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INTRODUÇÃO: O aumento da prevalência de obesidade nos últimos 50 anos coincidiu com o avanço na tecnologia de processamento de alimentos e aumento de venda e consumo de ultraprocessados. Estes alimentos geralmente são densos energeticamente, contêm grande quantidade de açúcar de adição, gordura saturada e sal, além de baixo teor de fibra, proteína, vitaminas e minerais, o que fomentou o desenvolvimento da classificação NOVA, que divide os alimentos de acordo com o grau de processamento em quatro grupos: in natura ou minimamente processado (G1), ingredientes culinários (G2), processados (G3) e ultraprocessados (UP). Diversos estudos populacionais sugerem uma forte associação entre consumo de UP e doenças metabólicas como obesidade e diabetes melitos tipo 2. Estudos recentes indicam que alimentos UP modificam a composição e o metabolismo da microbiota intestinal (MI), que participa ativamente da homeostase energética e da adiposidade do hospedeiro. Entretanto, ainda são escassos os estudos em humanos, e, até o momento, nenhum avaliou as espécies das bactérias intestinais, de acordo com a NOVA. OBJETIVO: Avaliar a relação do consumo alimentar com o perfil metabólico e a MI de mulheres com obesidade, eutrofia e magreza constitucional. MÉTODOS: Essa tese foi composta pela compilação de dois artigos. O primeiro avaliou a associação de espécies da MI produtoras de butirato com parâmetros antropométricos, metabólicos e consumo alimentar. O segundo analisou a MI de acordo com o consumo de UP. A casuística consistiu em 59 mulheres de 18 a 40 anos (20 com obesidade, 20 com eutrofia e 19 com magreza constitucional). Foram avaliados o consumo alimentar (utilizando a classificação NOVA), os parâmetros antropométricos, clínicos e metabólicos e a MI (a partir do DNA bacteriano coletado de amostras fecais). RESULTADOS: Não houve diferença no consumo alimentar entre as mulheres com obesidade, eutrofia e magreza constitucional. A leptina ajustada para massa gorda associou-se positivamente com UP (p=0,049) e negativamente com alimentos in natura e minimamente processados (p=0,037). O consumo de UP e alimentos do G1 foi correlacionado a diferenças na abundância de 9 e 15 espécies, respectivamente. Ao analisar as espécies produtoras de butirato individualmente, Faecalibacterium prausnitzii, Clostridium sp. e Anaerostipes sp. correlacionaram-se a um melhor perfil metabólico, sendo que esta última se correlacionou diretamente com o consumo de alimentos in natura e minimamente processados. Por outro lado, as espécies Coprococcus catus e Coprococcus comes associaram-se a um pior perfil metabólico. CONCLUSÕES: O consumo de alimentos UP foi diretamente associado a resistência à leptina, ao passo que a maior abundância de Anaerostipes sp. se correlacionou com melhor perfil metabólico e maior consumo de alimentos in natura e minimamente processado, sugerindo um efeito protetor relacionado ao consumo de alimentos do G1 em detrimento dos UP INTRODUCTION: The increase in the prevalence of obesity in the last 50 years has overlapped with advances in food processing technology and an increase in sale and consumption of ultra-processed (UP) foods. These foods are generally energy-dense, contain large amounts of sugar, saturated fat and salt, in addition are low in fiber, protein, vitamins and minerals, which led to the development of the NOVA classification, dividing foods according to degree of processing into four groups: in natura or minimally processed (G1), culinary ingredients (G2), processed (G3), and UP. Several population studies suggest a strong association between UP consumption and metabolic diseases such as obesity and type 2 diabetes mellitus. Recent studies indicate that UP foods modify the composition and metabolism of the gut microbiota (GM), which actively participates in energy homeostasis and host adiposity. Studies in humans are still scarce, and, to date, none have evaluated the species of gut bacteria, according to NOVA. OBJECTIVE: To evaluate the relationship between food consumption and metabolic profile and GM of women with obesity, normal weight and constitutional thinness. METHODS: This thesis was composed by the compilation of two articles. The first evaluated the association of butyrate- producing GM species with anthropometric and metabolic parameters, and food consumption. The second analyzed the GM according to UP consumption. The sample consisted of 59 women aged 18 to 40 years (20 with obesity, 20 with normal weight and 19 with constitutional thinness). Food consumption (using the NOVA classification), anthropometric, clinical and metabolic