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The prevalence of obesity is increasingly widespread, resembling a global epidemic. Lifestyle changes, such as consumption of high-energy-dense diets and physical inactivity, are major contributors to obesity. Common features of this metabolic pathology involve an imbalance in lipid and glucose homeostasis including dyslipidemia, insulin resistance and adipose tissue dysfunction. Moreover, the importance of the gut microbiota in the development and susceptibility to obesity has recently been highlighted. In recent years, new strategies based on the use of functional foods, in particular bioactive peptides, have been proposed to counteract obesity outcomes. In this context, the present study examines the effects of a lupin protein hydrolysate (LPH) on obesity, dyslipidemia and gut dysbiosis in mice fed a high-fat diet (HFD). After 12 weeks of LPH treatment, mice gained less weight and showed decreased adipose dysfunction compared to the HFD-fed group. HFD-induced dyslipidemia (increased triglycerides, cholesterol and LDL concentration) and insulin resistance were both counteracted by LPH consumption. Discriminant analysis differentially distributed LPH-treated mice compared to non-treated mice. HFD reduced gut ecological parameters, promoted the blooming of deleterious taxa and reduced the abundance of commensal members. Some of these changes were corrected in the LPH group. Finally, correlation analysis suggested that changes in this microbial population could be responsible for the improvement in obesity outcomes. In conclusion, this is the first study to show the effect of LPH on improving weight gain, adiposopathy and gut dysbiosis in the context of diet-induced obesity, pointing to the therapeutic potential of bioactive peptides in metabolic diseases., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Most known types of nonsyndromic monogenic obesity are caused by rare mutations in genes of the leptin-melanocortin pathway controlling appetite and adiposity. In contrast, congenital generalized lipodystrophy represents the most extreme form of leanness in humans caused by recessive mutations in four genes involved in phospholipid/triglyceride synthesis and lipid droplet/caveolae structure. In this disease, the inability to store triglyceride in adipocytes results in hypoleptinemia and ectopic hepatic and muscle fat accumulation leading to fatty liver, hypertriglyceridemia and severe insulin resistance. As a result of hypoleptinemia, patients with lipodystrophy show alterations in eating behaviour characterized by constant increased energy intake. As it occurs in obesity caused by genetic leptin deficiency, exogenous leptin rapidly reduces hunger scores in patients with congenital generalized lipodystrophy, with additional beneficial effects on glucose homeostasis and metabolic profile normalization. The melanocortin-4 receptor agonist setmelanotide has been used in the treatment of monogenic obesities. There is only one report on the effect of setmelanotide in a patient with partial lipodystrophy resulting in mild reductions in hunger scores, with no improvements in metabolic status. The assessment of contrasting phenotypes of obesity/leanness represents an adequate strategy to understand the pathophysiology and altered eating behaviour associated with adipose tissue excessive accumulation/paucity., (© 2020 World Obesity Federation.)

Backgroud: The prevalence of obesity has systematically been increased in the population, including children and adolescents, around the world., Objectives: To describe reference percentile curves for waist circumference (WC) in Brazilian children and provide cut-off values of WC to identify children at risk for obesity., Methods: A multicenter, prospective, cross-sectional study was performed with children aged from 6 to 10 years old, enrolled in public and private elementary schools from 13 cities of the São Paulo State. Height, weight, and WC were measured in duplicate in 22,000 children (11,199 boys). To establish the WC best cut-off value for obesity diagnosis, ROC curves with children classified as normal weight and obese were calculated, according to BMI curves, stratified by gender and age, and the Youden Index was utilized as the maximum potential effectiveness of this biomarker. A p < 0.05 was considered statistically significant., Results: WC values increased with age in both boys and girls. The prevalence of obesity in each age group varied from 17% (6 years old) to 21.6% (9 years old) among boys, and from 14.1% (7 years old) to 17.3 % (9 years old) among girls. ROC analyses have shown the 75th percentile as a cut-off for obesity risk, and the diagnosis of obesity is classified on the 85th percentile or more., Conclusion: Age and gender specific reference curves of WC for Brazilian children and cut-off values for obesity risk may be used for national screening and interventional studies to reduce the obesity burden in Brazil. (Arq Bras Cardiol. 2020; 114(3):530-537).

Obesity is a global pandemic complex to treat due to its multifactorial pathogenesis-an unhealthy lifestyle, neuronal and hormonal mechanisms, and genetic and epigenetic factors are involved. Scientific evidence supports the idea that obesity and metabolic consequences are strongly related to changes in both the function and composition of gut microbiota, which exert an essential role in modulating energy metabolism. Modifications of gut microbiota composition have been associated with variations in body weight and body mass index. Lifestyle modifications remain as primary therapy for obesity and related metabolic disorders. New therapeutic strategies to treat/prevent obesity have been proposed, based on pre- and/or probiotic modulation of gut microbiota to mimic that found in healthy non-obese subjects. Based on human and animal studies, this review aimed to discuss mechanisms through which gut microbiota could act as a key modifier of obesity and related metabolic complications. Evidence from animal studies and human clinical trials suggesting potential beneficial effects of prebiotic and various probiotic strains on those physical, biochemical, and metabolic parameters related to obesity is presented. As a conclusion, a deeper knowledge about pre-/probiotic mechanisms of action, in combination with adequately powered, randomized controlled follow-up studies, will facilitate the clinical application and development of personalized healthcare strategies.

Mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) is a mitochondrial-derived peptide that attenuates weight gain and hyperinsulinemia when administered to high fat-fed mice. MOTS-c is therefore a potential regulator of metabolic homeostasis under conditions of high-energy supply. However, the effect of insulin resistance and obesity on plasma MOTS-c concentration in humans is unknown. To gain insight into MOTS-c regulation, we measured plasma MOTS-c concentration and analyzed its relationship with insulin sensitivity surrogates, in lean and obese humans (n=10 per group). Obese individuals had impaired insulin sensitivity as indicated by low Matsuda and high Homeostatic Model Assessment (HOMA) indexes. Although plasma MOTS-c concentration was similar in lean and obese individuals (0.48±0.16 and 0.52±0.15 ng/mL; p=0.60), it was correlated with HOMA (r=0.53; p<0.05) and Matsuda index (r=-0.46; p<0.05). Notably, when the groups were analyzed separately, the associations remained only in lean individuals. We conclude that plasma MOTS-c concentration is unaltered in human obesity. However, MOTS-c associates positively with insulin resistance mostly in lean individuals, indicating that plasma MOTS-c concentration depends on the metabolic status in this population. Such dependence seems altered when obesity settles. The implications of plasma MOTS-c for human metabolic homeostasis deserve future examination., Competing Interests: Competing interests: None declared., (© American Federation for Medical Research (unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Objective: Infants born from overweight and obese mothers with glucose-controlled gestational diabetes (GDM) tend to be large-for-gestational age (LGA). It is hypothesized that this is due to an excessive rise in maternal triglyceride levels., Methods: Two-hundred and seventy nine singleton GDM pregnancies were divided into three groups according to prepregnancy BMI: normal weight (BMI = 20-24.9; n = 128), overweight (BMI = 25-29.9; n = 105), and obese (BMI ≥ 30; n = 46). Individual z-scores (ZS) of maternal triglycerides and of newborn weight (NWZS) were calculated as deviations from published 50th percentiles. Mean z-scores (MZS) were the average of triglyceride ZSs. MZS of triglycerides, HbA1c and NWZS were compared. Variables are expressed as mean ± SD., Results: In the three groups respectively: LGA (%) = 10.1%, 19.0% and 30.4% (P = 0.015). Birth weight (g) = 3274.2 ± 501.3, 3342.4 ± 620.2 and 3366.3±644.7 (RSPEARMAN  = 0.111, P = 0.027). HbA1c (%) = 5.2 ± 0.39, 5.3 ± 0.50 and 5.4 ± 0.47 (P = NS). Triglyceride MZS = 1.20 ± 1.13, 1.52 ± 1.37 and 1.62 ± 1.42 (RSPEARMAN = 0.116, P = 0.024). Correlations between triglyceride MZS and NWZS were, respectively: r = 0.12 (P = NS), r = 0.42 (P <0.001), and r = 0.47 (P < 0.001)., Conclusions: In overweight and obese GDM mothers, maternal triglycerides are partially responsible for LGA infants despite good maternal glucose control during pregnancy., (Copyright © 2014 The Obesity Society.)

Introduction: Leptin (LEP) is mainly produced in adipose tissue and acts in the hypothalamus to regulate energy intake. Mutations in the LEP gene or its receptor (LEPR) that produce monogenic obesity are infrequent. However, LEP and LEPR polymorphisms have been associated with obesity multifactorial, due to the association found with body weight and eating behavior., Aim: Measure the association between LEP and LEPR polymorphisms with childhood obesity and eating behavior., Methods: 221 Chilean obese children (BMI above the 95th percentile) were recruited. Parents of 134 of these children were also recruited to determine the association between LEP and LEPR polymorphisms with obesity in a case study-parent trio. Eating behavior was measured through the questionnaire of three factors progenitors' version (TFEQ-P19) and eating behavior in children (CEBQ)., Results: No significant difference between the studied polymorphisms and childhood obesity, after correction for multiple comparisons, was observed. The dimensions; "Slow eating", "emotional eating", "enjoyment of food" and "uncontrolling eating" were significant associated with certain polymorphisms of LEP and LEPR., Conclusions: There would be an association between polymorphisms of the LEP and LEPR genes with eating behavior in Chilean obese children., (Copyright AULA MEDICA EDICIONES 2014. Published by AULA MEDICA. All rights reserved.)

Obesity is a multifactorial disease, with epigenetic alterations. Have been described modifications in the expression of some microRNAs, and some proteins related to obesity. The objective was to determine and correlate, in obese patients, the gene expression of LEP, LEPR, IGF1, IL10 and of miR-27a, miR-27b, miR-143 and miR-145. RNA was extracted from biopsies of subcutaneous fat, liver and visceral fat of 15 obese subjects submitted to bariatric surgery and of 15 non-obese subjects submitted to cholecystectomy for cDNA synthesis and for RT-PCR. The microRNAs were chosen using the TargetScan software. An increased expression of LEP and IGF1 was detected in the subcutaneous fat of the obese group compared to control, while the expression of IGF1 was higher in the control group than in the obese one. MiRNA-27a had a higher expression in the omentum of the obese patients and there was also a correlation in the expression of miRNA-145 and LEPR in the omentum of this group.

Background: Metabolic Syndrome (MS) is highly prevalent among obese children and adolescents and is considered a predictor for the development of type 2 diabetes mellitus and cardiovascular disease. Obesity is associated with an increase in circulating levels of interleukins 6 (IL6) and 18 (IL18), which in turn would depend on polymorphisms of IL6, IL6R and IL18 genes., Aim: To evaluate the association between genetic polymorphisms of IL6 (rs1800795, rs1800796 and rs1800797), IL6R (rs2228145) and IL18 (rs360719, rs187238 and rs204355) and MS and/or its components in a sample of Chilean obese children., Patients and Methods: These polymorphisms were genotyped in 259 obese children aged 10 ± 2 years with a body mass index of 26.1 ± 4.1 kg/m². Sixty eight had metabolic syndrome (26.3%). The association of their alleles, genotypes and haplotypes with the MS and its components was assessed., Results: IL6, IL6R and IL18 variants showed no association with SM nor with any of the phenotypes that compose it. However, IL18 haplotypes (rs360719-rs187238-rs204355) TCT and CGT were associated with triglycerides ≤ 110 mg/dL and HDL < 40 mg/dL, respectively., Conclusions: IL6 and IL6R variants are not associated with MS or with any of its phenotypes. Although an association between IL18 haplotypes and certain MS component has been detected herein, it is necessary to replicate our findings in independent studies due to the low frequency of these allele combinations detected in our sample.

