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Sedentary lifestyle and consumption of high-calorie foods have caused a relentless increase of overweight and obesity prevalence at all ages. Its presently epidemic proportion is disquieting due to the tight relationship of obesity with metabolic syndrome and several other comorbidities which do call for urgent workarounds. The usual ineffectivenes...
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Maternal overnutrition has been reported to affect brain plasticity of the offspring by altering gene expression, regulating both synaptic plasticity and adult neurogenesis. However, whether perinatal metabolic stress may influence the accumulation of misfolded proteins and the development of neurodegeneration remains to be clarified. We investigat...
Citations
... The perinatal period has been suggested to have a critical impact on the development of obesity [45] and obesityrelated conditions such as cardiometabolic diseases and MAFLD [46][47][48]. Studies have suggested exposure to maternal over-nutrition or undernutrition increases susceptibility to MAFLD in childhood and hastens progression to NASH across the lifespan, especially when offspring are exposed in the postnatal period to a high-fat (Western-style) diet [47]. ...
The historical use of the term non-alcoholic fatty liver disease (NAFLD) in obese/overweight children has been controversial as to the appropriateness of this terminology in children, and lately, in adults too. Newer game-changer terminology, metabolic (dysfunction)-associated fatty liver disease (MAFLD), for this condition signifies a positive step forward that addresses the limitations of the previous definition for both adults and children. The prevalence of MAFLD has surged in tandem with the global rise in obesity rates, establishing itself as a predominant cause of chronic liver disease in both adult and pediatric populations. The adoption of the recently proposed nomenclature reflects a more encompassing comprehension of the disease and its etiology compared to its predecessor, NAFLD. Notably, the revised terminology facilitates the recognition of MAFLD as an autonomous condition while acknowledging the potential coexistence of other systemic fatty liver disorders. Particularly in children, this includes various paediatric-onset genetic and inherited metabolic disorders, necessitating thorough exclusion, especially in cases where weight loss interventions yield no improvement or in the absence of obesity. MAFLD presents as a multifaceted disorder; evidence suggests its origins lie in a complex interplay of nutritional, genetic, hormonal, and environmental factors. Despite advancements, current non-invasive diagnostic biomarkers exhibit limitations in accuracy, often necessitating imaging and histological evaluations for definitive diagnosis. While dietary and lifestyle modifications stand as cornerstone measures for MAFLD prevention and management, ongoing evaluation of therapeutic agents continues. This article provides an overview of the latest developments and emerging therapies in the realm of paediatric MAFLD.
... The increasing prevalence of childhood overweight and obesity has become a pressing global public health issue, particularly in China [1,2]. The development of obesity is influenced by complex factors, including lifestyle habits, dietary patterns, and genetic predispositions [2,3]. Among these factors, the infancy stage has been identified as a critical and sensitive time window for future health [4]. ...
Background: Breastfeeding appears to reduce the risk of childhood overweight/obesity. However, it remains unclear whether this protective effect persists among high-risk populations. This study aims to investigate the association of breastfeeding with the risk of overweight/obesity in early childhood and whether this association is altered by gestational diabetes mellitus (GDM) or size at birth. Methods: Feeding practices during the first 12 months of age and weight and length at 12–36 months of age were collected. Full breastfeeding includes exclusive and predominant breastfeeding. Children with body mass index (BMI) values greater than 1 standard deviation from the mean of sex- and age-specific BMI were classified as overweight/obese. Multiple generalized estimating equations models were applied to analyze the associations of full breastfeeding duration with overweight/obesity risk. Results: Among all participants (n = 9329), infants with a longer full-breastfeeding duration had a reduced risk of overweight/obesity in early childhood compared with those breastfed for less than one month. Infants exposed to GDM and those born large for gestational age (LGA) had a higher risk of overweight/obesity in early childhood. Among infants of mothers with GDM (n = 1748), infants with full breastfeeding for greater than 6 months (aOR: 0.58; 95% CI: 0.44, 0.78) showed a decreased risk of overweight/obesity in early childhood compared with those breastfed for less than one month. Among LGA infants (n = 1279), infants with full breastfeeding for 3–5 months (aOR: 0.66; 95% CI: 0.57, 0.76) and greater than 6 months (aOR: 0.70; 95% CI: 0.56, 0.88) showed a decreased risk of overweight/obesity in early childhood. Similar results were observed among LGA infants of mothers with GDM. Conclusions: Initiating and prolonging breastfeeding would reduce the risk of overweight/obesity in early childhood, and LGA infants and infants born to mothers with GDM would experience greater benefits.
