Weight gain induced by an isocaloric pair-fed high fat diet: A nutriepigenetic study on FASN and NDUFB6 gene promoters

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

doi:10.1016/j.ymgme.2010.07.017

Cited by 81 publications

(62 citation statements)

References 40 publications

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“…Nevertheless, this result agrees with a previous report performed in the same obesity model 32 . In this study, higher liver triglyceride contents were detected in HFD-fed rats,…”

Section: Discussionsupporting

confidence: 94%

Fat intake leads to differential response of rat adipocytes to glucose, insulin and ascorbic acid

García-Díaz

Campión

Arellano

et al. 2012

Exp Biol Med (Maywood)

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Antioxidant-based treatments have emerged as novel and interesting approaches to counteract fat accumulation in obesity and associated metabolic disturbances. Adipocytes from rats that were fed on chow or high-fat diet (HFD) for 50 d were isolated (primary adipocytes) and incubated (72 h) on low (LG; 5.6 mmol/L) or high (HG; 25 mmol/L) glucose levels, in the presence or absence of 1.6 nmol/L insulin and 200 μmol/L vitamin C (VC). Adipocytes from HFD-fed animals presented lower insulin-induced glucose uptake, lower lactate and glycerol release, and lower insulin-induced secretion of some adipokines as compared with controls. HG treatment restored the blunted response to insulin regarding apelin secretion in adipocytes from HFD-fed rats. VC treatment inhibited the levels of nearly all variables, irrespective of the adipocytes’ dietary origin. The HG treatment reduced adipocyte viability, and VC protected from this toxic effect, although more drastically in control adipocytes. Summing up, in vivo chow or HFD intake determines a differential response to insulin and glucose treatments that appears to be dependent on the insulin-resistance status of the adipocytes, while VC modifies some responses from adipocytes independently of the previous dietary intake of the animals.

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“…Nevertheless, this result agrees with a previous report performed in the same obesity model 32 . In this study, higher liver triglyceride contents were detected in HFD-fed rats,…”

Section: Discussionsupporting

confidence: 94%

Fat intake leads to differential response of rat adipocytes to glucose, insulin and ascorbic acid

García-Díaz

Campión

Arellano

et al. 2012

Exp Biol Med (Maywood)

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“…There are a number of techniques to study the epigenetic DNA methylation pattern, such as BSP [16], pyrosequencing [4], Combined Bisulfite Analysis (COBRA) [41], methylation microarrays [7], MSP [19] or Maldi-TOF mass spectrometry [25], and they have differences in their specificity, sensibility, accuracy and cost. We have recently published two reports identifying by BSP different diet-related epigenetic marks in leptin [29] and TNF-alpha [11] that could be used as biomarkers of weight loss.…”

Section: Discussionmentioning

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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“…Although the intake of a hypercaloric diet is important, macronutrient distribution is also determinant in these epigenetic processes as has been demonstrated when adult rats were fed a pair-fed HFD and changes in fatty acid synthase promoter methylation were found in adipose tissue (Lomba et al, 2010). This kind of experiments is not easy to accomplish in humans, but it has been recently published that a dietary pattern characterized by a high intake of vegetables and fruits (called a "prudent" diet) may protect against the global DNA hypomethylation observed with a "Western" dietary pattern characterized by a high intake of meats, grains, dairy, oils, and potatoes (Zhang et al, 2011b).…”

Section: Hypercaloric and High-fat Dietsmentioning

confidence: 99%

“…Although one of the most widely used models of diet-induced obesity in animals is the intake of a high-fat diet, and some works have analysed the epigenetic modifications induced by this dietary approach in rodents (Lomba et al, 2010), it is still unknown the capacity of the different types of fatty acids to induce epigenetic modifications. Few studies have evidenced the role of n-3 and n-6 PUFA on DNA methylation, although there are examples concerning effects of eicosapentaenoic (Ceccarelli et al, 2011), docosahexaenoic (Kulkarni et al, 2011) and arachidonic (Kiec-Wilk et al, 2011) fatty acids on DNA methylation.…”

Section: Fatty Acid and Amino Acidsmentioning

confidence: 99%

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

Milagro

Mansego

Miguel

et al. 2013

Molecular Aspects of Medicine

257

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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Weight gain induced by an isocaloric pair-fed high fat diet: A nutriepigenetic study on FASN and NDUFB6 gene promoters

Cited by 81 publications

References 40 publications

Fat intake leads to differential response of rat adipocytes to glucose, insulin and ascorbic acid

Fat intake leads to differential response of rat adipocytes to glucose, insulin and ascorbic acid

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

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

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