Obesity induced by a pair-fed high fat sucrose diet: methylation and expression pattern of genes related to energy homeostasis

Lomba, Almudena; Milagro, Fermı́n I.; García-Díaz, Diego F.; Marti, Amelia; Campión, Javier; Martínéz, J. Alfredo

doi:10.1186/1476-511x-9-60

Cited by 67 publications

(51 citation statements)

References 48 publications

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“…Thus, changes in the DNA methylation pattern as a result of dietary treatments or conditions have been studied in the last years, comparing vegetarians with omnivores [39], the effects of different obesogenic diets [26,31] or different dietary treatments to lose weight [7]. Interventional studies are showing that the DNA methylation profile previous to the treatment might be able to predict the response to the low calorie diet.…”

Section: Introductionmentioning

confidence: 99%

Leptin and TNF-alpha promoter methylation levels measured by MSP could predict the response to a low-calorie diet

et al. 2011

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Obesity-associated adipose tissue enlargement is characterized by an enhanced proinflammatory status and an elevated secretion of adipokines such as leptin and cytokines such as TNF-alpha. Among the different mechanisms that could underlie the interindividual differences in obesity, epigenetic regulation of gene expression has emerged as a potentially important determinant. Therefore, twenty-seven obese women (age: 32-50 years; baseline Body Mass Index, BMI: 34.4±4.2 Kg/m 2 ) were prescribed an eightweek Low-Calorie-Diet and epigenetic marks were assessed. Baseline and endpoint anthropometric parameters were measured and blood samples were drawn. Genomic DNA and RNA from adipose tissue biopsies were isolated before and after the dietary intervention. Leptin and TNF-alpha promoter methylation were measured by MSP after bisulfite treatment and gene expression was also analyzed.Obese women with a successful weight loss (≥5% of initial body weight, n=21) improved the lipid profile and fat mass percentage (-12%, p<0.05). Both systolic (-5%, p<0.05) and diastolic (-8%, p<0.01) blood pressures significantly decreased. At baseline women with better response to the dietary intervention showed lower promoter methylation levels of leptin (-47%, p<0.05) and TNF-alpha (-39%, p=0.071) than the non-responder group (n=6), while no differences were found between responder and non-responder group in leptin and TNF-alpha gene expression analysis. These data suggest that leptin and TNF-alpha methylation levels could be used as epigenetic biomarkers concerning the response to a Low-CalorieDiet. Indeed, methylation profile could help to predict the susceptibility to weight loss as well as some comorbidities such as hypertension or type 2 diabetes.

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Section: Introductionmentioning

confidence: 99%

Leptin and TNF-alpha promoter methylation levels measured by MSP could predict the response to a low-calorie diet

et al. 2011

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“…Consumption of high-caloric diets is one of the driving forces for obesity development, producing not only an energy imbalance, but also a drastic impact on the microbial community residing the gastrointestinal tract (Duca et al, 2013;Wu et al, 2011). Despite the fact that the surrounding physiological mechanisms are not fully understood, high energy yielding diets rich in fat and sugars have been closely related to obesity (Lomba et al, 2010). In this context, further investigation of the impact of these types of diets on gut microbiota and their metabolic consequences is required (Daniel et al, 2013;Duca et al, 2013), in order to identify changes caused in the gut that could be involved in the development of the disease.…”

Section: Introductionmentioning

confidence: 99%

Shifts in microbiota species and fermentation products in a dietary model enriched in fat and sucrose

Etxeberría

Arias

Boqué

et al. 2015

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The gastrointestinal tract harbours a "superorganism" called the gut microbiota, which is known to play a crucial role in the onset and development of diverse diseases. This internal ecosystem, far from being a static environment, could be willingly manipulated by diet and dietary components. Feeding animals with high-fat sucrose diets entails diet-induced obesity, a model which is usually used in research to mimic the obese phenotype of Western societies.The aim of the present study was to identify gut microbiota dysbiosis and associated metabolic changes produced in 5 male Wistar rats fed a high-fat sucrose (HFS) diet for six weeks and to compare it with the basal microbial composition. For this purpose, DNA extracted from faeces at baseline and after the treatment was analysed by amplification of the V4-V6 region of the 16S ribosomal DNA (rDNA) gene using 454 pyrosequencing. Short-chain fatty acids (SCFA), acetate, propionate and butyrate, were also evaluated by gas chromatography-mass spectrometry (GC-MS).At the end of the treatment, gut microbiota composition significantly differed at phylum level (Firmicutes, Bacteroidetes and Proteobacteria) and class level (Erisypelotrichi, Deltaproteobacteria, Bacteroidia and Bacilli). Interestingly, Clostridia class showed a significant decrease after the HFS-diet treatment, which correlated with visceral adipose tissue, and is likely mediated by dietary carbohydrates. Of particular interest, Clostridium cluster XIVa species were significantly reduced and changes were identified in the relative abundance of other specific bacterial species (Mitsuokella jalaludinii, Eubacterium ventriosum, Clostridium sp. FCB90-3, Prevotella nanceiensis, Clostridium fusiformis, Clostridium sp. BNL1100 and Eubacterium cylindroides) that, in some cases, showed opposite trends to their relative families.These results highlight the relevance of characterizing gut microbial population differences at species level and contribute to understand the plausible link between the 1 diet and specific gut bacterial species that are able to influence the inflammatory status, intestinal barrier function and obesity development.

