Studies have examined the possible utility of epigenetic phenomena (DNA methylation changes, covalent histone modifications, and miRNA expression patterns) in predicting individual responses to ...different lifestyle programs. Nonetheless, most available evidence is focused on identifying epigenetic marks eventually associated with body composition and adiposity outcomes, whereas their roles in metabolic endings remain less explored. This document comprehensively reviewed the evidence regarding the use of epigenetic signatures as putative biomarkers of metabolic outcomes (glycemic, lipid, blood pressure, and inflammatory/oxidative stress features) in response to different lifestyle interventions in humans. Although more investigation is still necessary in order to translate this knowledge in clinical practice, these scientific insights are contributing to the design of advanced strategies for the precise management of cardiometabolic risk, gaining understanding on metabolic heterogeneity, allowing for the prediction of metabolic outcomes, and facilitating the design of epigenome-based nutritional strategies for a more customized approach for metabolic alterations treatment under the scope of precision nutrition.
Background
This study aimed to investigate the putative role of the triglyceride‐glucose index (TyG index) computed as lnTG (mg/dl) × glucose (mg/dl)/2 and derived proxies as predictors of adiposity ...and weight loss changes after a low‐calorie diet (LCD) intervention.
Methods
A total of 744 adult participants from the multicentre DIOGenes intervention study were prescribed a LCD (800 kcal/day) during 8 weeks. Body composition and fat content at baseline and after 8 weeks were estimated by DEXA/BIA. A multivariate analysis approach was used to estimate the difference in ΔWeight1–2 (kg), ΔBMI1–2 (kg/m2) or ΔFat1–2 (%) between the basal value (point 1) and after 8 weeks following a LCD (point 2), respectively. The TyG index at baseline (TyG1), after following the LCD for 8 weeks (TyG2) or the TyG index differences between both time points (ΔTyG1–2) were analysed as predictors of weight and fat changes.
Results
TyG1 was associated with ΔWeight1–2 (kg) and ΔBMI1‐2 (kg/m2), with β = 0.812 (p = .017) and β = 0.265 (p = .018), respectively. Also, TyG2 values were inversely related to ΔFat1–2 (%), β = −1.473 (p = .015). Moreover, ΔTyG1–2 was associated with ΔWeight1–2 (kg) and ΔFat1–2 (%), β = 0.689 (p = .045) and β = 1.764 (p = .002), respectively. Furthermore, an association between TyG2 and resistance to fat loss was found (p = .015).
Conclusion
TyG1 index is a good predictor of weight loss induced by LCD. Moreover, TyG2 was closely related to resistance to fat loss, while ΔTyG1–2 values were positively associated with body fat changes. Therefore, TyG index and derived estimations could be used as markers of individualized responses to energy restriction and a surrogate of body composition outcomes in clinical/epidemiological settings in obesity conditions.
Currently, metabolic-associated fatty liver disease (MAFLD) is a leading global cause of chronic liver disease, and is expected to become one of the most common indications of liver transplantation. ...MAFLD is associated with obesity, involving multiple mechanisms such as alterations in lipid metabolism, insulin resistance, hyperinflammation, mitochondrial dysfunction, cell apoptosis, oxidative stress, and extracellular matrix formation. However, the onset and progression of MAFLD is variable among individuals, being influenced by intrinsic (personal) and external environmental factors. In this context, sequence structural variants across the human genome, epigenetic phenomena (i.e., DNA methylation, histone modifications, and long non-coding RNAs) affecting gene expression, gut microbiota dysbiosis, and metabolomics/lipidomic fingerprints may account for differences in MAFLD outcomes through interactions with nutritional features. This knowledge may contribute to gaining a deeper understanding of the molecular and physiological processes underlying MAFLD pathogenesis and phenotype heterogeneity, as well as facilitating the identification of biomarkers of disease progression and therapeutic targets for the implementation of tailored nutritional strategies. This comprehensive literature review highlights the potential of nutrigenetic, nutriepigenetic, nutrimetagenomic, nutritranscriptomics, and nutrimetabolomic approaches for the prevention and management of MAFLD in humans through the lens of precision nutrition.
