Predisposition To Obesity Research Articles

Leveraging Artificial Intelligence (AI) in Finding the Interconnected Epidemics and Genetic Predisposition of Obesity and Type 2 Diabetes: A Review

Leveraging Artificial Intelligence (AI) in Finding the Interconnected Epidemics and Genetic Predisposition of Obesity and Type 2 Diabetes: A Review

Association between cardiovascular risk factors and dilated and hypertrophic cardiomyopathy: Mendelian randomization analysis

Backgroundand aims: Dilated cardiomyopathy is a major cause of heart failure, and hypertrophic cardiomyopathy is a common cause of sudden cardiac death in young adults. Epidemiological studies reporting the association between these cardiomyopathies and common cardiovascular risk factors, including smoking, alcohol, and obesity, are limited, and the published studies are mostly observational, making them vulnerable to bias. Methods and resultsWe performed a two-sample Mendelian randomization analysis to assess whether cardiovascular risk factors were causally associated with dilated and hypertrophic cardiomyopathies. Independent genetic variants associated with body mass index, smoking, and alcohol were selected as instrumental variables, with two sets of instrumental variables utilized for alcohol. Dilated cardiomyopathy data on 355,318 samples and hypertrophic cardiomyopathy data on 489,727 samples were obtained from a European population-based genome-wide association study (GWAS) meta-analysis. The large GWAS data sample size improved the statistical power. Our results showed significant associations between a genetic predisposition for smoking and the risk of dilated cardiomyopathy (odds ratio (OR) = 1.33; 95% confidence level (CI): 1.07–1.67; p = 0.012) and between a genetic predisposition for obesity and the risk of dilated cardiomyopathy (OR = 1.62; 95% CI, 1.30 – 2.02; p = 1.51 × 10-5). The results of the other associations were not significant. ConclusionsThis study suggests that smoking and obesity are causally associated with an increased risk of dilated cardiomyopathy.

G-Protein-Coupled Receptor 120 Agonist Mitigates Steatotic and Fibrotic Features Triggered in Obese Mice by the Administration of a High-Fat and High-Carbohydrate Diet.

Nonalcoholic fatty liver disease (NALFD) represents a complex condition ranging from simple steatosis (nonalcoholic fatty liver, NAFL) to inflammation, and fibrosis is one of the main features of nonalcoholic steatohepatitis (NASH). The pathogenesis of NAFLD is not well established but involves several factors (i.e., predisposition of genetic variants, obesity, and unhealthy lifestyle as unbalanced diets) that lead to an alteration of lipid homeostasis and consequently to an abnormal accumulation of triglycerides and other lipids in the liver parenchyma. Currently, no resolutive pharmacological treatment for NAFLD is available, and the only therapeutic approach is a healthy diet and physical exercise. In this study, we investigated the potential beneficial effect of GprA, a new synthetic agonist of G-protein-coupled receptor 120/free fatty acid receptor 4 (GPR120/FFAR4), in the progression of NAFL/NASH in mice fed for different periods (26 weeks and 30 weeks), with a high-fat (40% kcal) and high-carbohydrate diet, also called a Western-style diet (WSD). In our experimental model, the histological, protein, and transcriptomic analyses highlighted that the GprA can reduce signs of steatosis in WSD-fed mice. Furthermore, in 30 week-treated mice, GprA is also effective in the reduction of collagen deposition and fibrosis development. Altogether, our data validate the central role of FFAR4 in the context of NAFL/NASH onset and progression and reveal that GprA could represent an interesting candidate for the development of a new therapeutic approach in NAFLD treatment.

Gene Polymorphisms LEP, LEPR, 5HT2A, GHRL, NPY, and FTO-Obesity Biomarkers in Metabolic Risk Assessment: A Retrospective Pilot Study in Overweight and Obese Population in Romania