... In addition, a thorough examination of the data reveals that both male and female progeny are almost equally affected by the detrimental consequences of chronic maternal WR consumption. A possible common mechanism behind these diet-induced modifications is via the programmed transmission of certain epigenetic marks [27,48,55]. Gene regulatory factors, including covalent chemical changes (such as methylation) to DNA, histone post-translational modifications, and various RNA species, may be passed from parental gametes to the zygote during both mitosis and meiosis [61]. ...
... Noteworthy alterations in gene expression are discernible in genes related to adipose tissue development, hyperphagia, regulation of energy balance, lipid metabolism, insulin-associated signaling, and the development of adipocytokines and proinflammatory factors such as leptin and adiponectin, as well as pancreatic islet beta cell development. Collectively, these changes contribute to diminished insulin sensitivity [8,23,24]. The study further identified elevated IR in the cases, as indicated by elevated HOMA-IR and reduced QUICKI and GIR, which are aligned with previous studies [25,26]. ...
Background
Maternal obesity is a global health concern that leads to metabolic alterations in the offspring, making them vulnerable to metabolic disorders in adulthood. Early identification of such neonates would provide opportunities to positively alter modifiable risk factors for non-communicable diseases (NCDs) to prevent their occurrence later in life.
Objectives
This study aimed to assess and contrast insulin resistance (IR) levels in neonates born to mothers with obesity and those born to healthy, non-obese mothers.
Methods
This case-control study was conducted after approval from the institutional ethics committee. A total of 98 healthy, non-obese pregnant females were included in Group 1, and 68 obese pregnant females were included in Group 2. The participants were followed up until delivery and cord blood samples were collected after delivery. Neonatal glucose and insulin concentrations were estimated, and indices of IR such as homeostatic model assessment for insulin resistance (HOMA-IR), quantitative insulin-sensitivity check index (QUICKI), and glucose-to-insulin ratio were calculated. Neonatal IR indices and anthropometric measurements were compared between the groups using the Z test and correlated with the maternal pre-pregnancy body mass index (BMI) using Pearson’s correlation. Additionally, Pearson’s correlations were examined between neonatal IR indices and anthropometric measurements. Statistical significance was set at p <0.05.
Results
Neonates in Group 2 exhibited significantly higher anthropometric parameters and IR indices than those in Group 1. A statistically significant positive correlation was identified between maternal pre-pregnancy BMI, neonatal anthropometric parameters, and IR. Furthermore, a statistically significant positive correlation was observed between neonatal IR and the anthropometric parameters.
Conclusion
Neonates born to obese mothers exhibited higher anthropometric parameters and insulin resistance than those born to non-obese, healthy mothers. Assessment of IR at birth can help identify neonates who are at higher risk of developing NCD in later life. Timely promotion of a healthy lifestyle can reduce the occurrence of NCDs in later life.
... Genetic predisposition to food tastes and preferences Food preferences and aversions play an important role in food choices, especially in children. 2 Despite the scarcity of studies, genetic factors seem to influence the development of food preferences, the regulation of appetite and metabolism, body fat distribution, and the presence of behaviors such as eating speed, responsiveness to satiety, and pleasure when eating. 2,9 Examples of this is the evidence that suggests that human beings' preference for sweet or salty flavors over bitter flavors, which characterized scarce and caloric foods and potentially toxic foods respectively, was inherited from primates. 10 In the past, a mix of innate preferences and the capacity to develop new preferences (i.e., learning what is nutritious and safe to eat) seemed to be crucial to survival. ...
... Alterations in different affected genes have variable penetrance and expression and result in a variety of manifestations and symptoms of obesity, such as hyperphagia, severe early-onset obesity, hormonal disorders such as hyperinsulinism and hypothyroidism, accelerated linear growth, hypertension, energy homeostasis impairment, and gastrointestinal disorders. 9,23 On the other hand, polygenic obesity is the most common cause of obesity in children and to which the obesity epidemic is attributed. It results from the interaction of a complex genetic history consisting of the combination of effects of genetic variants common in the general population, in combination with the environment or independently. ...
... The FTO gene, expressed in the hypothalamus, is located on chromosome 16 and encodes an enzyme implicated in the control of energy homeostasis, food intake, and energy expenditure. 9 Genetic variants that are more often present in children with obesity than in children without obesity seem to be related to increased production, secretion, and circulating levels of pro-inflammatory molecules, including tumor necrosis factor-alpha (TNF-a) and interleukin-6 (IL-6), which have been associated with hypertriglyceridemia, liver inflammation, and adipose tissue inflammation. 9 The field of studies in the epigenetics of childhood obesity is new and growing rapidly. ...
Objective:
To investigate the relationship between the biopsychosocial environment and eating habits and behaviors that lead to the selection and consumption of certain food from the earliest stages of life. To clarify whether there is an interaction between genetic and epigenetic factors, and how they shape eating habits.