Dyslipidemias are known risk factors for chronic diseases. Precision nutrition interventions are designed according to characteristics, such as diet, phenotype, and genotype. This systematic review ...aims to define a panel of genetic variants associated with lipid abnormalities that could be later used in nutrigenetic intervention studies. A systematic review is conducted following the PRISMA‐P. Studies published from January 2010 to December 2020 in English language and humans are included from PubMed and ScienceDirect databases. Articles that demonstrate a strong association between polymorphisms (single nucleotide variation) of genes involved in lipid metabolism and increased risk for dyslipidemia are included. A total of 3031 articles are screened, but only 51 articles fulfill the inclusion criteria. The genes included are FABP2, MTTP related to CM synthesis and secretion; LPL, LIPC involved in triglyceride hydrolysis; CETP, APOA1, LCAT, ABCA1, and APOA5 related to lipoprotein metabolism, and APOE, LDLR, SCARB1, APOC3 involved in lipid clearance. In this systematic review, genetic variants related to chylomicron synthesis, triglyceride hydrolysis, lipoprotein metabolism, and lipid clearance demonstrate a strong association with lipid abnormalities, which can be used to design precision nutrition interventions that may help to prevent and treat dyslipidemia effectively.
This systematic review highlights those genetic variants related to chylomicron synthesis and secretion (FABP2, MTTP), triglyceride hydrolysis (LPL, LIPC), lipoprotein metabolism (CETP, APOA1, LCAT, ABCA1, and APOA5), and lipid clearance (APOE, LDLR, SCARB1, APOC3) that increase the risk of cardiovascular diseases by altering lipid levels. This finding can be used to design precision nutrition interventions to prevent and treat dyslipidemia effectively.
Aim and objective
Emerging translational evidence suggests that epigenetic alterations (DNA methylation, miRNA expression, and histone modifications) occur after external stimuli and may contribute ...to exacerbated inflammation and the risk of suffering several diseases including diabetes, cardiovascular diseases, cancer, and neurological disorders. This review summarizes the current knowledge about the harmful effects of high-fat/high-sugar diets, micronutrient deficiencies (folate, manganese, and carotenoids), obesity and associated complications, bacterial/viral infections, smoking, excessive alcohol consumption, sleep deprivation, chronic stress, air pollution, and chemical exposure on inflammation through epigenetic mechanisms. Additionally, the epigenetic phenomena underlying the anti-inflammatory potential of caloric restriction,
n
-3 PUFA, Mediterranean diet, vitamin D, zinc, polyphenols (i.e., resveratrol, gallic acid, epicatechin, luteolin, curcumin), and the role of systematic exercise are discussed.
Methods
Original and review articles encompassing epigenetics and inflammation were screened from major databases (including PubMed, Medline, Science Direct, Scopus, etc.) and analyzed for the writing of the review paper.
Conclusion
Although caution should be exercised, research on epigenetic mechanisms is contributing to understand pathological processes involving inflammatory responses, the prediction of disease risk based on the epigenotype, as well as the putative design of therapeutic interventions targeting the epigenome.