Genome-wide association studies (GWAS) have successfully revealed numerous susceptibility loci for obesity. The PREDATORR study (2014) shows that in Romania, 346% of adults aged 20–79 y/o are overweight, and 31.4% are obese with a high risk of cardiometabolic complications, a number that puts almost 67% of Romania’s population in the abnormal weight group. Our study aims to investigate the current status of the genetic foundation in metabolic disease associated with obesity, applied to a pilot group of patients specifically examining the impact of known polymorphisms and their haplotype of six food intake-regulating genes, namely leptin (LEP), leptin receptor (LEP-R), serotonin receptor (5HTR2A), ghrelin (GHRL), neuropeptide Y (NPY), and fat-mass and obesity-associated protein (FTO) with the following polymorphisms: LEP A-2548G, LEPR A-223G, 5HTR2A G-1439A, GHRL G-72T, NPY T-29063C, FTO A-T, and body mass index (BMI). A notable link between the LEP-2548 rs7799039 gene’s AG genotype and the risk of obesity was observed, particularly pronounced in males aged 40–49, with an approximately seven-fold increased likelihood of obesity. The 5HTR2A rs6311 AA genotype was associated with a higher BMI, which was not statistically significant. The FTO rs9939609 gene’s AA genotype emerged as a significant predictor of obesity risk. Besides these significant findings, no substantial associations were observed with the LEPR, 5HTR2A, GHRL, and NPY genes. Haplotype association analysis showed a suggestive indication of GRGMLA (rs7799039, rs1137101, rs6311, rs696217, rs16139, rs9939609 sequence) haplotype with a susceptibility effect towards obesity predisposition. Linkage disequilibrium (LD) analysis showed statistically significant associations between LEP and LEPR gene (p = 0.04), LEP and GHRL gene (p = 0.0047), and GHRL and FTO gene (p = 0.03). Our study, to the best of our knowledge, is one of the very few on the Romanian population, and aims to be a starting point for further research on the targeted interventional strategies to reduce cardiometabolic risks.

Deciphering the Interplay between Genetic Risk Scores and Lifestyle Factors on Individual Obesity Predisposition.

Obesity's variability is significantly influenced by the interplay between genetic and environmental factors. We aimed to integrate the combined impact of genetic risk score (GRSBMI) with physical activity (PA), sugar-sweetened beverages (SSB), wine intake, and eating habits score (EHS) on obesity predisposition risk. Adults' (n = 5824) data were analyzed for common obesity-related single nucleotide polymorphisms and lifestyle habits. The weighted GRSBMI was constructed and categorized into quartiles (Qs), and the adjusted multivariate logistic regression models examined the association of GRSBMI with obesity (BMI ≥ 30) and lifestyle factors. GRSBMI was significantly associated with obesity risk. Each GRSBMI unit was associated with an increase of 3.06 BMI units (p ≤ 0.0001). PA markedly reduced obesity risk across GRSBMI Qs. Inactive participants' (≥90 min/week) mean BMI was higher in GRSBMI Q3-Q4 compared to Q1 (p = 0.003 and p < 0.001, respectively). Scoring EHS ≥ median, SSBs (≥1 cup/day), and non-wine drinking were associated with higher BMI within all GRSBMI Qs compared to EHS < median, non-SSBs, and non-wine drinkers. Mean BMI was higher in GRSBMI Q4 compared to other quartiles (p < 0.0001) in non-wine drinkers and compared to Q1 for SSB's consumers (p = 0.07). A higher GRSBMI augmented the impact of lifestyle factors on obesity. The interplay between GRSBMI and modifiable lifestyle factors provides a tailored personalized prevention and treatment for obesity management.

Higher Prevalence of the Periodontal Pathogen Selenomonas noxia among Pediatric and Adult Patients May Be Associated with Overweight and Obesity.

New evidence has suggested that oral and gut microflora may have significant impacts on the predisposition, development, and stability of obesity in adults over time-although less is known about this phenomenon in children. Compared with healthy-weight controls, overweight and obese adult patients are now known to harbor specific pathogens, such as Selenomonas noxia (S. noxia), that are capable of digesting normally non-digestible cellulose and fibers that significantly increase caloric extraction from normal dietary intake. To evaluate this phenomenon, clinical saliva samples (N = 122) from subjects with a normal BMI (18-25) and a BMI over 25 (overweight, obese) from an existing biorepository were screened using qPCR. The prevalence of S. noxia in samples from normal-BMI participants were lower (21.4%) than in overweight-BMI (25-29; 46.1%) and obese-BMI (30 and above; 36.8%) samples-a strong, positive correlation that was not significantly affected by age or race and ethnicity. These data strongly suggest that S. noxia may be intricately associated with overweight and obesity among patients, and more research will be needed to determine the positive and negative feedback mechanisms that may be responsible for these observations as well as the interventions needed to remove or reduce the potential effects of this oral pathogen.

