistance without obesity interference. Thus, we aimed to assess the effects of a rich fish oil dietetic intervention on glucose tolerance, serum insulin and adiponectin, and adipose tissue gene expression of adiponectin and TNF-alpha of paradoxically sleep deprived (PSD) rats. The study was performed in thirty day-old male Wistar randomly assigned into two groups: rats fed with control diet (soybean oil as source of fat) and rats fed with a fish oil rich diet. After 45 days of treatment, the animals were submitted to PSD or maintained as home cage control group for 96 h. Body weight and food intake were carefully monitored in all groups. At the end of PSD period, a glucose tolerance test was performed and the total blood and adipose tissues were collected. Serum insulin and adiponectin were analyzed. Adipose tissues were used for RT-PCR to estimate the gene expression of adiponectin and TNF-alpha. Results showed that although fish oil diet did not exert any effect upon these measurements, PSD induced a reduction in adiponectin gene expression of retroperitoneal adipose tissues, with no change in serum adiponectin concentration or in adiponectin and TNF-alpha gene expression of epididymal adipose tissue. Thus, the stress induced by sleep deprivation lead to a desbalance of adiponectin gene expression.
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PMID:Dietary fish oil did not prevent sleep deprived rats from a reduction in adipose tissue adiponectin gene expression. 1898 29

The risk of venous thromboembolism (VTE) is elevated in cancer, and thrombosis is the second leading cause of death in patients with malignancy. Many risk factors for cancer-associated thrombosis have been identified. These include patient-associated factors such as age, obesity and medical comorbidities; cancer-associated factors such as site and stage of cancer; and treatment-associated factors, particularly chemotherapy and hospitalization. In addition, several candidate biomarkers for cancer-associated thrombosis have been identified recently. Despite the high rate and significant impact of VTE in cancer outpatients, prior attempts at thromboprophylaxis in this population have not consistently demonstrated a benefit. This chapter will focus on risk stratification approaches, including a recently developed predictive model which can be used to identify those patients at highest risk. This model-based approach may have a significant impact on cancer-related morbidity, mortality and cost of care by directing targeted thromboprophylaxis in the future.
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PMID:Risk stratification for cancer-associated venous thromboembolism. 1928 71

Mouse models with physiological and behavioral differences attributable to differential plasticity of hippocampal and amygdalar neuronal networks are rare. We previously generated ataxin-2 (Atxn2) knockout mice and demonstrated that these animals lacked obvious anatomical abnormalities of the CNS, but showed marked obesity and reduced fertility. We now report on behavioral changes as a consequence of Atxn2-deficiency. Atxn2-deficiency was associated with impaired long-term potentiation (LTP) in the amygdala, but normal LTP in the hippocampus. Intact hippocampal plasticity was associated behaviorally with normal Morris Water maze testing. Impaired amygdala plasticity was associated with reduced cued and contextual fear conditioning. Conditioned taste aversion, however, was normal. In addition, knockout mice showed decreased innate fear in several tests and motor hyperactivity in open cage testing. Our results suggest that Atxn2-deficiency results in a specific set of behavioral and cellular disturbances that include motor hyperactivity and abnormal fear-related behaviors, but intact hippocampal function. This animal model may be useful for the study of anxiety disorders and should encourage studies of anxiety in patients with spinocerebellar ataxia type 2 (SCA2).
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PMID:Dissociated fear and spatial learning in mice with deficiency of ataxin-2. 1961 10


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