The burden of obesity on infectious disease

Karlsson, Erik A.; Beck, Melinda A.

doi:10.1258/ebm.2010.010227

Cited by 263 publications

(249 citation statements)

References 209 publications

(178 reference statements)

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“…Thus, it has been hypothesized that altered immune cell metabolism and epigenetic modifications could influence the immune response to infectious disease in the obese host (Karlsson and Beck, 2010), and be responsible of the increased susceptibility to infection with a number of different pathogens. However, there are few reports observing the effect of nutritional factors on the epigenetic modification of immune cells and further studies are needed.…”

Section: Infectionsmentioning

confidence: 99%

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Milagro

Mansego

Miguel

et al. 2013

Molecular Aspects of Medicine

252

161

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Nutritional factors play a life-long role in human health. Indeed, there is growing evidence that one of the mechanisms by which nutrients and bioactive compounds affect metabolic traits is epigenetics. Complex interactions among food components and histone modifications, DNA methylation, non-coding RNA expression and chromatin remodeling factors lead to a dynamic regulation of gene expression that controls the cellular phenotype. Although perinatal period is the time of highest phenotypic plasticity, contributing largely to developmental programming, also during adulthood there is evidence about a nutritional influence on epigenetic regulation. Similarly to type 2 diabetes, hypertension, atherosclerosis and other metabolic disorders, obesity predisposition and weight loss outcomes have been repeatedly associated to changes in epigenetic patterns. Different non-nutritional risk factors that usually accompany obesity seem also to be involved in these epigenetic modifications, especially hyperglycemia, inflammation, hypoxia and oxidative stress. There are currently three major objectives in epigenetic research in relation to obesity: to search for epigenetic biomarkers to predict future health problems or detect the individuals at most risk, to understand the obesity-related environmental factors that could modulate gene expression by affecting epigenetic mechanisms, and to study novel therapeutic strategies based on nutritional or pharmacological agents that can modify epigenetic marks. At this level, the major tasks are: development of robust epigenetic biomarkers of weight regulation, description of those epigenetic marks more susceptible to be modified by dietary exposures, identification of the active ingredients (and the doses) that alter the epigenome, assessment of the real importance of other obesity-related factors on epigenetic regulation, determination of the period of life in which best results are obtained, and understanding of the importance of the inheritance of these epigenetic marks.

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Section: Infectionsmentioning

confidence: 99%

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Milagro

Mansego

Miguel

et al. 2013

Molecular Aspects of Medicine

252

161

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“…According to the World Health Organization, worldwide obesity has doubled since 1980 (Pi-Sunyer 2002, Karlsson & Beck 2010). In this context, a better understanding of adipose tissue biology could contribute to the control of energy metabolism and obesity, at least in the most extreme situations.…”

Section: Introductionmentioning

confidence: 99%

ChemR23 knockout mice display mild obesity but no deficit in adipocyte differentiation

Rouger¹,

Denis²,

Luangsay³

et al. 2013

Journal of Endocrinology

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Chemerin was initially described as a chemoattractant factor for leukocyte populations. More recently, the protein has also been reported to be an adipokine, regulating adipocyte differentiation in vitro via its receptor ChemR23, and to be correlated with BMI and other parameters of the metabolic syndrome in humans. The aim of this study was to investigate the role of the chemerin/ChemR23 axis in the regulation of metabolism in vivo, using a mouse knockout (KO) model for ChemR23 (Cmklr1) in a C57BL/6 genetic background. Body weight and adipose tissue mass did not differ significantly in young animals, but were significantly higher in ChemR23 KO mice aged above 12 months. Glucose tolerance was unaffected. No significant modifications in the levels of blood lipids were observed and no increase in the levels of inflammatory markers was observed in the adipose tissue of KO mice. A high-fat diet did not exacerbate the obese phenotype in ChemR23 KO mice. No obvious defect in adipocyte differentiation was detected, while a marker of lipogenic activity (GPD1 expression) was found to be elevated. In conclusion, the chemerin/ChemR23 system does not appear to play a major role in adipocyte differentiation in vivo, but it may be involved in adipose tissue homeostasis.

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“…Alguns estudos apontam a presença elevada de marcadores como as adipocinas e o PCR em pessoas obesas com periodontite, que com o tratamento periodontal ou com a perda de massa adiposa acarretam o processo de retroalimentação dessas condições 32 . Acrescenta-se, também, que o reconhecimento de patógenos pelo organismo e a ação do sistema imune inato são fundamentais para a eliminação do agente patógeno 33 . Mediante esses fatores, o prejuízo da ação do sistema imune inato em indivíduos obesos 25 pode acarretar um verdadeiro risco de infecções de vários tipos.…”

Section: Obesidade E Doenças Periodontaisunclassified

Obesidade e saúde bucal: impacto da obesidade sobre condições bucais

Saporiti

Vera

Arruda

et al. 2015

Rev. da Fac. de Odontologia, UPF

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IntroduçãoA obesidade caracteriza-se por danos à condição de saúde causados pelo acúmulo excessivo ou anormal de gordura corpórea 1 . Essa doença não pode ser considerada como uma simples desordem, mas sim, um grupo heterogêneo de condições com múltiplas e complexas causas. O peso corporal é, então, determinado pela interação entre fatores biológicos, ambientais, sociais e comportamentais, agindo na regulação entre o armazenamento e o gasto energético. Diversas são as causas atribuídas à etiologia da obesidade, destacando fatores psicossociais, comportamentais e biológicos. Embora o componente genético tenha um papel inquestionável na etiologia da obesidade, o notável aumento na prevalên-cia dessa condição pode ser mais bem explicado por mudanças sociais e comportamentais, resultados da transição sociodemográfica.A epidemia da obesidade era uma realidade predominante dos países ricos e desenvolvidos 2 . Ao passo que países de baixa e de média renda começam a se tornar mais globalizados, há uma mudança considerável no padrão nutricional, e nos hábi-tos de vida, acarretando, consequentemente, uma significante elevação da prevalência dessa doença. Assim, após a década de 1990, a obesidade assume

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The burden of obesity on infectious disease

Cited by 263 publications

References 209 publications

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

ChemR23 knockout mice display mild obesity but no deficit in adipocyte differentiation

Obesidade e saúde bucal: impacto da obesidade sobre condições bucais

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