Brain-derived neurotrophic factor gene rs925946 associates with Israeli females' obesity predisposition: An interaction between genetics, eating habits, and physical inactivity

The global obesity pandemic presents a pressing health challenge, with an increasing prevalence shaped by an intricate interplay of genetics and environment. Brain-derived neurotrophic factor (BDNF) plays a pivotal role in regulating feeding behavior and energy expenditure. BDNF single nucleotide polymorphisms have been linked to obesity risk. We hypothesized that BDNF rs925946 is positively associated with obesity susceptibility in the Israeli population. We aimed to study BDNF rs925946 association with obesity susceptibility and its interaction with environmental factors, including eating habits, sugar-sweetened beverages, and physical activity. A data cohort of 4668 Israeli adults (≥18 years, Jewish) was analyzed. Participants' genotypic data for the BDNF rs925946 and lifestyle and eating behavior questionnaire data were analyzed for the association between obesity predisposition and gene–environment interactions. Female (n = 3259) BDNF rs925946 T-allele carriers had an elevated obesity odd (odds ratio [OR] = 1.2; 95% confidence interval [CI], 1.03–1.4, P = .02). BDNF rs925946 genotype interacted significantly with physical inactivity, sugar-sweetened beverage consumption, and eating habits score to enhance obesity odds (OR = 1.4; 95% CI, 1.14–1.7; OR = 1.54, 95% CI, 1.1–2.15; and OR = 1.4; 95% CI, 1.2–2.11, respectively). Our data demonstrated a significant association between BDNF rs925946 T-allele female carriers and a higher obesity predisposition, affected by modifiable lifestyle factors.

Weight development from childhood to motherhood—embodied experiences in women with pre-pregnancy obesity: a qualitative study

BackgroundPre-pregnancy obesity increases the risk of perinatal complications. Post-pregnancy is a time of preparation for the next pregnancy and lifestyle advice in antenatal care and postpartum follow-up is therefore recommended. However, behavioral changes are difficult to achieve, and a better understanding of pregnant women’s perspectives and experiences of pre-pregnancy weight development is crucial.MethodsWe used a qualitative design and conducted semi-structured interviews with 14 women in Norway with pre-pregnancy obesity 3–12 months postpartum. Data were analyzed using thematic analysis.ResultsFour themes addressing women’s experiences and understanding of their weight development were generated: (1) Unmet essential needs, (2) Genetic predisposition for obesity, challenging life course transitions and turning points, (3) Under a critical eye: an ever-present negative bodily awareness, and (4) Wrestling with food. Parents’ inability to meet children’s essential needs caused weight gain through an unbalanced diet, increased stress, and emotional eating patterns. Body criticism and a feeling of not belonging led to negative body awareness that influenced behavioral patterns and relationships. Participants reporting having had a good childhood more often described their weight development as a result of genetic predisposition, challenging life course transitions and turning points, such as illness and injuries. Nevertheless, these participants also described how eating patterns were influenced by stress and negative emotions.ConclusionsHealthcare providers should pay attention to the insider perspectives of pre-pregnancy weight development. An open and shared understanding of the root causes of these women’s weight development can form a basis for more successful lifestyle guidance.

Predisposition of the Common MC4R rs17782313 Female Carriers to Elevated Obesity and Interaction with Eating Habits.