Some high-carbohydrate diets may lead to obesity and multiple metabolic disorders, including hypertriglyceridemia (HTG). This lipid abnormality is considered an important risk factor for ...cardiovascular disease and type 2 diabetes. The sweet taste receptor TAS1R2 polymorphism (Ile191Val) has been reported to be associated with carbohydrate intake. The aim of this study was to analyze the association of the TAS1R2 gene polymorphism with carbohydrate intake and HTG among the population of West Mexico. In a cross-sectional study, 441 unrelated subjects were analyzed for TAS1R2 genotypes (Ile/Ile, Ile/Val and Val/Val) by an allelic discrimination assay. Biochemical tests and a three-day food record were assessed. The Val/Val genotype carriers had a higher intake of total carbohydrates, fiber and servings of cereals and vegetables than the other genotype carriers. The Val/Val genotype conferred a higher risk for HTG than the Ile/Val and Ile/Ile genotypes (OR = 3.26, 95%CI 1.35-7.86, p = 0.006 and OR = 2.61, 95%CI 1.12-6.07, p = 0.02, respectively). Furthermore, the Val/Val genotype was associated with approximately 30% higher triglycerides compared with Ile/Val and Ile/Ile genotypes (β = 44.09, 95%CI 9.94-78.25, p = 0.01 and β = 45.7, 95%CI 10.85-80.54, p = 0.01, respectively). In conclusion, the Val/Val genotype of TAS1R2 was associated with a higher carbohydrate intake and HTG.
Liver cirrhosis(LC) is a chronic illness caused by inflammatory responses and progressive fibrosis. Globally, the most common causes of chronic liver disease include persistent alcohol abuse, ...followed by viral hepatitis infections and nonalcoholic fatty liver disease. However, regardless of the etiological factors, the susceptibility and degree of liver damage may be influenced by genetic polymorphisms that are associated with distinct ethnic and cultural backgrounds. Consequently, metabolic genes are influenced by variable environmental lifestyle factors, such as diet, physical inactivity, and emotional stress, which are associated with regional differences among populations. This Topic Highlight will focus on the genetic and environmental factors that may influence the metabolism of alcohol and nutrients in the setting of distinct etiologies of liver disease. The interaction between genes and environment in the current-day admixed population, Mestizo and Native Mexican, will be described. Additionally, genes involved in immune regulation, insulin sensitivity, oxidative stress and extracellular matrix deposition may modulate the degree of severity. In conclusion, LC is a complex disease. The onset, progression, and clinical outcome of LC among the Mexican population are influenced by specific genetic and environmental factors. Among these are an admixed genome with a heterogenic distribution of European, Amerindian and African ancestry; a high score of alcohol consumption; viral infections; a hepatopathogenic diet; and a high prevalence of obesity. The variance in risk factors among populations suggests that intervention strategies directed towards the prevention and management of LC should be tailored according to such population-based features.
Betaine, an osmolyte derivative of the metabolite choline and the amino acid glycine, acts as a methyl donor in the conversion of homocysteine to methionine and is involved in the maintenance of ...adequate lipid metabolism. There is growing evidence for the role of betaine in the development of various lipid-related diseases, including dyslipidemia and cardiovascular risk. This study aimed to analyze associations between betaine intake and blood lipid profiles in Mexican subjects.
A total of 212 adults were randomly recruited in the city of Tijuana, Baja California, Mexico. Betaine intake was estimated using Nutritionist Pro software. Body composition and metabolic measurements were obtained by conventional methods. In the total sample, the average intake of betaine was 14.32 mg/d. Individuals were categorized into three groups according to tertiles of betaine consumption: tertile/group 1 (<4.16 mg/d), tertile/group 2 (4.16-12.02 mg/d), and tertile/group 3 (>12.02 mg/d).
Compared to group 3, subjects within group 1 had higher serum levels of total cholesterol (
= 0.001), LDL-c (
= 0.026), and non-HDL-c (
= 0.021). In addition, significant negative Pearson correlations were found between betaine intake and the serum levels of total cholesterol (r = -0.432, 95% CI, -0.684, -0.185,
= 0.001), LDL-c (r = -0.370, 95% CI, -0.606, -0.134,
= 0.002), and non-HDL-c (r = -0.351, 95%CI, -0.604, -0.098,
= 0.007).
Our results show that a low intake of betaine is associated with elevated blood cholesterol levels in Mexican subjects. On this basis, betaine consumption could be used as an additional dietary measure for cardiovascular care. However, additional studies are required to confirm our results in other Mexican regions as well as in other populations worldwide.
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