parameters, and GM (from bacterial DNA collected from fecal samples) were evaluated. RESULTS: There was no difference in food consumption between women with obesity, normal weight and constitutional thinness. Leptin adjusted to fat mass was positively associated with UP consumption (p=0.049) and negatively associated with in natura and minimally processed foods (p=0.037). The consumption of UP and G1 food was correlated with differences in the abundance of 9 and 15 species, respectively. When analyzing the butyrate- producing species individually, Faecalibacterium prausnitzii, Clostridium sp and Anaerostipes sp correlated with a better metabolic profile, the latter being directly correlated with the consumption of in natura/minimally processed foods. On the other hand, the species Coprococcus catus and Coprococcus comes were associated with a worse metabolic profile. CONCLUSIONS: The consumption of UP foods was directly associated with leptin resistance, whereas the greater abundance of Anaerostipes sp. correlated with better metabolic profile and higher consumption of in natura and minimally processed foods, suggesting a protective effect related to the consumption of G1 foods to the detriment of UP foods

Background/Aims: Taste is recognized as an important predictor of food choices. Thus, polymorphisms in genes encoding taste receptors may explain the variability in food preference and intake. Here, we aimed to determine whether genetic variation in the CD36 gene affects food intake and risk of obesity. Methods: A cross-sectional study was conducted with obese Brazilian children and adolescents (n = 466; BMI-for-age z-score [zBMI] 3.29 ± 0.61) and normal-weight children (n = 114; zBMI -0.11 ± 0.7). To assess the obesity risk according to genotypes, a logistic regression adjusted for age and gender was performed. Two 24-h food recalls assessed total energy (kcal/day) and macronutrient (% kcal and g/day) intake, consumption of sweet and fatty tasting foods (portion and g/day), as well as the most commonly consumed foods (mL or g/day). The food portion sizes were measured according to Brazilian guidelines. The genetic variant rs1761667 (A/G) in CD36 was genotyped by real-time PCR. Results: We found no relationship between rs1761667 genotypes and obesity risk. A significant genetic association between CD36 genotype and fat intake was observed for the A allele of rs1761667, which was associated with a decreased intake of total fat (g/day) (p = 0.01), polyunsaturated and monounsaturated fatty acids (% kcal and g/day), total sugars (g/day) (p = 0.01), fatty foods (portion and g/day) (p < 0.001 for both), and vegetable oils (mL/day) (p = 0.02) only in obese subjects. No differences were found between normal-weight children. Conclusion: The A allele of the rs1761667 single nucleotide polymorphism in CD36 is associated with decreased fat and sugar intake in obese children and adolescents.

Polymorphisms near the MC4R gene may be related to an increased risk for obesity, but studies of variations in this gene and its relation to cardiometabolic profiles and food intake are scarce and controversial. The aim of this study is to evaluate the influence of the variants rs12970134 and rs17782313 near the MC4R gene in food intake, binge eating (BE) behavior, anthropometric parameters, body composition, metabolic profile, and cardiometabolic risk factors in obese children and adolescents. This is a cross-sectional study that included obese children and adolescents. We evaluated anthropometric, metabolic parameters and cardiometabolic risk factors, including hypertension, impaired fasting glucose, hypertriglyceridemia, and low HDL-cholesterol. BE was assessed through the BE scale, and a 24-h recall was used to evaluate total caloric intake and percentage of macronutrients and types of dietary fat. The MC4R variants rs12970134 and rs17782313 were genotyped using TaqMan assay. To assess the magnitude of risk, a logistic regression adjusted for Z-BMI, age, and gender was performed, adopting the significance level of 0.05. The study included 518 subjects (52.1 % girls, 12.7 ± 2.7 years old, Z-BMI = 3.24 ± 0.57). Carriers of the variant rs17782313 exhibit increased triglyceride levels (108 ± 48 vs. 119 ± 54, p = 0.034) and an increased risk of hypertriglyceridemia (OR 1.985, 95 % CI 1.288-3.057, p = 0.002). There was no association of the SNP rs12970134 with clinical, metabolic, or nutritional parameters. The variant rs12970134 and rs17782313 did not influence food intake or the presence of BE. The variant rs17782313 is associated with an increased risk of hypertriglyceridemia in obese children and adolescents.