Metabolic syndrome (MS) related to adult type 2 diabetes mellitus and cardiovascular disease is prevalent among obese children/adolescents. Genetic variants of the leptin-melanocortin system have been associated with components of MS. The aim of our study is to estimate the prevalence of MS (according to Cook's criteria) in a Chilean cross-sectional sample of 259 obese children (47.1% girls, aged 6-12 years), and to assess the association between common genetic variants of leptin-melanocortin pathway genes (LEP, LEPR, POMC, MC3R and MC4R) with components of the MS using logistic regression. We observed an overall MS prevalence of 26.3% (32.2% in girls and 21.1% in boys) in obese Chilean children. No associations were detected between genetic variants of leptin-melanocortin genes and MS components. MS prevalence among our obese children sample is similar to those previously described in Chile, demonstrating the increased risk of diseases in adulthood that obese children carry.

Background: Iron bioavailability in obese subjects after the ingestion of a nutritional supplement was the aim of this work., Methods: Fourteen persons were studied before and after bariatric surgery after the ingestion of a nutritional formulation containing 25 mg iron, 25 g fiber and 800 mg calcium., Results: The following ferremia values (median and minimum--maximum) were obtained before and after bariatric surgery, respectively: Fasting, 105 (70 - 364) μg/dL and 198 (38 - 617) μg/dL; 1 hour, 103 (63 - 305) μg/dL and 160 (11 - 207) μg/dL; 2 hours, 103 (62 - 150) μg/dL and 141 (10 - 412) μg/dL; 3 hours. 97 (63 - 190) μg/dL and 153 (6 - 270) μg/dL; 4 hours, 91 (58 - 163) μg/dL and 156 (40 - 251) μg/dL (p>0.05), with no association of serum iron levels with time. There was a difference in total triglycerides (95 ± 29 mg/dL and 60 ± 10 mg/dL) which were correlated with a decrease in serum ferritin levels (r = 0,926, p = 0.008), UIBC (r = 0.910, p = 0.01), total cholesterol (r = 0,918, p = 0.01) and LDL-c fraction (r = 0.830, p = 0.04), with an increase in HDL-c fraction (r = 0,807, p = 0.05)., Conclusion: Iron bioavailability in obese subjects was affected by the ingestion of the nutritional formulation containing calcium and fiber, a fact that may cause these patients to develop iron deficiency., (Copyright © AULA MEDICA EDICIONES 2013. Published by AULA MEDICA. All rights reserved.)

The adipose tissue expansion is accompanied by remodeling of extracellular matrix performed by matrix metalloproteinases (MMPs). Higher plasma and tissue MMP-9 levels are found in obese; therefore, we evaluated if the functional C(-1562)T polymorphism (rs3918242) located in promoter region of the MMP-9 gene is associated with obesity in women. We studied 112 lean and 114 obese women. Plasma MMP-9 and tissue inhibitor of MMP-9 (TIMP)-1 were measured using enzyme-linked immunosorbent assay. We found different genotype frequencies between lean and obese women (p=0.008), prevailing T-allele in obese (2.3-fold). However, although obese women present higher levels of plasma MMP-9, lack of modulation by the polymorphism was found (all p>0.05). Our findings suggest that C(-1562)T polymorphism may contribute to pathogenetic mechanisms involved in the development of obesity in women.

Objectives: To compare the plasma concentrations of matrix metalloproteinase (MMP)-9, tissue inhibitor of MMP (TIMP)-1, MMP-8, and myeloperoxidase (MPO) for obese and lean women., Design and Methods: We recruited 30 lean and 36 obese women without comorbidities. The MMP-9, TIMP-1, and MMP-8 levels were measured using enzyme-linked immunosorbent assay (ELISA). MPO activity was assessed by a colorimetric assay., Results: Obese women had higher MMP-9 levels and MMP-9:TIMP-1 ratios than lean women. Conversely, the MMP-8 levels and MMP-8:TIMP-1 ratios in the obese women were significantly lower than those in the lean women despite neutrophil activation, which was assessed by MPO activity., Conclusion: We observed that MMP-9 and MMP-8 had distinct profiles, which suggested that these 2 enzymes play different roles in obesity., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Objective: The objective of this study was to determine whether constant daily vitamin supplementation would be sufficient to prevent possible vitamin deficiencies in obese patients undergoing bariatric surgery., Methods: The study was conducted on 58 men and women (mean age 41 ± 10 y) who underwent Roux-en-Y gastric bypass RYGB and were assessed preoperatively and at 3, 6, and 12 mo after surgery. During the postoperative period, the patients received a multivitamin-mineral supplement on a daily basis., Results: Serum β-carotene and vitamin C were lower starting from the third postoperative month and continued to be low after 12 mo, and vitamin A was decreased by the sixth month and increased by 12 mo. Vitamin B12 levels were stable up to 6 mo but were decreased by 12 mo. Folic acid levels increased from the third month and remained higher throughout follow-up. One year after surgery there were 19% and 21% increases in the number of patients with vitamin A and vitamin C deficiency, respectively, and a 4% decreased of patients with folic acid deficiency., Conclusion: Weight loss and improvement in patients' general condition followed surgery, but serum levels of some vitamins were decreased despite the use of a vitamin-mineral supplement. These patients need continuous follow-up and individualized prescription of supplementation after the surgical procedure to prevent and treat vitamin deficiencies., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Background: Inadequate eating behavior and physical inactivity contribute to the current epidemic of childhood obesity. The aim of this study was to assess the association between eating behavior scores and childhood obesity in Chilean children., Design and Methods: We recruited 126 obese, 44 overweight and 124 normal-weight Chilean children (6-12 years-old; both genders) according to the International Obesity Task Force (IOTF) criteria. Eating behavior scores were calculated using the Child Eating Behavior Questionnaire (CEBQ). Factorial analysis in the culturally-adapted questionnaire for Chilean population was used to confirm the original eight-factor structure of CEBQ. The Cronbach's alpha statistic (>0.7 in most subscales) was used to assess internal consistency. Non-parametric methods were used to assess case-control associations., Results: Eating behavior scores were strongly associated with childhood obesity in Chilean children. Childhood obesity was directly associated with high scores in the subscales "enjoyment of food" (P < 0.0001), "emotional overeating" (P < 0.001) and "food responsiveness" (P < 0.0001). Food-avoidant subscales "satiety responsiveness" and "slowness in eating" were inversely associated with childhood obesity (P < 0.001). There was a graded relation between the magnitude of these eating behavior scores across groups of normal-weight, overweight and obesity groups., Conclusion: Our study shows a strong and graded association between specific eating behavior scores and childhood obesity in Chile.

