Association of MFSD3 promoter methylation level and weight regain after gastric bypass: Assessment for 3 y after surgery

Nicoletti, Carolina Ferreira; Pinhel, Marcela Souza; Noronha, Natália Yumi; Jácome, Amalia; Crujeiras, Ana B.; Nonino, Carla Barbosa

doi:10.1016/j.nut.2019.04.010

Cited by 12 publications

(8 citation statements)

References 28 publications

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“…35 In addition, weight loss therapies are also able to modulate the obesityrelated methylation profile. 28,30,59,60 In line with these results, weight loss therapies based dietary energy restriction were able to reverse the obesity-related methylation levels of ACE2 with a putative increase in the transcript levels. However, after 6 months of bariatric surgery, the methylation and transcript levels of ACE2 did no change respect to baseline, even though patients showed a weight loss higher than 20%.…”

Section: Discussionsupporting

confidence: 61%

Adipose tissue and blood leukocytes ACE2 DNA methylation in obesity and after weight loss

Izquierdo

Carreira

Boughanem

et al. 2021

Eur J Clin Investigation

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Background: Obesity was consistently associated with a poor prognosis in patients with COVID-19. Epigenetic mechanisms were proposed as the link between obesity and comorbidities risk.Aim: To evaluate the methylation levels of angiotensin-converting enzyme 2 (ACE2) gene, the main entry receptor of SARS-CoV-2, in different depots of adipose tissue (AT) and leukocytes (PBMCs) in obesity and after weight loss therapy based on a very-low-calorie ketogenic diet (VLCKD), a balanced hypocaloric diet (HCD) or bariatric surgery (BS).

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Section: Discussionsupporting

confidence: 61%

Adipose tissue and blood leukocytes ACE2 DNA methylation in obesity and after weight loss

Izquierdo

Carreira

Boughanem

et al. 2021

Eur J Clin Investigation

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“…On the other hand, obesity is associated with a specific methylation profile in several tissues [35e38] and the obesityrelated methylome is related to complications such as insulin resistance [39] and cancer [40,41]. Moreover, several methylation marks were identified as potential biomarkers for predicting the success of weight loss therapies during the active phase of treatment [42e46] or during the period of weight loss maintenance [47,48]. Therefore, DNA methylation was proposed as a target for preventing and managing obesity [48e51].…”

Section: Introductionmentioning

confidence: 99%

Epigenetic landscape in blood leukocytes following ketosis and weight loss induced by a very low calorie ketogenic diet (VLCKD) in patients with obesity

et al. 2021

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Background: The molecular mechanisms underlying the potential health benefits of a ketogenic diet are unknown and could be mediated by epigenetic mechanisms. Objective: To identify the changes in the obesity-related methylome that are mediated by the induced weight loss or are dependent on ketosis in subjects with obesity underwent a very-low calorie ketogenic diet (VLCKD). Methods: Twenty-one patients with obesity (n ¼ 12 women, 47.9 ± 1.02 yr, 33.0 ± 0.2 kg/m 2 ) after 6 months on a VLCKD and 12 normal weight volunteers (n ¼ 6 women, 50.3 ± 6.2 yrs, 22.7 ± 1.5 kg/m 2 ) were studied. Data from the Infinium MethylationEPIC BeadChip methylomes of blood leukocytes were obtained at time points of ketotic phases (basal, maximum ketosis, and out of ketosis) during VLCKD (n ¼ 10) and at baseline in volunteers (n ¼ 12). Results were further validated by pyrosequencing in representative cohort of patients on a VLCKD (n ¼ 18) and correlated with gene expression. Results: After weight reduction by VLCKD, differences were found at 988 CpG sites (786 unique genes). The VLCKD altered methylation levels in patients with obesity had high resemblance with those from normal weight volunteers and was concomitant with a downregulation of DNA methyltransferases (DNMT)1, 3a and 3b. Most of the encoded genes were involved in metabolic processes, protein metabolism, and muscle, organ, and skeletal system development. Novel genes representing the top scoring associated events were identified, including ZNF331, FGFRL1 (VLCKD-induced weight loss) and CBFA2T3, C3orf38, JSRP1, and LRFN4 (VLCKD-induced ketosis). Interestingly, ZNF331 and FGFRL1 were validated in an independent cohort and inversely correlated with gene expression. Conclusions: The beneficial effects of VLCKD therapy on obesity involve a methylome more suggestive of normal weight that could be mainly mediated by the VLCKD-induced ketosis rather than weight loss.

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“…In addition to the genetic polymorphisms, epigenetics could also play important roles on weight regain. Although the association between weight regain and DNA methylation of some genes, including proopiomelanocortin (POMC), neuropeptide Y (NPY), mal, T cell differentiation protein 2 (MAL2), family with sequence similarity 129, member A (FAM129A), periplakin (PPL), PDZ domain containing ring finger 4 (PDZRN4) and major facilitator superfamily domain containing 3 (MFSD3), has been reported (91)(92)(93) , future epigenetic studies regarding the relationship between post-transcriptional modification and the impacts of genetic polymorphisms on long-term weight maintenance in different populations are also required.…”

Section: Future Directions and Clinical Applicationsmentioning

confidence: 99%

The impact of genetic polymorphisms on weight regain after successful weight loss

2020

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Abstract Obesity is associated with an increased risk of various diseases and mortality. Although nearly 50 % of adults have been reported trying to lose weight, the prevalence of obesity has increased. One factor that hinders weight loss-induced decrease in obesity prevalence is weight regain. Although behavioural, psychological and physiological factors associated with weight regain have been reviewed, the information regarding the relationship between weight regain and genetics has not been previously summarised. In this paper, we comprehensively review the association between genetic polymorphisms and weight regain in adults and children with obesity after weight loss. Based on this information, identification of genetic polymorphism in patients who undergo weight loss intervention might be used to estimate their risks of weight regain. Additionally, the genetic-based risk estimation may be used as a guide for physicians and dietitians to provide each of their patients with the most appropriate strategies for weight loss and weight maintenance.

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Association of MFSD3 promoter methylation level and weight regain after gastric bypass: Assessment for 3 y after surgery

Cited by 12 publications

References 28 publications

Adipose tissue and blood leukocytes ACE2 DNA methylation in obesity and after weight loss

Adipose tissue and blood leukocytes ACE2 DNA methylation in obesity and after weight loss

Epigenetic landscape in blood leukocytes following ketosis and weight loss induced by a very low calorie ketogenic diet (VLCKD) in patients with obesity

The impact of genetic polymorphisms on weight regain after successful weight loss

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