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“…Estudios con roedores con dietas ricas en carbohidratos, grasas o combinaciones que imitan los hábitos nutricionales de diferentes poblaciones humanas, diferentes combinaciones y cantidades de carbohidratos (entre 10% y 30%) y grasas (entre 20% y 40%) tuvieron como resultado un incremento del peso corporal, un aumento de la grasa abdominal, hipertrigliceridemia, hiperglucemia, hiperleptinemia, resistencia a la insulina y un incremento de los ácidos grasos libres circulantes 11,13,14 , concluyendo que las dietas altas en carbohidratos y lípidos generan en los roedores la mayoría de las complicaciones presentes en el síndrome metabólico humano.…”

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Efecto de la administración subcrónica de glucosamina oral en la regulación del peso corporal, glucemia y dislipidemias provocada por una dieta hipercalórica en rata Wistar

Barrientos‐Alvarado

Vázquez²,

Oscoy³

et al. 2014

Rev. Nutr.

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ObjetivoEste estudio evaluó el efecto de la glucosamina oral en el sobrepeso y dislipidemia provocada por una dieta hipercalórica en ratas. MétodosEn 4 grupos de ratas Wistar: alimentados con dieta comercial para roedores y agua de beber sin grupo de control y con glucosamina (500 mg/kg-1 por día) grupo glucosamina y con dieta hipercalórica enriquecida al 24% (g/g) compuesta por manteca de cerdo y agua de beber sin grupo hipercalórico y con glucosamina grupo hipercalórico + grupo glucosamina, durante 22 semanas, se evaluaron el peso corporal, grasa abdominal, niveles de glucemia, triglicéridos, colesterol total y lipoproteínas de alta densidad en suero. ResultadosSe observó un aumento del peso corporal y glucemia en suero con dislipidemias en el grupo con dieta hipercalórica grupo hipercalórico versus grupo de controle (p<0.001); al administrarse glucosamina para esta misma dieta grupo hipercalórico + grupo glucosamina se minimizaron los efectos presentados, disminuyendo la cantidad de grasa abdominal y los niveles del perfil lípido en suero (p>0.05) y regulándose el peso corporal, las lipoproteínas de alta densidad y la glucemia basal (p<0.05). ConclusionLa glucosamina reguló el peso corporal y la glucemia en sangre y minimizó las dislipidemias provocadas por la dieta hipercalórica, favoreciendo el aumento de colesterol lipoproteínas de alta densidad en las ratas. No afectó el peso corporal y el metabolismo lipídico cuando se administró con dieta comercial.Palabras ilave: Glucemia. Glucosamina. HDL-colesterol. Peso corporal. A B S T R A C T Objective This study evaluated the effect of oral glucosamine on overweight and dyslipidemia caused by a high-fat diet in rats. Methods Four groups of Wistar rats: fed with commercial rodent food and drinking water without (control group) and with glucosamine (500 mg kg-1 per day) and a high-fat diet enriched with 24% (g/g) butter pork and drinking water without and with glucosamine, for 22 weeks; the body weight, abdominal fat, blood glucose, triglycerides, total cholesterol, and high density lipoprotein in serum were evaluated. Results Body

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Obesity induced by a pair-fed high fat sucrose diet: methylation and expression pattern of genes related to energy homeostasis

Cited by 67 publications

References 48 publications

Leptin and TNF-alpha promoter methylation levels measured by MSP could predict the response to a low-calorie diet

Leptin and TNF-alpha promoter methylation levels measured by MSP could predict the response to a low-calorie diet

Shifts in microbiota species and fermentation products in a dietary model enriched in fat and sucrose

Efecto de la administración subcrónica de glucosamina oral en la regulación del peso corporal, glucemia y dislipidemias provocada por una dieta hipercalórica en rata Wistar

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