We investigated the impact of obesity on the abnormalities of systolic and diastolic regional left ventricular (LV) function in patients with or without hypertension or hypertrophy, and without heart failure. We studied 120 individuals divided into 6 groups of 20 patients (42 ± 6 years, 60 females) using standard and pulsed-wave tissue Doppler imaging (TDI) echocardiography, and heterogeneity index (HI): nonobese (I: no hypertension, no hypertrophy, control group; II: hypertension, no hypertrophy; III: hypertension and hypertrophy) and obese (IV: no hypertension, no hypertrophy; V: hypertension, no hypertrophy; VI: hypertension and hypertrophy). The criterion for obesity was BMI ≥30 kg/m2, for hypertension was blood pressure ≥ 140/90 mm Hg, for hypertrophy in nonobese was LV mass/body surface area (BSA) >134 g/m(2) (men) and >110 mg/m2 (women), and in obese was LV mass/height(2.7) >50 (men) and >40 (women). Obese groups had normal LV ejection fraction compared with nonobese groups, but decreased longitudinal and radial systolic myocardial peak velocities (S'), and early diastolic myocardial peak velocity (E'). Also, a great variability of E' and late diastolic myocardial peak velocity (A') from the longitudinal basal region was observed in obese groups (E'basal nonobese: 11 ± 7 vs. obese 19 ± 11, P < 0.001, A'basal nonobese: 7 ± 4 vs. obese 11 ± 7, P < 0.001). Our findings were more evident when comparing groups IV with V and VI, with the latter having concentric hypertrophy and obvious segmental systolic and diastolic dysfunctions. Subclinical myocardial alterations and increased variability of the velocities were observed in obese groups, especially with hypertension and hypertrophy, reflecting impaired regional LV relaxation, segmental atrial, and systolic dysfunctions.

Introduction: The melanocortin system plays an important role in energy homeostasis. Mice genetically deficient in the melanocortin-3 receptor gene have a normal body weight with increased body fat, mild hypophagia compared to wild-type mice. In humans, Thr6Lys and Val81Ile variants of the melanocortin-3 receptor gene (MC3R) have been associated with childhood obesity, higher BMI Z-score and elevated body fat percentage compared to non-carriers. The aim of this study is to assess the association in adults between allelic variants of MC3R with weight loss induced by energy-restricted diets., Subjects and Methods: This research is based on the NUGENOB study, a trial conducted to assess weight loss during a 10-week dietary intervention involving two different hypo-energetic (high-fat and low-fat) diets. A total of 760 obese patients were genotyped for 10 single nucleotide polymorphisms covering the single exon of MC3R gene and its flanking regions, including the missense variants Thr6Lys and Val81Ile. Linear mixed models and haplotype-based analysis were carried out to assess the potential association between genetic polymorphisms and differential weight loss, fat mass loss, waist change and resting energy expenditure changes., Results: No differences in drop-out rate were found by MC3R genotypes. The rs6014646 polymorphism was significantly associated with weight loss using co-dominant (p = 0.04) and dominant models (p = 0.03). These p-values were not statistically significant after strict control for multiple testing. Haplotype-based multivariate analysis using permutations showed that rs3827103-rs1543873 (p = 0.06), rs6014646-rs6024730 (p = 0.05) and rs3746619-rs3827103 (p = 0.10) displayed near-statistical significant results in relation to weight loss. No other significant associations or gene*diet interactions were detected for weight loss, fat mass loss, waist change and resting energy expenditure changes., Conclusion: The study provided overall sufficient evidence to support that there is no major effect of genetic variants of MC3R and differential weight loss after a 10-week dietary intervention with hypo-energetic diets in obese Europeans.

Background and Aims: Currently, obesity has become a worldwide health problem affecting even children and yet little is known about its role as a determinant of high blood pressure in this age group. The aim of this epidemiological study was to determine the relationship between the increment of body mass index (BMI) and waist circumference (WC) on systolic blood pressure (SBP) and diastolic blood pressure (DBP) in children and teenagers., Methods: The study was performed in Mexico City schools. Overweight was established if BMI ranged from >or=85(th) to <95(th) percentiles and obesity if BMI was >or=95(th) percentile. WC was classified in two categories, one ranging between the 75(th) and 89.9(th) percentiles and >90(th) percentile. Blood pressure was measured four times during one visit by the auscultatory method. High blood pressure was defined if the levels were >or=90(th) percentile according to the guidelines of the 2004 North American Task Force., Results: Ages of the study population ranged from 5-8 (n = 474), 9-12 (n = 643) and 13-17 (n = 912) years, respectively. The levels of blood pressure and prevalence of high blood pressure were higher in overweight and obese children and adolescents. In both genders, the prevalence of SBP and DBP increased directly correlated with increments in age, BMI and WC, although prevalence and odd ratios of high blood pressure were higher in individuals with increased WC in comparison to BMI., Conclusions: Increases in WC and BMI are parameters directly associated with high blood pressure in children and adolescents.