The global rise in obesity is attributed to genetic predisposition interaction with an obesogenic environment. Melanocortin 4 receptor (MC4R) rs17782313 polymorphism has been linked to common obesity with varying influence across different populations. MC4R is a crucial player in the leptin proopiomelanocortin pathway that regulates weight hemostasis. We aimed to study MC4R rs17782313 and its interaction with eating behaviors on obesity predisposition in the Israeli population. Adults' (n = 5785, >18 y) genotype and anthropometric and demographic data were analyzed using logistic regression models adjusting for age, sex, T1DM, and T2DM. MC4R rs17782313 significantly predisposes to elevated obesity risk under the recessive and additive models (OR = 1.38, 95% CI: 1.1-1.72, p = 0.005 and OR = 1.1, 95% CI: 1.01-1.2, p = 0.03, respectively) adjusted for confounders (age, sex, T1DM, and T2DM). Stratification by sex demonstrated that carrying the common MC4R rs17782313 is significantly associated with an elevated predisposition to obesity under the recessive model among females only (OR = 1.41, 95% CI: 1.09-1.82, p = 0.01), with an average of 0.85 BMI increment compared with wild type and one risk allele carriers. MC4R rs17782313 significantly interacted with several eating behaviors to enhance the risk of obesity. Our findings demonstrate that MC4R rs17782313 homozygous female carriers are significantly predisposed to obesity amplified by eating behaviors.

The association between body mass index elevation and differentiation in vitamin D receptor gene expression, genetic polymorphism, and oxidative stress in adult Egyptian individuals

Vitamin D plays a central role in maintaining calcium, phosphorus, and bone homeostasis in close interaction with the parathyroid hormone. Obesity is a significant health problem worldwide, particularly in developed nations. The current study was carried out to investigate the possible relationship between body mass index (BMI) elevation and differentiation in 25-hydroxyvitamin D (VD), vitamin D receptor (VDR) gene expression, and genetic polymorphism besides oxidative stress in adult Egyptian individuals. This was done to explore the mechanisms underlying the suggested role of the VD/VDR complex in the pathogenesis of obesity. A total of 70 subjects (30 obese, 25 overweight, and 15 normal, age: 20–50 years, without other chronic diseases) were selected. The study focused on the determination of VD, VDR gene polymorphism, VDR gene expression, alkaline phosphatase, calcium, phosphorus, glucose, lipid profile, oxidative stress including, oxidant (malondialdehyde), and anti-oxidants (reduced glutathione and superoxide dismutase). The results showed that elevation in BMI led to the percentage of the Ff 'allele' becoming predominant, while the percentage of the FF 'allele' was in the normal BMI range. Also, BMI elevation caused significant reductions in VD and VDR expression, with significant elevations in alkaline phosphatase and the levels of calcium and phosphate in serum. Also, oxidative stress increases with increasing BMI. Elevation in BMI causes a reduction in VD concentration and VDR gene expression levels. Also, the percentage of heterozygous mutant genotype Ff 'allele' is predominantly in the obese human, in contrast to normal subjects, where the percentage of homozygous wild genotype FF 'allele' is predominant. In general, the genetic expression and polymorphism of VD and VDR can be used as a genetic marker for predisposition, diagnosis, prognosis, and progression of obesity.

Hypothalamic α7 nicotinic acetylcholine receptor (α7nAChR) is downregulated by TNFα-induced Let-7 overexpression driven by fatty acids.

The α7nAChR is crucial to the anti-inflammatory reflex, and to the expression of neuropeptides that control food intake, but its expression can be decreased by environmental factors. We aimed to investigate whether microRNA modulation could be an underlying mechanism in the α7nAchR downregulation in mouse hypothalamus following a short-term exposure to an obesogenic diet. Bioinformatic analysis revealed Let-7 microRNAs as candidates to regulate Chrna7, which was confirmed by the luciferase assay. Mice exposed to an obesogenic diet for 3 days had increased Let-7a and decreased α7nAChR levels, accompanied by hypothalamic fatty acids and TNFα content. Hypothalamic neuronal cells exposed to fatty acids presented higher Let-7a and TNFα levels and lower Chrna7 expression, but when the cells were pre-treated with TLR4 inhibitor, Let-7a, TNFα, and Chrna7 were rescued to normal levels. Thus, the fatty acids overload trigger TNFα-induced Let-7 overexpression in hypothalamic neuronal cells, which negatively regulates α7nAChR, an event that can be related to hyperphagia and obesity predisposition in mice.