OBJECTIVE: To analyze the LEPR gene in obese children and to investigate the associations between molecular findings and anthropometric and metabolic features. SUBJECTS AND METHODS: Thirty-two patients were evaluated regarding anthropometric characteristics, blood pressure, heart rate, serum glucose, insulin, leptin levels, and lipid profile. The molecular study consisted of the amplification and automatic sequencing of the coding region of LEPR in order to investigate new mutations. RESULTS: We identified a high prevalence of metabolic disorders: impaired fasting glucose in 12.5% of the patients, elevated HOMA-IR in 85.7%, low HDL-cholesterol levels in 46.9%, high triglyceride levels in 40.6%, and hypertension in 58.6% of the patients. The molecular study identified 6 already described allelic variants: rs1137100 (exon-2), rs1137101 (exon-4), rs1805134 (exon-7), rs8179183 (exon-12), rs1805096 (exon-18), and the deletion/insertion of the pentanucleotide CTTTA at 3'untranslated region. CONCLUSIONS: The frequency of alleles observed in this cohort is similar to that described in the literature, and was not correlated with any clinical feature. The molecular findings in the analysis of the LEPR did not seem to be implicated in the etiology of obesity in these patients. OBJETIVO: Analisar o LEPR em crianças obesas e investigar associações entre achados moleculares e características antropométricas e metabólicas. SUJEITOS E MÉTODOS: Foram avaliados 32 pacientes quanto às características antropométricas, à pressão arterial, à frequência cardíaca, às dosagens séricas de glicemia, à insulina, à leptina e ao perfil lipídico. O estudo molecular consistiu na amplificação e no sequenciamento automático da região codificadora do LEPR para pesquisar mutações. RESULTADOS: Identificou-se uma alta prevalência de distúrbios metabólicos: glicemia de jejum alterada em 12,5%, HOMA-IR elevado em 85,7%, níveis de HDL-colesterol baixos em 46,9%, níveis de triglicérides elevados em 40,6% e hipertensão arterial em 58,6%. O estudo molecular identificou 6 variações alélicas já descritas na literatura: rs1137100 (éxon-2), rs1137101 (éxon-4), rs1805134 (éxon-7), rs8179183 (éxon-12), rs1805096 (éxon-18) e deleção/inserção do pentanucleotídeo CTTTA na região 3' não traduzida. CONCLUSÕES: A frequência das variações alélicas observada é semelhante à descrita na literatura e não se correlacionou com nenhuma característica clínica. Os resultados da análise molecular do LEPR não parecem estar implicados na etiologia da obesidade desses pacientes.

INTRODUÇÃO: O aumento mundial da prevalência de obesidade atribui-se principalmente a mudanças nos hábitos alimentares e na prática de atividade física, que afetam indivíduos predispostos geneticamente. Alterações genéticas podem provocar desequilíbrio na regulação homeostática afetando sinalizadores periféricos e centrais. Um componente do controle central fica no núcleo arqueado hipotalâmico, sendo o receptor tipo 4 de melanocortina (MC4R) de suma importância. Mutações no MC4R têm sido relatadas como causa mais frequente de obesidade monogênica. Há evidência de que polimorfismos de nucleotídeo único (SNP) localizados próximos ao MC4R possam estar relacionados ao aumento do risco para obesidade, porém estudos de variantes nesse gene avaliando o consumo alimentar são escassos e controversos. OBJETIVO: Avaliar a influência de variantes alélicas no MC4R sobre consumo alimentar, presença de compulsão alimentar periódica (CAP), composição corporal e perfil clínico e metabólico em crianças e adolescentes obesos. MÉTODOS: Trata-se de um estudo transversal realizado com crianças e adolescentes obesos. Foram avaliados parâmetros antropométricos, metabólicos e fatores de risco cardiometabólicos, incluindo hipertensão arterial sistêmica, glicemia de jejum alterada, hipertrigliceridemia e HDL-colesterol baixo. A CAP foi avaliada utilizando a Escala de Compulsão Alimentar Periódica e o consumo alimentar por meio do Recordatório de 24 horas, analisando consumo calórico total, percentual de macronutrientes e fibras, além da frequência na omissão do café da manhã, adequação de macronutrientes, frações lipídicas e colesterol. Para verificar o efeito dos SNPs no risco para a obesidade foi incluído um grupo controle composto por 137 crianças e adolescentes eutróficos. Foi realizado o sequenciamento do gene MC4R e a genotipagem por PCR em tempo real das variantes rs17782313 e rs12970134, adotando-se o modelo recessivo para a análise. A análise estatística para comparação dos grupos foi conduzida por meio