A number of studies have yielded controversial results on the association between polymorphisms in UCP2 and UCP3 genes with obesity and its comorbidities. The discrepancy among studies might be partially explained by the lack of consideration of the effect of adjacent loci in the same haplotype and the exclusion of key lifestyle factors in the statistical analysis. In this study, we have assessed the association between three genetic variants of the UCP2-UCP3 gene cluster, the -866G/A (rs659366) and the 45bp insertion (in position 173247 of the AC019121) of the UCP2 gene, the -55C/T (rs1800849) polymorphism of the UCP3 gene and their estimated haplotypes with childhood obesity and insulin resistance. This research was designed as a case-control study and information about several environmental parameters such as leisure time physical activity and time spent watching television were included. The study sample consisted in 193 obese children and adolescents (cases) and 170 controls aged 6-18. We found that the individual polymorphisms were not associated with obesity, but the (-866G; rs659366)-(Del; 45bp)-(-55T; rs1800849) haplotype was significantly associated with obesity and its presence in the control group increased about nine times the insulin resistance risk. Thus, the (-866A; rs659366)-(Ins; 45bp)-(-55C; rs1800849) haplotype may protect against insulin resistance in the obese population group.

Objective: To investigate dyspnea in individuals with Class II or III obesity and look for correlations among the respiratory data related to such individuals., Methods: This study involved 49 subjects with a body mass index >35 kg/m(2), divided into two groups (those with dyspnea and those without). The baseline dyspnea index was evaluated, as were spirometry findings, maximal respiratory pressures and arterial blood gas analysis., Results: Of the 49 subjects evaluated, 37 reported dyspnea and 12 reported no dyspnea. The baseline dyspnea index differed between the two groups. The mean values were within the range of normality for all subjects and all parameters, except for the following: ratio of residual volume to total lung capacity; expiratory reserve volume; and the alveolar-arterial oxygen gradient. The subjects with dyspnea presented significantly lower values for expiratory reserve volume, maximal expiratory pressure and arterial pH. In all subjects, body mass index correlated significantly with the following: baseline dyspnea index; the residual volume/total lung capacity ratio; the forced expiratory volume in one second/forced vital capacity ratio; forced expiratory flow between 25% and 75% of forced vital capacity; arterial oxygen tension; the alveolar-arterial oxygen gradient; and arterial carbon dioxide tension. The baseline dyspnea index was found to correlate significantly with the following parameters: residual volume/total lung capacity ratio; expiratory reserve volume; arterial oxygen tension; the alveolar-arterial oxygen gradient; and arterial carbon dioxide tension., Conclusion: Dyspnea is a common complaint in individuals with class II or III obesity. Such individuals present a pronounced reduction in expiratory reserve volume and an increase in the alveolar-arterial oxygen gradient. The correlations found suggest that obese individuals present dysfunction of the lower airways, and that obesity itself plays a role in the genesis of dyspnea.

Purpose: The aim of this review is to update concepts of the nonalcoholic fatty liver disease (NAFLD) and to establish a relationship between this condition and obesity., Methods: By means of a comprehensive literature review where special attention was devoted to articles published in the last 5 years, NAFLD is discussed in view of new concepts, diagnosis, staging, and treatment., Results: NAFLD is emerging as one of the main causes of chronic liver disease and it is believed to be the hepatic component of the metabolic syndrome, whose central features include obesity, hyperinsulinemia, peripheral insulin resistance, diabetes, dyslipidemia, and hypertension. The surgical treatment of morbid obesity is one of the options available for the treatment of NAFLD., Conclusion: Nonalcoholic fatty liver disease is strongly related with obesity.

This review focuses on methodological aspects and main results of different family studies that have been conducted to assess the existence of a genetic contribution in human obesity. A genetic component in the etiology of obesity has been elucidated through specific study designs answering different research questions such as: a) Do obesity aggregate in families? b) Is there a genetic contribution to familial clustering? c) Is it possible to localize chromosomal regions that contain susceptibility genes to obesity? d) Is it possible to estimate the risk for developing obesity depending on the genotype profile in candidate genes? There are sufficient evidences indicating the existence of a moderate familial clustering of obesity defined as body mass index >/=30 with a stronger aggregation with more extreme values of body mass index. Twin studies have demonstrated that the familial aggregation of obesity has a genetic component and is not only due to cultural or environmental factors clustered in families. Linkage studies have identified markers and genes related to obesity in virtually all human chromosomes. However, some of these linkage studies have produced conflicting results. Discordant results are even more pronounced in case-control studies that evaluate the association between alleles at candidate genes and obesity. Topics related to study design will acquire increasing importance in order to avoid methodological problems related to trait definition, sample sizes, population stratification by ethnicity and other confounding factors.

Objective: To establish the frequency of the Trp64Arg polymorphism of the beta3 adrenergic receptor (ADRB3) in women with polycystic ovary syndrome (PCOS) from a Chilean population, focusing particularly on the interaction with body weight. In addition, we evaluated the relationship of the Trp64Arg variant with other metabolic components of this syndrome., Patients and Design: In a case-control design study, a total of 106 women with clinical and hormonal evidence of PCOS and 82 healthy women (HW) were evaluated., Measurements: An oral glucose tolerance test (OGTT) was performed and serum glucose and insulin were measured before the glucose load and 30, 60, 90 and 120 min after. Lipid profile was determined in the basal sample. Insulin resistance was assessed by the homeostatic model assessment (HOMA(IR)) and insulin sensitivity index (ISI) composite. A polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) analysis was performed to determine the Trp64Arg polymorphism of ADRB3., Results: The frequency of the heterozygous condition was similar between PCOS and HW (39%vs. 35%). Only two subjects were homozygous for arginine, both belonging to the PCOS group and having a body mass index (BMI) > 30 kg/m2. In the crude analysis, hypothesis tests and odds ratios show that there is no evidence of association between the ADRB3 Trp64Arg variant and PCOS (P = 0.47). Moreover, when data were stratified by BMI categories, the statistical test for interaction between Trp64 carrier status and obesity was not significant (P = 0.29). This variant was present in 52% of the obese PCOS patients and 40% of the obese HW. In normal weight and obese PCOS carriers, the presence of the Trp64Arg variant was associated with high triglyceride (TG) levels. A major effect of the Trp64Arg variant on insulin resistance parameters could not be demonstrated., Conclusions: The frequency of the Trp64Arg polymorphism was similar in healthy women and PCOS women, and a possible interaction between the effect of this variant and obesity in PCOS could not be demonstrated. However, our results showed an association between triglyceride levels and the presence of this genetic variant in PCOS women.

