Database : MEDLINE
Search on : Obesity [Words]
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[PMID]: 29524863
[Au] Autor:Kasselman LJ; Vernice NA; DeLeon J; Reiss AB
[Ad] Address:Winthrop Research Institute and Department of Medicine, NYU Winthrop Hospital, Mineola, NY, USA. Electronic address: lkasselman@nyuwinthrop.org.
[Ti] Title:The gut microbiome and elevated cardiovascular risk in obesity and autoimmunity.
[So] Source:Atherosclerosis;271:203-213, 2018 Mar 02.
[Is] ISSN:1879-1484
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Cardiovascular disease associated with obesity and autoimmunity is the leading cause of death in these populations and significant residual risk remains despite current treatment approaches. Obesity, type 1 diabetes mellitus (T1DM), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE) are linked to chronic inflammation, and subjects with these disorders have characteristic shifts in their gut microbiome composition. Recent data suggest that alterations in gut microbial and metabolic composition may be responsible, in part, for induction of chronic inflammation, thus promoting cardiovascular disease. Common microbiome changes observed in obesity, T1DM, RA, and SLE include a decrease in the ratio of bacteria, such as Gram-positive Firmicutes to Gram-negative Bacteroidetes, as well as an overabundance or depletion of certain species, including Prevotella copri. The consequent effects of these shifts include alterations in the metabolic composition of the gut, hyper-activation of toll-like receptor 4 (TLR-4), upregulation of inflammatory pathways, e.g. c-Jun N-terminal kinase and nuclear factor-kappa B (NFκB), increased intestinal permeability, increased C-reactive protein, and increased levels of trimethylamine N-oxide (TMAO). Differential microbiome compositions may also explain sex differences observed in autoimmunity, where a male gut microbiome promotes anti-inflammatory processes as compared to a female pro-inflammatory gut microbiome. Intervention at the level of the microbiota appears to attenuate symptoms in these inflammatory syndromes with probiotic treatment, such as Lactobacilli, playing a uniquely beneficial role in restoring intestinal health, decreasing inflammation, and reducing cardiovascular disease. This review will discuss obesity, T1DM, RA, and SLE in the context of how each unique microbiome profile contributes to elevated cardiovascular risk.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 272782 MEDLINE  
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[PMID]: 29524783
[Au] Autor:Safahani M; Aligholi H; Noorbakhsh F; Djalali M; Pishva H; Mousavi SMM; Alipour F; Gorji A; Koohdani F
[Ad] Address:Department of Cellular and Molecular Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Title:Resveratrol promotes the arcuate nucleus architecture remodeling to produce more anorexigenic neurons in high-fat-diet-fed mice.
[So] Source:Nutrition;50:49-59, 2017 Dec 02.
[Is] ISSN:1873-1244
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Adult hypothalamic neurogenesis has been considered a central regulator of energy balance. Resveratrol (RSV), a natural polyphenol, influences the body fat mass and reduces the amount of adipose tissue. The present study was designed to evaluate the effect of RSV on dynamic of hypothalamic neurons in a diet-induced obesity model of mice. METHODS: Apoptosis, neurogenesis, the expression of the main trophic factors, and the fate of newborn cells were evaluated in the hypothalamus of adult male C57 BL/6 J mice fed a normal diet, a high-fat (HF) diet, or an HF diet supplemented with 400 mg/kg RSV (HF + RSV) for 6 wk. RESULTS: The HF diet caused an increase in neuronal apoptosis in the hypothalamus, which coincided with an increase in the number of newborn cells in the arcuate nucleus, suggesting that compensatory mechanisms developed to overcome deleterious effects of the HF diet. Addition of RSV to the HF diet enhanced the production of newborn cells in all studied regions of the hypothalamus. These changes were paralleled by enhancement of the expression of ciliary neurotrophic factor. Interestingly, a considerable proportion of newborn cells expressed neuropeptide Y in the arcuate nucleus of the HF group, and conversely, most of them differentiated to proopiomelanocortin neurons in HF + RSV mice. CONCLUSIONS: Diets rich in fat changed hypothalamic neuronal balance toward orexigenic versus anorexigenic neurons. Administration of RSV to the HF diet reversed this balance toward generation of anorexigenic neurons. These data point to the potential for RSV in regulation of body weight, possibly via modulation of hypothalamic neurogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 272782 MEDLINE  
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[PMID]: 29524629
[Au] Autor:Craft CS; Broekelmann TJ; Mecham RP
[Ad] Address:Division of Bone and Mineral Research, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, United States.
