Ghrelin and eating disorders

Background Ghrelin is a potent hormone with central and peripheral action. This hormone plays an important role in the regulation of appetite, food intake, and energy balance. Studies have suggested that ghrelin is involved with eating disorders (ED), particularly bingeing and purging. Genetic variants have also been studied to explain changes in eating behavior. Methods We conducted a literature review; we searched PubMed, Scientific Electronic Library Online (SciELO), and LILACS databases using the keywords “eating disorder”, “ghrelin”, “polymorphism”, “anorexia nervosa”, “bulimia nervosa”, “binge eating disorder”, and their combinations. We found 319 articles. Thirty-nine articles met the inclusion criteria. Results High levels of ghrelin were found in patients with anorexia nervosa (AN), especially in the purging subtype (AN-P). There was also a positive correlation between fasting ghrelin level and frequency of episodes of bingeing/purging in bulimia nervosa (BN) and the frequency of bingeing in periodic binge eating disorder (BED). Some polymorphisms were associated with AN and BN. Conclusion Changes in ghrelin levels and its polymorphism may be involved in the pathogenesis of EDs; however, further studies should be conducted to clarify the associations

Effects of Perilipin1 (PLIN1) gene variation on metabolic syndrome risk and weight loss in obese children and adolescents

Introdução: Perilipina, a proteína mais abundante no adipócito, tem um papel importante na regulação da lipólise intracelular. Polimorfismos genéticos no lócus da perilipina1 (PLIN1) foram estudados e associados à obesidade e aos riscos de alterações dos fatores da síndrome metabólica (SM) em populações diferentes. Objetivo: Avaliamos crianças e adolescentes obesos (CAO) antes e após tratamento multidisciplinar com reeducação alimentar e estímulo à prática de atividade física, por um período de 20 semanas. Estudamos a associação entre SNPs (Polimorfismos de um Único Nucleotídeo) e dados antropométricos e metabólicos, como também a resposta à perda de peso após a intervenção. Metodologia: Foram avaliados 234 CAO (idade 10,6±1,3 anos) (IMC 30,4±4,5 kg/m2; ZIMC 2,31±0,28). As genotipagens dos SNPs PLIN1* 6209T>C, PLIN4* 11482G>A e PLIN6* 14995A>T foram realizadas através de PCR em Tempo Real. A ingestão alimentar foi calculada pelo método de registro da ingestão de três dias. O SM foi avaliado pelos critérios do IDF. Resultados: As freqüências dos alelos PLIN1*, 0,48; PLIN4*, 0,30 e PLIN6*, 0,26 foram semelhantes às outras populações; PLIN1* e PLIN4* mostraram um desequilíbrio de ligação (DL) (D=0,999, r=0,67). Antes da intervenção, não houve diferenças nas medidas antropométricas, porém a presença do alelo A no PLIN4 foi associada a triglicérides mais elevados (111±49 x 93,9±42,5 mg/dL P= 0,003), HDLC mais baixo (40±9 x 43,6±10mg/dL P=0,003) e HOMA-IR maior (4,0± 2,3 x 3,5±2,1 P=0,015). A presença do alelo A no PLIN4* associou-se a um risco relativo maior de ter SM (ajustado por idade e sexo: 2,4 (95% Intervalo de confiança: 1,1-4,9) para heterozigoto e 3,5 (95% Intervalo de confiança: 1,2-9,9) para homozigoto. Os resultados do PLIN1* foram semelhantes devido ao DL. Após intervenção, a presença do alelo T no PLIN6* foi associada a uma resposta melhor na perda de peso (3,3±3,7 x 1,9±3,5 kg; P=0,002) e uma maior perda de ZIMC (0,23±0,18 x 0,18±0,15; P=0,01). Discussão: Este estudo mostrou a influência da presença do alelo A no PLIN4* sobre o risco de ter SM em crianças e adolescentes obesos similares em termos antropométricos e de ingestão alimentar. Foi mostrado também que a presença do alelo T no PLIN6* influencia uma melhor resposta de perda de peso durante intervenção multidisciplinar. Conclusões: Os resultados sugerem que os polimorfismos da Perilipina têm influência nas co-morbidades associadas à obesidade e podem ajudar nas estratégias aplicadas no tratamento multidisciplinar em crianças e adolescentes obesosIntroduction: Genetic polymorphisms at the perilipin1 (PLIN1) locus have been investigated for their potential utility as markers for obesity and metabolic syndrome (MS). We examined in obese children and adolescents (OCA) aged 714 yr the association of single-nucleotide polymorphisms (SNP) at the PLIN1 locus with anthropometric, metabolic traits, and weight loss after 20-wk multidisciplinary behavioral and nutritional treatment without medication. Design: A total of 234 OCA (body mass index (BMI) = 30.4 ± 4.5 kg/m2; BMI Z-score = 2.31 ± 0.28) were evaluated at baseline and after intervention. We genotyped four SNPs (PLIN1* 6209T>C, PLIN4* 11482G>A and PLIN6* 14995A>T). Results: Allele frequencies were similar to other populations, PLIN1* and PLIN4* were in linkage disequilibrium (D´= 0.999; P=0.001). At baseline, no anthropometric differences were observed, but minor allele A at PLIN4* was associated with higher triglycerides (111 ± 49 vs. 94 ± 42 mg/dl; P = 0.003), lower high-density lipoprotein cholesterol (40 ± 9 vs. 44 ± 10 mg/dl; P = 0.003) and higher homeostasis model assessment for insulin resistance (4.0±2.3 vs. 3.5±2.1; P=0.015). Minor allele A at PLIN4*was associated with MS risk (age and sex adjusted) hazard ratio 2.4 (95% confidence interval = 1.1 4.9) for genotype GA and 3.5 (95% confidence interval = 1.29.9) for AA. After intervention, subjects carrying minor allele T at PLIN6* had increased weight loss (3.3±3.7 vs. 1.9±3.4 kg; P=0.002) and increased loss of the BMI Z-score (0.23±0.18 vs. 0.18±0.15; P=0.01). Due to group size, risk of by-chance findings cannot be excluded. Conclusion: The minor A allele at PLIN4* was associated with higher risk of MS at baseline, whereas the PLIN6* SNP was associated with better weight loss, suggesting that these polymorphisms may predict outcome strategies based on multidisciplinary treatment for OC