Objective: To assess the association between the Ala54Thr genetic polymorphism of the fatty acid-binding protein 2 (FABP2) gene with insulin resistance and obesity., Research Methods and Procedures: According to a sampling scheme based on BMI, 33 adult obese women (BMI > or = 30) and 30 adult normal-weight women (BMI > 18.5 and < 25 kg/m(2)) were recruited for this study. Women with chronic inflammatory diseases or acute pathology were excluded. Glucose, insulin, leptin, lipids, and tumor necrosis factor alpha (TNF alpha) were measured in fasting plasma samples. Insulin resistance was estimated through the homeostasis model assessment for insulin resistance method. The Ala54Thr allelic variant was determined by polymerase chain reaction, followed by restriction fragment-length polymorphism analysis., Results: The Thr54 allele was more frequent in obese than in nonobese women (47.0% vs. 31.7; p = 0.08). Among obese women, higher TNF alpha concentrations were found when comparing the Thr54/Thr54 genotype (30.0 +/- 7.1 pg/mL) with either the Ala54/Thr54 genotype (21.2 +/- 8.4 pg/mL) or the Ala54/Ala44 genotype (20.1 +/- 7.0 pg/mL) (p < 0.05). In addition, higher fasting plasma insulin and leptin levels were found among Thr54/Thr54 homozygotes compared with the other genotypes (p < 0.05)., Discussion: Our results suggest that the Ala54Thr polymorphism of the FABP2 gene is associated with obesity and insulin resistance. The effect of this polymorphism might be mediated by elevated production of TNF alpha.

Abstract Background Inadequate eating behavior and physical inactivity contribute to the current epidemic of childhood obesity. The aim of this study was to assess the association between eating behavior scores and childhood obesity in Chilean children. Design and methods We recruited 126 obese, 44 overweight and 124 normal-weight Chilean children (6-12 years-old; both genders) according to the International Obesity Task Force (IOTF) criteria. Eating behavior scores were calculated using the Child Eating Behavior Questionnaire (CEBQ). Factorial analysis in the culturally-adapted questionnaire for Chilean population was used to confirm the original eight-factor structure of CEBQ. The Cronbach's alpha statistic (>0.7 in most subscales) was used to assess internal consistency. Non-parametric methods were used to assess case-control associations. Results Eating behavior scores were strongly associated with childhood obesity in Chilean children. Childhood obesity was directly associated with high scores in the subscales "enjoyment of food" (P < 0.0001), "emotional overeating" (P < 0.001) and "food responsiveness" (P < 0.0001). Food-avoidant subscales "satiety responsiveness" and "slowness in eating" were inversely associated with childhood obesity (P < 0.001). There was a graded relation between the magnitude of these eating behavior scores across groups of normal-weight, overweight and obesity groups. Conclusion Our study shows a strong and graded association between specific eating behavior scores and childhood obesity in Chile.

BackgroundSystemic inflammation may play a role in shaping breast composition, one of the strongest risk factors for breast cancer. Pubertal development presents a critical window of breast tissue susceptibility to exogenous and endogenous factors, including pro-inflammatory markers. However, little is known about the role of systemic inflammation on adolescent breast composition and pubertal development among girls.MethodsWe investigated associations between circulating levels of inflammatory markers (e.g., interleukin-6 (IL-6), tumor necrosis factor receptor 2 (TNFR2), and C-reactive protein (CRP)) at Tanner stages 2 and 4 and breast composition at Tanner stage 4 in a cohort of 397 adolescent girls in Santiago, Chile (Growth and Obesity Cohort Study, 2006-2018). Multivariable linear models were used to examine the association between breast composition and each inflammatory marker, stratifying by Tanner stage at inflammatory marker measurement. Accelerated failure time models were used to evaluate the association between inflammatory markers concentrations at each Tanner stage and time to menarche.ResultsIn age-adjusted linear regression models, a doubling of TNFR2 at Tanner 2 was associated with a 26% (95% CI 7-48%) increase in total breast volume at Tanner 4 and a 22% (95% CI 10-32%) decrease of fibroglandular volume at Tanner 4. In multivariable models further adjusted for body fatness and other covariates, these associations were attenuated to the null. The time to menarche was 3% (95% CI 1-5%) shorter among those in the highest quartile of IL-6 at Tanner 2 relative to those in the lowest quartile in fully adjusted models. Compared to those in the lowest quartile of CRP at Tanner 4, those in the highest quartile experienced 2% (95% CI 0-3%) longer time to menarche in multivariable models.ConclusionsSystemic inflammation during puberty was not associated with breast volume or breast density at the conclusion of breast development among pubertal girls after adjusting for body fatness; however, these circulating inflammation biomarkers, specifically CRP and IL-6, may affect the timing of menarche onset.