Clostridium butyricum Reduces Obesity in a Butyrate-Independent Way

Accumulating evidence from recent studies links the gut microbiota to obesity, and microbiome therapy has been examined as a treatment. Clostridium butyricum (C. butyricum), an intestinal symbiont, protects the host from a range of diseases. Studies have shown a negative correlation between the relative abundance of C. butyricum and a predisposition for obesity. However, the physiological function and material basis of C. butyricum for obesity are unclear. Here, five C. butyricum isolates were administered to mice on a high-fat diet (HFD) to determine their anti-obesity effects. All isolates suppressed the formation and inflammation of subcutaneous fat, and the two effective strains considerably reduced weight gain and ameliorated dyslipidemia, hepatic steatosis, and inflammation. These positive effects were not achieved by increasing the concentration of intestinal butyrate, and the effective strains could not be replaced by sodium butyrate (NaB). We also discovered that oral supplementation with the two most effective strains changed the metabolism of tryptophan and purine and altered the composition of the gut microbiota. In summary, C. butyricum improved the metabolic phenotypes under the HFD by controlling the composition of the gut microbiota and modulating intestinal metabolites, thereby demonstrating its ability to fight obesity and providing a theoretical foundation for microbial preparations production.

Intraindividual variability in brain activation—A novel correlate of obesity risk among female college students

There are published data describing impairments in the brain function of adolescents or young adults who have a genetic or familial predisposition for obesity. From these descriptions, it is often assumed that the impairments are appropriately captured by a central tendency estimate and therefore consistently detectable. The present study questions this assumption and shows that the variability in brain function over the time course of a cognitive task is a better predictor of familial risk than its central tendency. Sixty-nine female young adults lacking an obese parent and 24 female young adults with an obese parent were compared on the average amplitude and inter-trial variability (ITV) in amplitude of their P300 electroencephalographic responses to rarely-occurring stimuli during a selective attention task. Simple group comparisons revealed statistically significant findings with effect sizes that were markedly greater for analyses of P300 ITV versus P300 average amplitude. It is suggested that the elevation in P300 ITV among young adults with familial risk indicates temporal instability in systems responsible for the maintenance of attention. These fluctuations may episodically disrupt their attention to satiety cues as well as other cues that influence behavior regulation.

Parental Obesity Predisposition and Age of Onset Associate with Poor Response to Bariatric and Metabolic Surgery

IntroductionParental predisposition and age of onset may be independently associated with 1-year total weight loss (TWL) failure (< 20%) after metabolic–bariatric surgery (MBS).MethodsThis cohort study includes all cases of the German StuDoQ|MBE register (2015–2019) with data on parental predisposition, obesity onset, and at least 1-year follow up after primary MBS procedures (n = 14,404). We provide descriptive statistics of the cohort in terms of the main outcome and 1-year TWL failure, and provide characteristics of surgery type subgroups. Finally, we provide a multivariate logistic regression model of 1-year TWL failure.Results58.8% and 45.7% of patients reported maternal and paternal predisposition for obesity, respectively. Average onset of obesity was 15.5 years and duration of disease 28.3 years prior to MBS. SG is the most frequently performed procedure (47.2%) followed by RYGB (39.7%) and OAGB (13.1%). Mean 1-year TWL is 32.7 ± 9.3%, and 7.8% (n = 1,119) of patients show TWL failure (< 20%). Multivariate analysis shows independent association of early onset of obesity (< 18 years), male sex, age at operation, pre-operative BMI, pre-operative weight loss, sleeve gastrectomy (SG), and type 2 diabetes (T2D) with 1-year TWL failure (p < 0.001).ConclusionThe proportions of MBS patients that report on paternal and maternal predisposition for obesity are 45.7% and 58.8% respectively, and average age at onset is 15.5 years. 7.8% of patients do not meet current target criteria of successful response to surgery at 1 year. Early onset, male sex, age at operation, pre-operative BMI, pre-operative weight loss, SG, and T2D are independently associated with weight loss failure.Graphical abstract

Interactive effects of FTO rs9939609 and obesogenic behavioral factors on adiposity-related anthropometric and metabolic phenotypes