Variantes genéticos influenciando a efetividade das estratégias de perda de peso

Body weight excess has an increasingly high prevalence in the world. Obesity is a complex disease of multifactorial origin with a polygenic condition affected by environmental factors. Weight loss is a primary strategy to treat obesity and its morbidities. Weight changes through life depend on the interaction of environmental, behavioral and genetic factors. Interindividual variation of weight loss in response to different types of interventions (behavioral, caloric restriction, exercise, drug or surgery) has been observed. In this article, currently available data on the role of candidate gene polymorphisms in weight loss are reviewed. Even though control of weight loss by genotype was described in twin and family studies, it is premature to recommend use of genotyping in the design of therapeutic diets or drug treatment. Future studies will have to be large in order to assess the effects of multiple polymorphisms, and will have to control factors other than diet.A prevalência do excesso de peso cresce no mundo todo. De origem multifatorial, a obesidade é uma doença complexa, com condição poligênica afetada por fatores ambientais. A perda de peso é a estratégia primária utilizada para prevenir e tratar a obesidade bem como suas comorbidades. Mudanças de peso durante a vida dependem da interação entre fatores ambientais, comportamentais e genéticos. Observa-se grande variação da perda de peso entre indivíduos em resposta a diferentes modelos de intervenções (comportamentais, restrições da ingesta cálorica, exercícios físicos, drogas antiobesidade ou cirurgias). Este artigo é uma revisão atual da literatura disponível, que busca abordar o papel dos polimorfismos dos genes candidatos à obesidade e sua influência na perda de peso. Apesar da interação do genótipo na perda de peso corporal, descrita nos estudos de gêmeos e familiares, é prematuro recomendar o uso da genotipagem para estratégias de perda de peso. É necessário ampliar as pesquisas sobre os efeitos sinérgicos dos polimorfismos genéticos com coorte maior e associá-los não somente à restrição alimentar mas também às outras intervenções que auxiliam na perda de peso

Binge eating symptoms, diet composition and metabolic characteristics of obese children and adolescents

This study aimed to determine the occurrence of symptoms of binge eating (BE) among children and adolescents seeking treatment for their obesity, as well as to evaluate their diet composition and metabolic characteristics. The Binge Eating scale (BES) was answered by 128 children and adolescents (10.77 +/- 2.04 years, BMI 29.15 +/- 4.98 kg/m(2), BMI Z score 2.28 +/- 0.46, 53.91% pubescent), who were classified into two subgroups-binge eaters (score greater than or equal to IS points) and non-binge eaters (score lower than 18 points). Anthropometric data, body composition and Tanner stages were collected and dietary evaluation conducted. Blood pressure was determined, and glucose, lipid profile and insulin assays were performed. insulin resistance was determined using HOMA-IR. BE symptoms were present in 39.06% of patients. Carbohydrate intake in diet composition was significantly higher among binge eaters. Children with BE did not demonstrate significant dissimilar metabolic characteristics when compared to their counterparts without BE. Therefore, BE seems to be a prevalent problem among children and adolescents seeking help for their obesity. When associated with obesity, this eating behaviour can influence macronutrient consumption through increased carbohydrate intake. Further research would be valuable to verify the reproducibility of these findings. (c) 2007 Elsevier Ltd. All rights reserved

Effects of Perilipin (PLIN) Gene Variation on Metabolic Syndrome Risk and Weight Loss in Obese Children and Adolescents

Context: Genetic polymorphisms at the perilipin (PLIN) locus have been investigated for their potential utility as markers for obesity and metabolic syndrome (MS). We examined in obese children and adolescents (OCA) aged 7–14 yr the association of single-nucleotide polymorphisms (SNP) at the PLIN locus with anthropometric, metabolic traits, and weight loss after 20-wk multidisciplinary behavioral and nutritional treatment without medication