Data source:
A narrative review based on research in PubMed and Web of Science electronic databases was carried out over the last 10 years, searching the title and summary fields using the keywords Children OR adolescents Feeding Behavior eating OR Dietary Habits OR Eating Behavior OR Eating Habits OR Children obesity.
Data synthesis:
The generational transmission of eating habits is related to the home, community, and school environments, mainly during the first years of life, and can exert the modulation of habits during all stages of life. During childhood, the family's role in consolidating eating habits is very broad and ranges from choosing foods to prioritizing family meals, including the lifestyle.
Conclusions:
Eating habits are transmitted from parents to children in different ways: environmental, emotional, social, and educational. In cases of obesity, a greater association of genetic influence can be observed.
... Obesity is distinguished by a singular and atypical deposition of adipose tissue, which incites maleficent and intimidating health consequences such as metabolic syndrome, Type 2 Diabetes Mellitus, and cardiovascular diseases. The budding pervasiveness of this condition on a global magnitude makes it an intimidating and exigent public health quandary that necessitates expeditious attention and intervention (1,2). Although the incontrovertible implication of genetic elements in the inception of obesity is acknowledged, the pivotal role of epigenetic modifications in regulating gene expression and influencing the pathophysiology of this malaise is gaining increasing recognition from the scientific community (3). ...
Epigenetics, a multifaceted and intricate scientific domain, plays a substantial role in the aetiology of non-communicable diseases, particularly obesity. Its unique capacity to regulate gene expression and cellular processes endows it with remarkable power and potential to mitigate and investigate this global scourge. In this review, the three most widely recognised and complex epigenetic mechanisms implicated in the pathophysiology of obesity - DNA methylation, histone modifications, and non-coding RNAs, and their multifarious and complex interplay with obesity are explored. The review highlights the potential of epigenetic interventions, particularly lifestyle modifications, in managing and ameliorating obesity and related disorders and their reversibility. These interventions present a promising target for designing and developing effective and sustainable strategies to alleviate the enormous burden of obesity worldwide. The crucial insights provided by this review are indispensable for informing and shaping public health policies and interventions that aim to combat and mitigate the insidious and pernicious impact of obesity on individuals and societies.
... Among the three mechanisms, sncRNAs have been primarily studied with paternal obesity partially due to its abundance and diversity in sperm [55]. They play a critical role in regulating gene expression both transcriptionally and post-translationally [56]. In line with this, research has shown that sncRNA content in HF mice sperm contribute to metabolic dysfunction in offspring mice [56,57]. ...
... They play a critical role in regulating gene expression both transcriptionally and post-translationally [56]. In line with this, research has shown that sncRNA content in HF mice sperm contribute to metabolic dysfunction in offspring mice [56,57]. Further, paternal exercise conferred a protective effect of metabolic status of offspring with increased sperm quality as evid enced by a better sncRNA expression level [55]. ...
This study investigates the effects of fish oil supplementation during the periconceptional period in male mice. Specifically, it examines the impact of fish oil on intergenerational health, as determined by skeletal muscle markers. To mimic paternal obesity, thirty mice were separated into three groups with distinct dietary regimes for 10 weeks: a high-fat diet (HF), a high-fat diet supplemented with fish oil (FO), and a low-fat diet (LF). Then, these mice mated with control female mice. Dams and offspring consumed a chow diet during gestation and lactation, and the offspring continued on a chow diet. To study short-term (8 weeks) and long-term (16 weeks) effects of FO, skeletal muscle was isolated at the time of sacrifice, and gene analyses were performed. Results suggest that offspring born to FO-supplemented sires exhibited a significant, short-term upregulation of genes associated with insulin signaling, fatty acid oxidation, and skeletal muscle growth with significant downregulation of genes involved in fatty acid synthesis at 8 weeks. Prominent differences in the above markers were observed at 8 weeks compared to 16 weeks. These findings suggest the potential benefits of FO supplementation for fathers during the periconceptional period in reducing the health risks of offspring due to paternal obesity.
... Environmental epigenetics is known to have a critical role in metabolic disease and obesity [4,5]. For example, the role of epigenetic transgenerational inheritance of obesity susceptibility has been observed in several populations [2,5,6], including humans [7][8][9][10]. ...