Numerous genetic variants have been linked to obesity predisposition, however, the interplay of genetic and behavioral factors is very crucial in determining the final phenotype. Therefore, this study examined the interactive effects of the FTO rs9939609 and various obesogenic behavioral factors on adiposity-related anthropometric and metabolic phenotypes in a sample of Pakistani population. A total of 612 participants encompassing 306 overweight/obese (cases) and an equal number (306) of age- and sex-matched normal-weight (controls) individuals were included in the study. Adiposity-related anthropometric parameters were collected by taking corresponding body measurements by following standard procedures. The metabolic parameters were assessed by performing corresponding biochemical assays. A standard questionnaire was devised for the collection of adiposity-related behavioral information. The FTO rs9939609 was genotyped by employing TaqMan allelic discrimination assay. The data was analyzed by using SPSS software. Interactive effects of the FTO rs9939609 and behavioral factors on obesity-related anthropometric and metabolic phenotypes were examined via linear regression by adjusting potential confounders and making correction for multiple comparisons. The results implied that the interaction between the FTO rs9939609 and low physical activity may significantly increase various adiposity-related anthropometric variables (p < 0.05). However, no such interactive effects were found on any adiposity-related metabolic variable. In conclusion, the interaction between the FTO rs9939609 and low physical activity may have a significant impact on obesity-related anthropometric traits in the Pakistani population.

Drinking Habits and Physical Activity Interact and Attenuate Obesity Predisposition of TMEM18 Polymorphisms Carriers.

The transmembrane protein 18 (TMEM18) gene plays a central and peripheral role in weight regulation. TMEM18 genetic polymorphisms have been identified as an important risk factor for obesity, depending on ethnic population and age. This research aimed to study the association of common TMEM18 polymorphisms with obesity and their interactions with modifiable factors, namely drinking habits (sugar-sweetened beverages (SSBs), flavored water and wine) and physical activity (PA) in the Israeli population. Adults (n = 3089) were analyzed for common TMEM18 polymorphisms and lifestyle and nutrition habits were obtained from questionnaires using adjusted (age, sex) binary logistic regression models. TMEM18 rs939583 and rs1879523 were significantly associated with increased obesity risk (OR = 1.35, 95% CI (1.17-1.57) and OR = 1.66, 95% CI (1.29-2.15), respectively). TMEM18 rs939583 interacted with consumption of 1-3 weekly glasses of wine and PA to attenuate obesity risk (OR = 0.82 95% CI (0.74-0.9; p &lt; 0.001) and OR = 0.74 95% CI (0.68-0.8), respectively), while physical inactivity, SSBs and flavored water consumption significantly enhanced obesity risk (OR = 1.54 95% CI (1.41-1.67), OR = 1.31 95% CI (1.14-1.51) and OR = 1.35 95% CI (1.13-1.62), respectively). PA duration was significantly associated with a lower BMI for rs939583 risk carriers, with a PA cutoff of &gt;30 min/week (p = 0.005) and &gt;90 min/week (p = 0.01). Common TMEM18 SNPs were significantly linked with adult obesity risk and interacted with modifiable lifestyle factors.

Development of a genetic risk score for obesity predisposition evaluation.

Obesity is a major public health issue resulting from an interaction between genetic and environmental factors. Genetic risk scores (GRSs) are useful to summarize the effects of many genetic variants on obesity risk. In this study, we aimed to assess the association of previously well-studied genetic variants with obesity and develop a genetic risk score to anticipate the risk of obesity development in the Iranian population. Among 968 participants, 599 (61.88%) were obese, and 369 (38.12%) were considered control samples. After genotyping, an initial screening of 16 variants associated with body mass index (BMI) was performed utilizing a general linear model (p < 0.25), and seven genetic variants were selected. The association of these variants with obesity was examined using a multivariate logistic regression model (p < 0.05), and finally, five variants were found to be significantly associated with obesity. Two gene score models (weighted and unweighted), including these five loci, were constructed. To compare the discriminative power of the models, the area under the curve was calculated using tenfold internal cross-validation. Among the studied variants, ADRB3 rs4994, FTO rs9939609, ADRB2 rs1042714, IL6 rs1800795, and MTHFR rs1801133 polymorphisms were significantly associated with obesity in the Iranian population. Both of the constructed models were significantly associated with BMI (p < 0.05) and the area under the mean curve of the weighted GRS and unweighted GRS were 70.22% ± 0.05 and 70.19% ± 0.05, respectively. Both GRSs proved to predict obesity and could potentially be utilized as genetic tools to assess the obesity predisposition in the Iranian population. Also, among the studied variants, ADRB3 rs4994 and FTO rs9939609 polymorphisms have the highest impacts on the risk of obesity.