BackgroundEstrogen receptor-α (ER-α) is a transcriptional regulator, which mediates estrogen-dependent breast development, as well as breast tumorigenesis. The influence of epigenetic regulation of ER-α on adolescent breast composition has not been previously studied and could serve as a marker of pubertal health and susceptibility to breast cancer. We investigated the association between ER-α DNA methylation in leukocytes and breast composition in adolescent Chilean girls enrolled in the Growth and Obesity Cohort Study (GOCS) in Santiago, Chile. Breast composition (total breast volume (BV; cm3), fibroglandular volume (FGV; cm3), and percent fibroglandular volume (%FGV)) was measured at breast Tanner stage 4 (B4). ER-α promoter DNA methylation was assessed by pyrosequencing in blood samples collected at breast Tanner stages 2 (B2; n = 256) and B4 (n = 338).ResultsAfter adjusting for fat percentage at breast density measurement, ER-α methylation at B2, and cellular heterogeneity, we observed an inverse association between B4 average ER-α DNA methylation and BV and FGV. Geometric mean BV was 15% lower (95% CI: - 28%, - 1%) among girls in the highest quartile of B4 ER-α methylation (6.96-23.60%) relative to the lowest (0.78-3.37%). Similarly, FGV was 19% lower (95% CI: - 33%, - 2%) among girls in the highest quartile of B4 ER-α methylation relative to the lowest. The association between ER-α methylation and breast composition was not significantly modified by body fat percentage and was not influenced by pubertal timing.ConclusionsThese findings suggest that the methylation profile of ER-α may modulate adolescent response to estrogen and breast composition, which may influence breast cancer risk in adulthood.

Copyright of Journal of Physical Education (24482455) is the property of Universidade Estadual de Maringa and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Brazilian Journal of Kineanthropometry & Human Performance is the property of Brazilian Journal of Kineanthropometry & Human Performance and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Physical Education (24482455) is the property of Universidade Estadual de Maringa and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archivos Latinoamericanos de Nutrición is the property of Sociedad Latinoamericana de Nutricion and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Obesity is a major public health concern nowadays, as the risk of developing cancer and other chronic diseases has increased considerably in this population. Using in vitro tests (Comet Assay and Micronucleus Test), we evaluated whether lymphocytes from obese individuals (BMI: 40-62 kg / m2) are sensitive to genotoxic and cytotoxic damage when exposed to anorexigenics sibutramine, femproporex and phytotherapics Cordia ecalyculata and Echinodorus grandiflorus. We found that both possessed weak genotoxic activity and did not detect cytotoxic activity or interference in the cell division mechanisms of lymphocytes among obese individuals. [ABSTRACT FROM AUTHOR]

Mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) is a mitochondrial-derived peptide that attenuates weight gain and hyperinsulinemia when administered to high fat-fed mice. MOTS-c is therefore a potential regulator of metabolic homeostasis under conditions of high-energy supply. However, the effect of insulin resistance and obesity on plasma MOTS-c concentration in humans is unknown. To gain insight into MOTS-c regulation, we measured plasma MOTS-c concentration and analyzed its relationship with insulin sensitivity surrogates, in lean and obese humans (n=10 per group). Obese individuals had impaired insulin sensitivity as indicated by low Matsuda and high Homeostatic Model Assessment (HOMA) indexes. Although plasma MOTS-c concentration was similar in lean and obese individuals (0.48±0.16 and 0.52±0.15 ng/mL; p=0.60), it was correlated with HOMA (r=0.53; p<0.05) and Matsuda index (r=-0.46; p<0.05). Notably, when the groups were analyzed separately, the associations remained only in lean individuals. We conclude that plasma MOTS-c concentration is unaltered in human obesity. However, MOTS-c associates positively with insulin resistance mostly in lean individuals, indicating that plasma MOTS-c concentration depends on the metabolic status in this population. Such dependence seems altered when obesity settles. The implications of plasma MOTS-c for human metabolic homeostasis deserve future examination. [ABSTRACT FROM AUTHOR]

Background/Aims: To evaluate the association between allelic variants of melanocortin receptors -3 and -4 (MC3R and MC4R, respectively) and leptin receptor (LEPR) genes with body mass index (BMI) and eating behavior. Methods: We selected 344 Chilean adults (57.8% women; age 39.1 ± 6.6 years) with a wide variation in BMI (30.3 ± 6.3 kg/m2). The Three-Factor Eating Questionnaire-R18 that measures uncontrolled eating (UE), emotional eating (EE) and cognitive restraint scores was adapted, validated and assessed for association with BMI. Genotypes were determined by polymerase chain reaction followed by restriction fragment length polymorphism techniques and Taqman assays. Results: Higher EE scores were found in obese vs. non-obese in both men (p = 0.01) and women (p < 0.001). UE scores were significantly associated with BMI only in women (p = 0.002). No significant differences in eating behavior scores or BMI were found by LEPR (rs1137101, rs8179183 and rs1137100 polymorphisms) or MC3R (rs3746619 and rs3827103). Carriers of the C allele for MC4R rs17782313 showed significantly higher scores of UE compared to non-carriers (2.3 ± 0.8 vs. 2.0 ± 0.7; p = 0.02). Additionally, we also report a monogenic case of obesity carrying the pathogenic mutation 449C>T (Thr150Ile) in MC4R gene with no apparent alterations in eating behavior scores. Conclusions: UE scores were higher in C-allele carriers of MC4R-rs17782313 compared to non-carriers. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Resistant hypertension ( RHTN) is a multifactorial and polygenic disease, frequently associated with obesity. Low plasma adiponectin levels, a hormone produced by the adipose tissue, were associated with RHTN. Single nucleotide polymorphisms ( SNPs) -11377C/G (rs266729) and +276G/T (rs1501299) in ADIPOQ (adiponectin gene) were associated with hypertension. This study evaluated the association between two SNPs (-11377C/G and +276G/T) and adiponectin levels in RHTN. This study comprised 109 patients with RHTN genotyped for both polymorphisms. A cross-sectional study was designed to compare features of CC homozygous versus G allele carriers for -11377C/G and GG homozygous versus T allele carriers for +276G/T. Office and ambulatory BP measurements were similar among genotypes subgroups in both SNPs as well as the markers of target organ damage (arterial stiffness, left ventricular mass index and microalbuminuria). Adiponectin concentrations were significantly higher in CC compared to G carrier for -11377C/G ( CC:7.0 (4.0-10.2 ) versus G allele:5.5 (2.5-7.9), p = 0.04) and lower in GG compared to T carrier for +276G/T ( GG:5.3 (2.3-7.7 ) versus T allele:7.1 (3.6-10.5), p = 0.04). Adjusting for systolic ambulatory BP, body mass index, age, gender, race and presence of type 2 diabetes, multiple linear regression analyses revealed that the minor alleles G (β-coefficient= -0.14, SE=0.07, p = 0.03) and T (β-coefficient=0.12, SE=0.06, p = 0.04) were independent predictors of adiponectin. The -11377C/G and +276G/T SNPs in ADIPOQ were associated with adiponectin levels in RHTN individuals. [ABSTRACT FROM AUTHOR]

