RESUMEN
Gut microbiota (GM) after bariatric surgery (BS) has been considered as a factor associated with metabolic improvements and weight loss. In this systematic review, we evaluate changes in the GM, characterized by 16S rRNA and metagenomics techniques, in obese adults who received BS. The PubMed, Scopus, Web of Science, and LILACS databases were searched. Two independent reviewers analyzed articles published in the last ten years, using Rayyan QCRI. The initial search resulted in 1275 documents, and 18 clinical trials were included after the exclusion criteria were applied. The predominance of intestinal bacteria phyla varied among studies; however, most of them reported a greater amount of Bacteroidetes (B), Proteobacteria (P), and diversity (D) after BS. Firmicutes (F), B, and the (F/B) ratio was inconsistent, increasing or decreasing after Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG) were conducted, compared to before surgery. There was a reduction in the relative proportion of F. Moreover, a higher proportion of Actinobacteria (A) was observed after RYGB was conducted. However, the same was not identified when SG procedures were applied. Genera abundance and bacteria predominance varied according to the surgical procedure, with limited data regarding the impact on phyla. The present study was approved by PROSPERO, under registration number CRD42020209509.
Asunto(s)
Cirugía Bariátrica , Derivación Gástrica , Microbioma Gastrointestinal , Obesidad Mórbida , Humanos , ARN Ribosómico 16S , Cirugía Bariátrica/métodos , Derivación Gástrica/métodos , Gastrectomía/métodos , Bacterias/genética , Obesidad Mórbida/cirugía , Resultado del TratamientoRESUMEN
Obesity is a multifactorial, complex, and public health problem worldwide. Interaction between genes and environment as associated with diet may predispose an individual to obesity. In this sense, nutrigenetics appears to be a strategy that can improve understanding of the gene-diet interaction. The aim of this literature review was to summarize data from studies of genes involved in the regulation of energy intake (melanocortin 4 receptor [MC4R], fat mass and obesity-associated [FTO], ghrelin [GHRL], leptin [LEP], and cholecystokinin [CCK]) and diet interaction in obesity. The presence of polymorphisms in MC4R, FTO, leptin, and the respective receptor appear to be associated with higher energy and total lipid consumption. Polymorphisms in FTO, leptin, and leptin receptor are also related to increased intake of saturated fatty acids. Individuals with the MC4R, FTO, and ghrelin polymorphisms, who submitted themselves for weight loss intervention, appeared to achieve weight loss similar to individuals without polymorphisms in these genes. Additionally, protein seems to interact with these genes, which increases or decreases appetite, or to drive or lessen body weight recovery. Additionally, polymorphisms in these genes were found to be associated with inappropriate eating behaviors, such as increased consumption of sweets and snacks, consumption of large food portions, desire to eat, and eating associated with emotional issues. Preliminary data has supported the gene-diet interaction in determining weight loss and gain in individuals with polymorphisms in the genes involved in energy intake. Despite the advent of nutrigenetics in obesity, it is still too early to define the dietary management for weight loss based on the presence or absence of obesity polymorphisms.