Prenatal Effects of Nicotine on Obesity Risks: A Narrative Review.

Nicotine usage by mothers throughout pregnancy has been observed to relate to numerous deleterious effects in children, especially relating to obesity. Children who have prenatally been exposed to nicotine tend to have lower birth weights, with an elevated risk of becoming overweight throughout development and into their adolescent and adult life. There are numerous theories as to how this occurs: catch-up growth theory, thrifty phenotype theory, neurotransmitter or endocrine imbalances theory, and a more recent examination on the genetic factors relating to obesity risk. In addition to the negative effect on bodyweight and BMI, individuals with obesity may also suffer from numerous comorbidities involving metabolic disease. These may include type 1 and 2 diabetes, high cholesterol levels, and liver disease. Predisposition for obesity with nicotine usage may also be associated with genetic risk alleles for obesity, such as the DRD2 A1 variant. This is important for prenatally nicotine-exposed individuals as an opportunity to provide early prevention and intervention of obesity-related risks.

Influence of High Energy Diet and Polygenic Predisposition for Obesity on Postpartum Health in Rat Dams.

It is estimated that 30% of pregnant women worldwide are overweight or obese, leading to adverse health effects for both mother and child. Women with obesity during pregnancy are at higher risk for developing both metabolic and mental disorders, such as diabetes and depression. Numerous studies have used rodent models of maternal obesity to understand its consequences on the offspring, yet characterization of changes in the dams is rare, and most rodent models rely solely on a high fat diet to induce maternal obesity, without regarding genetic propensity for obesity. Here we present the influence of both peripartum high energy diet (HE) and obesity-proneness on maternal health using selectively bred diet-resistant (DR) and diet-induced obese (DIO) rat dams. Outbred Sprague-Dawley rats were challenged with HE diet prior to mating and bred according to their propensity to gain weight. The original outbred breeding dams (F0) were maintained on low-fat chow during pregnancy and lactation. By comparison, the F1 dams consuming HE diet during pregnancy and lactation displayed higher gestational body weight gain (P < 0.01), and HE diet caused increased meal size and reduced meal frequency (P < 0.001). Sensitivity to the hormone amylin was preserved during pregnancy, regardless of diet. After several rounds of selective breeding, DIO and DR dams from generation F3 were provided chow or HE during pregnancy and lactation and assessed for their postpartum physiology and behaviors. We observed strong diet and phenotype effects on gestational weight gain, with DIO-HE dams gaining 119% more weight than DR-chow (P < 0.001). A high-resolution analysis of maternal behaviors did not detect main effects of diet or phenotype, but a subset of DIO dams showed delayed nursing behavior (P < 0.05). In generation F6/F7 dams, effects on gestational weight gain persisted (P < 0.01), and we observed a main effect of phenotype during a sucrose preference test (P < 0.05), with DIO-chow dams showing lower sucrose preference than DR controls (P < 0.05). Both DIO and DR dams consuming HE diet had hepatic steatosis (P < 0.001) and exhibited reduced leptin sensitivity in the arcuate nucleus (P < 0.001). These data demonstrate that both diet and genetic obesity-proneness have consequences on maternal health.

Бронхиальная астма у пациентов с ожирением (обзор литературы)

Bronchial asthma (BA) is a widespread disease affecting up to 339 million people worldwide. Currently, a number of BA phenotypes are distinguished: asthma associated with obesity, allergic, non-allergic, asthma with late onset, and asthma with fixed bronchial obstruction. According to the World Health Organization, more than 30% of the world population is obese. According to GINA, the phenotype “BA with obesity” is characterized by a more severe development of the decease, low level of disease control, resistance to baseline therapy, frequent hospitalizations for exacerbations, and the comorbid pathology in patients. In this connection, personalized approach is required, with individual selection of therapy, which is often not effective enough, which entails the need for further study of the disease development and its pathogenesis factors. To date, the role of obesity in the mechanisms of formation of a more severe development of BA has been actively studied. It has been shown that many other factors such as oxidative stress, changes in vitamin D and periostine levels, changes in airway physiology due to obesity, sleep disorders and genetic predisposition can influence the development and/or exacerbation of dyspnea in obese patients.