[Ti] Title:Microfibril-associated glycoproteins MAGP-1 and MAGP-2 in disease.
[So] Source:Matrix Biol;, 2018 Mar 07.
[Is] ISSN:1569-1802
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Microfibril-associated glycoproteins 1 and 2 (MAGP-1, MAGP-2) are protein components of extracellular matrix microfibrils. These proteins interact with fibrillin, the core component of microfibrils, and impart unique biological properties that influence microfibril function in vertebrates. MAGPs bind active forms of TGFß and BMPs and are capable of modulating Notch signaling. Mutations in MAGP-1 or MAGP-2 have been linked to thoracic aneurysms and metabolic disease in humans. MAGP-2 has also been shown to be an important biomarker in several human cancers. Mice lacking MAGP-1 or MAGP-2 have defects in multiple organ systems, which reflects the widespread distribution of microfibrils in vertebrate tissues. This review summarizes our current understanding of the function of the MAGPs and their relationship to human disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 272782 MEDLINE  
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[PMID]: 29524611
[Au] Autor:Black M; Joseph V; Mott L; Maheswaran R
[Ad] Address:School of Health and Related Research, The University of Sheffield, Regent Court, 30 Regent Street, Sheffield S1 4DA, UK. Electronic address: michelle.black1@nhs.net.
[Ti] Title:Increasing inequality in childhood obesity in primary schools in a northern English town.
[So] Source:Public Health;158:9-14, 2018 Mar 07.
[Is] ISSN:1476-5616
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To undertake an analysis of National Child Measurement Programme (NCMP) data to quantify the obesity prevalence gap over time between children in primary schools in the most and least deprived areas of Doncaster. STUDY DESIGN: The research design for this study was retrospective quantitative analysis of secondary data. METHODS: The study undertook secondary analysis of NCMP data on obesity prevalence in children in Reception Year and Year 6 in primary schools in Doncaster for the period 2006-2007 to 2014-2015. Data were combined into three 3-year periods (2006-2007 to 2008-2009; 2009-2010 to 2011-2012; and 2012-2013 to 2014-2015), and schools were grouped by deprivation based on the national Indices of Multiple Deprivation 2015. Analysis was undertaken to assess whether there is a difference in obesity prevalence for Reception Year and Year 6 children in schools in the most deprived areas compared with the least deprived (prevalence gap), over time. RESULTS: The difference in obesity prevalence between children attending schools in the most and least deprived areas has increased over time. For Reception Year children, the prevalence gap has widened from a difference of 1.01% higher in the most deprived schools in 2006-2007 to 2008-2009 to 3.64% higher in 2012-2013 to 2014-2015. In the same time periods, for Year 6 children, the obesity prevalence gap has also increased over time from 2.82% to 5.08%. CONCLUSIONS: There is inequality in relation to obesity in primary school children in Doncaster with those in schools in the most deprived areas carrying the greatest burden. Research is needed to understand why the plateau seen nationally is not reaching the most deprived children.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 272782 MEDLINE  
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[PMID]: 29524577
[Au] Autor:Javanrouh N; Daneshpour MS; Soltanian AR; Tapak L
[Ad] Address:Department of Biostatistics and Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran. Electronic address: n.Javanroh@umsha.ac.ir.
[Ti] Title:Kernel machine SNP set analysis provides new insight into the association between obesity and polymorphisms located on the chromosomal 16q.12.2 region: Tehran Lipid and Glucose Study.
[So] Source:Gene;, 2018 Mar 07.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Obesity is a serious health problem that leads to low quality of life and early mortality. To the purpose of prevention and gene therapy for such a worldwide disease, genome wide association study is a powerful tool for finding SNPs associated with increased risk of obesity. To conduct an association analysis, kernel machine regression is a generalized regression method, has an advantage of considering the epistasis effects as well as the correlation between individuals due to unknown factors. MATERIALS AND METHODS: In this study, information of the people who participated in Tehran cardio-metabolic genetic study was used. They were genotyped for the chromosomal region, evaluation 986 variations located at 16q12.2; build 38hg. Kernel machine regression and single SNP analysis were used to assess the association between obesity and SNPs genotyped data. RESULTS: We found that associated SNP sets with obesity, were almost in the FTO (P = 0.01), AIKTIP (P = 0.02) and MMP2 (P = 0.02) genes. Moreover, two SNPs, i.e., rs10521296 and rs11647470, showed significant association with obesity using kernel regression (P = 0.02). CONCLUSION: In conclusion, significant sets were randomly distributed throughout the region with more density around the FTO, AIKTIP and MMP2 genes. Furthermore, two intergenic SNPs showed significant association after using kernel machine regression. Therefore, more studies have to be conducted to assess their functionality or precise mechanism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 272782 MEDLINE  
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[PMID]: 29524474
[Au] Autor:Hege MA; Veit R; Krumsiek J; Kullmann S; Heni M; Rogers PJ; Brunstrom JM; Fritsche A; Preissl H
[Ad] Address:Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, 72076 Tübingen, Germany; German Center for Diabetes Research (DZD e.V.), 85764 Neuherberg, Germany.