Obesity is a multifactorial disease, with epigenetic alterations. Have been described modifications in the expression of some microRNAs, and some proteins related to obesity. The objective was to determine and correlate, in obese patients, the gene expression of LEP, LEPR, IGF1, IL10 and of miR-27a, miR-27b, miR-143 and miR-145. RNA was extracted from biopsies of subcutaneous fat, liver and visceral fat of 15 obese subjects submitted to bariatric surgery and of 15 non-obese subjects submitted to cholecystectomy for cDNA synthesis and for RT-PCR. The microRNAs were chosen using the TargetScan software. An increased expression of LEP and IGF1 was detected in the subcutaneous fat of the obese group compared to control, while the expression of IGF1 was higher in the control group than in the obese one. MiRNA-27a had a higher expression in the omentum of the obese patients and there was also a correlation in the expression of miRNA-145 and LEPR in the omentum of this group. [ABSTRACT FROM AUTHOR]

Congenital generalized lipodystrophy (CGL) is a rare autosomal recessive disorder characterized by extreme reduction of white adipose tissue (WAT) mass. CGL type 1 is the most frequent form and is caused by mutations in AGPAT2. Genetic and clinical studies were performed in two affected sisters of a Chilean family. These patients have notoriously dissimilar metabolic abnormalities that correlate with differential levels of circulating leptin and soluble leptin receptor fraction. Sequencing of AGPAT2 exons and exon-intron boundaries revealed two homozygous mutations in both sisters. Missense mutation c.299G>A changes a conserved serine in the acyltransferase NHX4D motif of AGPAT2 (p.Ser100Asn). Intronic c.493-1G>C mutation destroy a conserved splicing site that likely leads to exon 4 skipping and deletion of whole AGPAT2 substrate binding domain. In silico protein modeling provided insights of the mechanisms of lack of catalytic activity owing to both mutations. [ABSTRACT FROM AUTHOR]

Copyright of Revista Brasileira de Prescrição e Fisiologia do Exercício is the property of Instituto Brasileiro de Pesquisa e Ensino em Fisiologia do Exercicio and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Interamericana de Psicología is the property of Sociedad Interamericana de Psicologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: The global mortality caused by cardiovascular disease increases with weight. The Framingham study showed that obesity is a cardiovascular risk factor independent of other risks such as type 2 diabetes mellitus, dyslipidemia and smoking. Moreover, the main problem in the management of weight-loss is its maintenance, if it is achieved. We have designed a study to determine whether a group motivational intervention, together with current clinical practice, is more efficient than the latter alone in the treatment of overweight and obesity, for initial weight loss and essentially to achieve maintenance of the weight achieved; and, secondly, to know if this intervention is more effective for reducing cardiovascular risk factors associated with overweight and obesity. Methods: This 26-month follow up multi-centre trial, will include 1200 overweight/obese patients. Random assignment of the intervention by Basic Health Areas (BHA): two geographically separate groups have been created, one of which receives group motivational intervention (group intervention), delivered by a nurse trained by an expert phsychologist, in 32 group sessions, 1 to 12 fortnightly, and 13 to 32, monthly, on top of their standard program of diet, exercise, and the other (control group), receiving the usual follow up, with regular visits every 3 months. Discussion: By addressing currently unanswered questions regarding the maintenance in weight loss in obesity/ overweight, upon the expected completion of participant follow-up in 2012, the IMOAP trial should document, for the first time, the benefits of a motivational intervention as a treatment tool of weight loss in a primary care setting. Trial Registration: ClinicalTrials.gov Identifier: NCT01006213 [ABSTRACT FROM AUTHOR]

Metabolic-associated fatty liver disease (MAFLD) is the most important cause of liver disease worldwide. It is characterized by the accumulation of fat in the liver and is closely associated with abdominal obesity. In addition, oxidative stress and inflammation are significant features involved in MAFLD. Recently, our group demonstrated that lupin protein hydrolysates (LPHs) had lipid lowering, antioxidant, and anti-inflammatory effects. Sixty male mice fed with a Western diet were intragastrically treated with LPHs (or vehicle) for 12 weeks. Liver and adipose tissue lipid accumulation and hepatic inflammatory and oxidant status were evaluated. A significant decrease in steatosis was observed in LPHs-treated mice, which presented a decreased gene expression of CD36 and LDL-R, crucial markers in MAFLD. In addition, LPHs increased the hepatic total antioxidant capacity and reduced the hepatic inflammatory status. Moreover, LPHs-treated mice showed a significant reduction in abdominal adiposity. This is the first study to show that the supplementation with LPHs markedly ameliorates the generation of the steatotic liver caused by the intake of a Western diet and reduces abdominal obesity in ApoE−/− mice. Future clinical trials should shed light on the effects of LPHs on MAFLD. [ABSTRACT FROM AUTHOR]