Asunto(s)
Dioxigenasa FTO Dependiente de Alfa-Cetoglutarato/fisiología , Ingestión de Energía/genética , Leptina/fisiología , Obesidad/genética , Receptor de Melanocortina Tipo 4/fisiología , Receptores de Leptina/fisiología , Conducta Alimentaria/fisiología , Humanos , Nutrigenómica , Polimorfismo de Nucleótido SimpleRESUMEN
Genetic variants associated with dietary intake may be important as factors underlying the development of obesity. We investigated the associations between the obesity candidate genes (fat mass and obesity-associated (FTO), melanocortin-4 receptor (MC4R), leptin (LEP) and leptin receptor) and total energy intake and percentage of energy from macronutrients and ultra-processed foods before and during pregnancy. A sample of 149 pregnant women was followed up in a prospective cohort in Rio de Janeiro, Brazil. A FFQ was administered at 5-13 and 30-36 weeks of gestation. Genotyping was performed using real-time PCR. Associations between polymorphisms and the outcomes were investigated through multiple linear regression and ANCOVA having pre-pregnancy dietary intake as a covariate. The A-allele of FTO-rs9939609 was associated with a -6·5 % (95 % CI -12·3, -0·4) decrease in the percentage of energy from protein and positively associated with the percentage of energy from carbohydrates before pregnancy (ß=2·6; 95 % CI 0·5, 4·8) and with a 13·3 % (95 % CI 0·7, 27·5) increase in the total energy intake during pregnancy. The C-allele of MC4R-rs17782313 was associated with a -7·6 % (95 % CI -13·8, -1·0) decrease in the percentage of energy from protein, and positively associated with the percentage of energy from ultra-processed foods (ß=5·4; 95 % CI 1·1, 9·8) during pregnancy. ANCOVA results revealed changes in dietary intake from pre-pregnancy to pregnancy for FTO-rs9939609 (percentage of energy from ultra-processed foods, P=0·03), MC4R-rs17782313 (total energy intake, P=0·02) and LEP-rs7799039 (total energy intake, P=0·04; percentage of energy from protein, P=0·04). These findings suggest significant associations between FTO-rs9939609, MC4R-rs17782313 and LEP-rs7799039 genes and the components of dietary intake in pregnant women.
Asunto(s)
Dioxigenasa FTO Dependiente de Alfa-Cetoglutarato/genética , Dieta , Leptina/genética , Obesidad/genética , Receptor de Melanocortina Tipo 4/genética , Receptores de Leptina/genética , Adulto , Alelos , Carbohidratos de la Dieta/metabolismo , Femenino , Genotipo , Humanos , Modelos Lineales , Madres , Obesidad/metabolismo , Polimorfismo Genético , Polimorfismo de Nucleótido Simple , Embarazo , Estudios Prospectivos , Reacción en Cadena en Tiempo Real de la Polimerasa , Riesgo , Adulto JovenRESUMEN
BACKGROUND/AIMS: To determine the influence of the Pro12Ala polymorphism of the PPARγ2 gene and the dietary lipid intake on energy metabolism and nutritional outcomes in obese women after an acute fat load or following a low-calorie diet for 10 weeks. METHODS: Sixty obese women (aged 30-46 years) participated in the study and were assigned to 2 groups depending on the genotype: Pro12Pro and Pro12Ala/Ala12Ala carriers. At baseline and after 2 nutritional (short- or long-term) interventions, measurement of anthropometrical and body composition (bioelectrical impedance) variables, dietary assessments, energy metabolism (indirect calorimetry) measurements as well as biochemical and molecular (PPARγ2 genotype) analyses were performed. All women received a high-fat test meal to determine the postprandial metabolism (short term) and an energy-restricted diet for 10 weeks (long term). RESULTS: The frequencies of the Pro12Pro and Pro12Ala/Ala12Ala genotypes were 83.33 and 16.67%, respectively, and reached Hardy-Weinberg equilibrium. Interestingly, the postprandial energy expenditure after the fat load was higher in subjects carrying the Ala allele. At baseline, the habitual monounsaturated fatty acid (MUFA) intake inversely correlated with fat oxidation and body mass index in the obese Pro12Ala/Ala12Ala carriers, while a lower PUFA intake (%) in the long-term trial was associated with an increase in the respiratory quotient only in Ala carriers but not in the Pro12Pro genotyped group. CONCLUSIONS: The Pro12Ala polymorphism in the PPARγ2 gene influenced energy metabolism in the assayed short- and long-term situations since the response to both nutritional interventions differed according to the genotype. The results suggest that fat oxidation and energy expenditure may be lower in Pro12Pro carriers compared to Pro12Ala/Ala12Ala genotypes, while in obese women with Pro12Ala/Ala12Ala polymorphisms in the PPARγ2 gene fat oxidation was negatively correlated with the MUFA and PUFA (%) intake.