dos Testes T de Student ou Mann-Whitney U. Para avaliar a magnitude do risco, foi realizada regressão logística ajustada para Z-IMC, idade e gênero, com o nível de significância fixado em 0,05. RESULTADOS: Foram incluídos no estudo 536 obesos (52,1% meninas; 12,7 ± 2,7 anos; Z-IMC 3,24 ± 0,57). A frequência dos SNPs foi semelhante entre os grupos de obesos e controle. Os portadores do polimorfismo rs17782313 apresentaram maior nível de triglicérides (108 ± 48 vs.119 ± 54, p=0,034)e maior risco para hipertrigliceridemia (OR=1,985; IC95% 1,288-3,057; p=0,002). Não houve associação do rs12970134 com os parâmetros clínicos, metabólicos ou alimentares. No gene MC4R foram identificados 10 polimorfismos já descritos e uma variante nova, Asn72Ser (A/G), sendo 8 mutações do tipo missense e 3 sinônimas. CONCLUSÕES: Os SNPs rs17782313 e rs12970134 não influenciam o consumo alimentar nem a presença da CAP. O SNP rs17782313 está associado a maior risco de hipertrigliceridemia e maior nível sérico de triglicérides em crianças e adolescentes obesos. A presença de mutações que resultem na perda de função no gene MC4R é rara nessa coorte INTRODUCTION: The global increase in the prevalence of obesity is attributed mainly to changes in dietary habits and physical activity, which affects genetically predisposed individuals. Genetic alterations can cause imbalance in the homeostatic regulation affecting peripheral and central signals. One component of the central control is the arcuate nucleus of the hypothalamus, and the melanocortin type 4 receptor (MC4R) is of outstanding importance. Mutations in MC4R have been reported as the most frequent cause of monogenic obesity. Studies indicate that polymorphisms located near the MC4R may be related to increased risk for obesity, but the studies of variations in this gene and its relation to food intake are scarce and controversial. OBJECTIVE: To evaluate the influence of allelic variants of MC4R in food intake, binge eating behavior (BE), body composition, clinical and metabolic profile in obese children and adolescents. METHODS: This is a cross-sectional study with obese children and adolescents. Anthropometric, metabolic parameters and cardiometabolic risk factors including hypertension, impaired fasting glucose, hypertriglyceridemia and low HDL-cholesterol were evaluated. The BE was evaluated through the Binge Eating Scale, and to analyze the dietary intake 24 hour recall was used, evaluating total caloric intake, percentage of macronutrients, fiber, omission of breakfast, adequacy of macronutrients, lipid fractions and cholesterol. To investigate the effect of SNPs on obesity risk, a control group of 137 eutrophic children and adolescents was enrolled. The MC4R gene was sequenced and genotyping was performed by real-time PCR of the variants rs17782313 and rs12970134, adopting the recessive model for the analysis. Statistical analysis for group comparison was conducted using the Student T test or Mann-Whitney U test. To assess the magnitude of risk, logistic regression adjusted for Z-BMI, age and gender was performed, with the significance level of 0.05. RESULTS: The study included 536 subjects (52.1% girls, 12.7 ± 2.7 years-old, Z-BMI = 3.24± 0,57). The frequency of SNPs was similar between the obese and control groups. The C allele carriers for the rs17782313 polymorphism had increased triglyceride levels (108 ± 48 vs.119 ± 54, p = 0.034) and increased risk of hypertriglyceridemia (OR = 1.985, 95% CI 1.288-3.057, p = 0.002). There was no association of the SNP rs12970134 with clinical, metabolic or nutritional parameters. Ten polymorphisms already described and a new variant, Arn72Ser (A/G), were identified in the MC4R gene, with 8 missense mutations and 3 synonymous. CONCLUSIONS: The SNPs rs17782313 and rs12970134 did not influence food intake or the presence of BE. The SNP rs17782313 is associated with increased risk of elevated triglycerides and higher serum triglyceride levels in obese children and adolescents. The presence of mutations resulting in loss of function in the MC4R gene is rare in this cohort

The aim of this study is to compare the weight loss of obese adolescents on two different low-calorie diets: fixed diet plan and calorie-counting diet. This is a randomized clinical study with 66 obese adolescents (body mass index Z score (ZBMI)>+3, 13.7±0.7 years, 60.6% male) with anthropometric, food intake, physical activity, laboratory, body composition and stage of pubertal development data evaluated. There was a reduction in the ZBMI in both groups (P