[Ti] Title:Eating less or more - Mindset induced changes in neural correlates of pre-meal planning.
[So] Source:Appetite;, 2018 Mar 07.
[Is] ISSN:1095-8304
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Obesity develops due to an imbalance between energy intake and expenditure. Besides the decision about what to eat, daily energy intake might be even more dependent on the decision about the portion size to be consumed. For decisions between different foods, attentional focus is considered to play a key role in the choice selection. In the current study, we investigated the attentional modulation of portion size selection during pre-meal planning. We designed a functional magnetic resonance task in which healthy participants were directed to adopt different mindsets while selecting their portion size for lunch. Compared with a free choice condition, participants reduced their portion sizes when considering eating for health or pleasure, which was accompanied by increased activity in left prefrontal cortex and left orbitofrontal cortex, respectively. When planning to be full until dinner, participants selected larger portion sizes and showed a trend for increased activity in left insula. These results provide first evidence that also the cognitive process of pre-meal planning is influenced by the attentional focus at the time of choice, which could provide an opportunity for influencing the control of meal size selection by mindset manipulation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 272782 MEDLINE  
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[PMID]: 29524473
[Au] Autor:Norman Å; Nyberg G; Elinder LS; Berlin A
[Ad] Address:Department of Public Health Sciences, Karolinska Institutet, 171 77 Stockholm, Sweden. Electronic address: asa.norman@ki.se.
[Ti] Title:Parental strategies for influencing the diet of their children - A qualitative study from disadvantaged areas.
[So] Source:Appetite;, 2018 Mar 07.
[Is] ISSN:1095-8304
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: A social gradient is evident in the prevalence of childhood overweight and obesity, to the disadvantage of children with low socioeconomic status (SES). Parents have a substantial influence on their children's dietary behaviours and weight development through the way they interact with the children around food. This study aims to explore the variation of how parents with low SES influence their child's dietary behaviours. METHODS: A phenomenographic design and analysis was used on 29 sessions of motivational interviewing with mothers and fathers participating in the Healthy School Start intervention study in 2012. The parents had a maximum of 12 years of education and resided in areas targeted for socioeconomic development. In the sessions, parents explored changes that they wanted to make in the home environment regarding their child's dietary behaviours. RESULTS: Five categories of guidance of children's dietary habits were found ranging from silently guiding to enforcement. The categories of guidance were structurally related to each other through positive to negative impact of parental recognition of responsibility for the child's behaviours, level of trust in the child's satiety response, and level of parental emotional distress. CONCLUSION: The results suggest that parents use situation-specific guidance with both negative and positive impacts on child behaviours. Depending on the type of guidance used, parents are in need of different supporting strategies to enhance positive parent-child interplay. Suggestions for intervention strategies are provided where specific focus on parental responsibility recognition, emotional self-regulation, increased responsiveness, and cooperation between parents are highlighted.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 272782 MEDLINE  
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[PMID]: 29524451
[Au] Autor:Warren KR; Wehring HJ; Liu F; McMahon RP; Chen S; Chester C; Kelly DL
[Ad] Address:Maryland Psychiatric Research Center, University of Maryland, School of Medicine, PO Box 21247, Baltimore, MD 21228, United States; Morgan State University, Department of Psychology, 1700 East Cold Spring Lane, Baltimore, MD 21215, United States.
[Ti] Title:Effects of intranasal oxytocin on satiety signaling in people with schizophrenia.
[So] Source:Physiol Behav;, 2018 Mar 07.