The current study was designed to use an epigenome-wide association approach (EWAS) to identify potential systemic DNA methylation alterations that are associated with obesity using 22 discordant twin pairs. Buccal cells (from a cheek swab) were used as a non-obesity relevant purified marker cell for the epigenetic analysis. Analysis of differential DNA methylation regions (DMRs) was used to identify epigenetic associations with metabolic and dietary measures related to obesity with discordant twins. An edgeR analysis provided a DMR signature with p < 1e-04, but statistical significance was reduced due to low sample size and known multiple origins of obesity. A weighted gene coexpression network analysis (WGCNA) was performed and identified modules (p < 0.005) of epigenetic sites that correlated with different metabolic and dietary measures. The DMR and WGCNA epigenetic sites were near genes (e.g., CIDEC, SPP1, ZFPG9, and POMC) with previously identified obesity associated pathways (e.g., metabolism, cholesterol, and fat digestion). Observations demonstrate the feasibility of identifying systemic epigenetic biomarkers for obesity, which can be further investigated for clinical relevance in future research with larger sample sizes. The availability of a systemic epigenetic biomarker for obesity susceptibility may facilitate preventative medicine and clinical management of the disease early in life.
... In addition to psychological screenings, an individual's genetic makeup can be observed [40][41][42][43] to highlight a propensity towards behavioral addictions [44], giving clinicians further opportunities to tailor interventions and maximize the likelihood of the operation's success. Genetic addiction risk has been previously described to identify genetic polymorphisms (alleles) known to play a role in addiction, compulsive behaviors (such as overeating) [45,46], vulnerability to pain [47], and behavioral/conduct disorders [48]. ...
This study analyzed genetic risk assessments in patients undergoing bariatric surgery to serve as a predictive factor for weight loss parameters 1 year after the operation. Thirty (30) patients were assessed for Genetic Addiction Risk Severity (GARS), which analyzes neurogenetic polymorphisms involved in addiction and reward deficiency. Genetic and psychosocial data collected before the operation were correlated with weight loss data, including changes in weight, body mass index (BMI), and percent of expected weight loss (%EWL). Results examined correlations between individual gene risk alleles, 1-year body weight data, and psychosocial trait scores. Spearman’s correlations revealed that the OPRM1 (rs1799971) gene polymorphism had significant negative correlation with 1-year weight (rs = −0.4477, p < 0.01) and BMI (rs = −0.4477, p < 0.05). In addition, the DRD2 risk allele (rs1800497) was correlated negatively with BMI at 1 year (rs = −0.4927, p < 0.05), indicating that one risk allele copy was associated with lower BMI. However, this allele was positively correlated with both ∆Weight (rs = 0.4077, p < 0.05) and %EWL (rs = 0.5521, p < 0.05) at 1 year post-surgery. Moreover, the overall GARS score was correlated with %EWL (rs = 0.4236, p < 0.05), ∆Weight (rs = 0.3971, p < 0.05) and ∆BMI (rs = 0.3778, p < 0.05). Lastly, Food Cravings Questionnaire (FCQ) scores were negatively correlated with %EWL (rs = −0.4320, p < 0.05) and ∆Weight at 1 year post-surgery (rs = −0.4294, p < 0.05). This suggests that individuals with a higher genetic addiction risk are more responsive to weight loss treatment, especially in the case of the DRD2 polymorphism. These results should translate clinically to improve positivity and attitude related to weight management by those individuals born with the risk alleles (rs1800497; rs1799971).
... Although the pathophysiological mechanisms of fetal programming are complicated and not well defined, epigenetic modification is a crucial factor. An overlap of epigenetic modifications causing both neurodevelopmental disorders and obesity cannot be excluded [18,57], and could suggest a future direction for expanding this field of research. ...
Specific learning disorders (SLDs) are the most frequently diagnosed developmental disorders in childhood. Different neurocognitive patterns have been found in patients with overweight and obesity, but no data on childhood obesity and SLDs have been reported. To increase our understanding of the relationship between neuropsychological developmental and obesity, we assessed the prevalence of SLD in a pediatric population with obesity. We retrospectively included 380 children and adolescents with obesity. For all participants, auxological, metabolic, demographic features, relationship and social skills, anamnestic data on pregnancy and the perinatal period, stages of development and family medical history were reviewed. SLD was defined according to the DSM-5 criteria. A group of 101 controls of normal weight was included. The overall prevalence of SLD was 10.8%, and SLD was more prevalent in patients with obesity (p < 0.001), with male predominance (p = 0.01). SGA was associated with SLD (p = 0.02). Speech retardation (p < 0.001), limited relationships with peers (p < 0.001) and didactic support (p < 0.001) were noted in the SLD group compared to the group without SLD. A higher prevalence of family history of neuropsychiatric disorders was observed in the SLD group (p = 0.04). A higher fasting glucose level was detected in patients with obesity and SLD compared to subjects without SLD (p = 0.01). An association between obesity and SLD could not be excluded, and an overlap of pathogenic factors for both conditions should be considered.