[Is] ISSN:1873-507X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Overweight and obesity in schizophrenia are prevalent, affecting half to three-quarters of people with schizophrenia. Hyperphagia and increased meal size have also been implicated as significant contributors to the weight gain problem. Oxytocin has shown to play a role in appetite control in humans and is considered an anorexigenic peptide. This two-day, within-subjects, challenge study involved the examination of satiety after administration of 24 IU oxytocin (intranasal) vs. placebo in participants with a DSM-IV diagnosis of schizophrenia (N = 16). Self reported satiety along with a preload-test meal paradigm were utilized as well as related laboratory measures (insulin, glucose, and leptin), and measures of taste and smell. There were no statistically significant differences between the groups on self-reported satiety or test meal consumption, insulin or glucose levels, or sensory measures. A significant treatment difference was found (F = 5.22, df = 1,97.6, p = 0.025), with a decrease in leptin in the oxytocin group post-administration, but no time effect (F = 1.67, df = 6,95.1, p = 0.180) or treatment by time interaction (F = 1.36. df = 3,4.16, p = 0.261). Despite the small sample and mostly negative findings, we encourage more work to use higher and repeated doses of oxytocin, and to further examine the effect of oxytocin on leptin in schizophrenia as this may be important for understanding both weight control and psychopathology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 272782 MEDLINE  
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[PMID]: 29524411
[Au] Autor:Gui X; Sun L; Gu L; Cai H; Chen H
[Ad] Address:Department of Respiratory Medicine, The Affiliated Nanjing Drum Tower Hospital, Nanjing Medical University, 210008, China.
[Ti] Title:Leptin promotes pulmonary fibrosis development by inhibiting autophagy via PI3K/Akt/mTOR pathway.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Leptin, a protein-related product of the obesity gene, plays an important role in the pathogenesis of fibrotic diseases including pulmonary fibrosis. As a highly conservative process, autophagy regulates various biological functions. Otherwise, insufficient autophagy has been described in alveolar epithelial cells (AEC) to cope with the progression of pulmonary fibrosis. Hence, this study is to investigate the effects of leptin on fibrosis in TGF-ß1 induced epithelial mesenchymal transition (EMT) and the potential roles of autophagy in this processes. Our results showed that the elevated leptin level in serum correlated with the severity of lung fibrosis and leptin significantly promoted the EMT in A549 cells as evidenced by promoting collagen I and α-SMA production. Additionally, treatment with leptin decreased autophagosome formation, inhibited the lipidation of LC3I to LC3II, and up-regulated the expression of p62 via activating PI3K/Akt/mTOR pathway, which is indicative of inhibition of autophagy by leptin. Finally, rapmycin pretreatment reversed the pro-fibrogenic effects of leptin. Take together, our study suggested that leptin accelerated the EMT of A549 cells through inhibiting autophagy via PI3K/Akt/mTOR pathway.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 272782 MEDLINE  
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[PMID]: 29524401
[Au] Autor:Shao S; Yao Z; Lu J; Song Y; He Z; Yu C; Zhou X; Zhao L; Zhao J; Gao L
[Ad] Address:Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, PR China; Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, PR China; Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, PR China.
[Ti] Title:Ablation of prolactin receptor increases hepatic triglyceride accumulation.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Increasing prevalence of non-alcoholic fatty liver disease (NAFLD) worldwide has necessitated a more thorough understanding of it and expanded the scope of research in this field. Women are more resistant to NAFLD than men despite equal exposure to major risk factors, such as obesity or hyperlipidemia. Female resistance is hormone-dependent, as evidenced by the sharp increase in NAFLD incidence in post-menopausal women who do not take hormone replacement therapy. Here, we found that the estrogen-responsive pituitary hormone prolactin (PRL), through specific PRL receptor (PRLR), down-regulates hepatic triglyceride (TG) accumulation. PRL was demonstrated to significantly down-regulate hepatic TG accumulation in female mice and protect male mice from liver steatosis induced by high-fat diet. Interestingly, Ad-shPRLR injected mice, whose hepatic PRLR abundance was effectively decreased at the protein levels, exhibited significantly aggravated liver steatosis. PRL could decrease the expression of stearoyl-coenzyme A desaturase 1 (SCD1), the rate-limiting enzyme in the biosynthesis of monounsaturated fatty acids, in animal models and multiple hepatic cell lines. Following knockdown of PRLR, the changes to PRL-triggered SCD1 expression disappeared. Thus, PRL acted as a previously unrecognized master regulator of liver TG metabolism, indicating that modification of PRL via PRLR might serve as a potential therapeutic target for NAFLD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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