RESUMO

BACKGROUND: Different types of stress inflicted in early stages of life elevate the risk, among adult animals and humans, to develop disturbed emotional-associated behaviors, such as hyperphagia or depression. Early-life stressed (ELS) adults present hyperactivity of the hypothalamus-pituitary-adrenal (HPA) axis, which is a risk factor associated with mood disorders. However, the prevalence of hyperphagia (17%) and depression (50%) is variable among adults that experienced ELS, suggesting that the nature, intensity, and chronicity of the stress determines the specific behavioral alteration that those individuals develop. METHODS: We analyzed corticosterone serum levels, Crh, GR, Crhr1 genes expression in the hypothalamic paraventricular nucleus, amygdala, and hippocampus due to their regulatory role on HPA axis in adult rats that experienced maternal separation (MS) or limited nesting material (LNM) stress; as well as the serotonergic system activity in the same regions given its association with the corticotropin-releasing hormone (CRH) pathway functioning and with the hyperphagia and depression development. RESULTS: Alterations in dams' maternal care provoked an unresponsive or hyper-responsive HPA axis function to an acute stress in MS and LNM adults, respectively. The differential changes in amygdala and hippocampal CRH system seemed compensating alterations to the hypothalamic desensitized glucocorticoids receptor (GR) in MS or hypersensitive in LNM. However, both adult animals developed hyperphagia and depression-like behavior when subjected to the forced-swimming test, which helps to understand that both hypo and hypercortisolemic patients present those disorders. CONCLUSION: Different ELS types induce neuroendocrine, brain CRH and 5-hydroxytriptamine (5-HT) systems' alterations that may interact converging to develop similar maladaptive behaviors.

Assuntos

Hormônio Liberador da Corticotropina , Serotonina , Humanos , Ratos , Animais , Hormônio Liberador da Corticotropina/genética , Hormônio Liberador da Corticotropina/metabolismo , Serotonina/metabolismo , Sistema Hipotálamo-Hipofisário/metabolismo , Depressão/etiologia , Privação Materna , Sistema Hipófise-Suprarrenal/metabolismo , Encéfalo/metabolismo , Hiperfagia/metabolismo , Receptores de Glucocorticoides/genética , Receptores de Glucocorticoides/metabolismo , Estresse Psicológico

RESUMO

Maternal obesity and/or high-fat diet (HF) consumption can disrupt appetite regulation in their offspring, contributing to transgenerational obesity and metabolic diseases. As fatty acids (FAs) play a role in appetite regulation, we investigated the maternal and fetal levels of FAs as potential contributors to programmed hyperphagia observed in the offspring of obese dams. Female mice were fed either a control diet (CT) or HF prior to mating, and fetal and maternal blood and tissues were collected at 19 days of gestation. Elevated levels of linoleic acid were observed in the serum of HF dams as well as in the serum of their fetuses. An increased concentration of eicosadienoic acid was also detected in the hypothalamus of female HF-O fetuses. HF-O male fetuses showed increased hypothalamic neuropeptide Y (Npy) gene expression, while HF-O female fetuses showed decreased hypothalamic pro-opiomelanocortin (POMC) protein content. Both male and female fetuses exhibited reduced hypothalamic neurogenin 3 (NGN-3) gene expression. In vitro experiments confirmed that LA contributed to the decreased gene expression of Pomc and Ngn-3 in neuronal cells. During lactation, HF female offspring consumed more milk and had a higher body weight compared to CT. In summary, this study demonstrated that exposure to HF prior to and during gestation alters the FA composition in maternal serum and fetal serum and hypothalamus, particularly increasing n-6, which may play a role in the switch from POMC to NPY neurons, leading to increased weight gain in the offspring during lactation.

Assuntos

Neuropeptídeos , Obesidade Materna , Efeitos Tardios da Exposição Pré-Natal , Humanos , Feminino , Animais , Masculino , Gravidez , Camundongos , Dieta Hiperlipídica/efeitos adversos , Obesidade Materna/metabolismo , Ácidos Graxos/metabolismo , Pró-Opiomelanocortina/metabolismo , Obesidade/metabolismo , Aumento de Peso , Neuropeptídeos/metabolismo , Hipotálamo/metabolismo , Fenômenos Fisiológicos da Nutrição Materna , Efeitos Tardios da Exposição Pré-Natal/metabolismo

RESUMO

Syndromic obesity refers to obesity occurring with additional clinical findings, such as intellectual disability/developmental delay, dysmorphic features, and congenital malformations. PURPOSE OF REVIEW: To present a narrative review regarding the genetic etiology, clinical description, and molecular diagnosis of syndromic obesity, which is a rare condition with high phenotypic variability and genetic heterogeneity. The following syndromes are presented in this review: Prader-Willi, Bardet-Biedl, Pseudohypoparathyroidism, Alström, Smith-Magenis, Cohen, Temple, 1p36 deletion, 16p11.2 microdeletion, Kleefstra, SIM1-related, Börjeson-Forssman-Lehmann, WAGRO, Carpenter, MORM, and MYT1L-related syndromes. RECENT FINDINGS: There are three main groups of mechanisms for syndromic obesity: imprinting, transcriptional activity regulation, and cellular cilia function. For molecular diagnostic, methods of genome-wide investigation should be prioritized over sequencing of panels of syndromic obesity genes. In addition, we present novel syndromic conditions that need further delineation, but evidences suggest they have a higher frequency of obesity. The etiology of syndromic obesity tends to be linked to disrupted neurodevelopment (central) and is associated with a diversity of genes and biological pathways. In the genetic investigation of individuals with syndromic obesity, the possibility that the etiology of the syndromic condition is independent of obesity should be considered. The accurate genetic diagnosis impacts medical management, treatment, and prognosis, and allows proper genetic counseling.

Assuntos

Obesidade , Humanos , Obesidade/genética , Deficiência Intelectual/genética , Síndrome , Fenótipo , Síndrome de Bardet-Biedl/genética , Síndrome de Prader-Willi/genética , Síndrome de Prader-Willi/diagnóstico , Deficiências do Desenvolvimento/genética , Síndrome de Alstrom/genética

RESUMO

OBJECTIVE: The aim was to investigate the intergenerational inheritance induced by a high-fat diet on sensitivity to insulin and leptin in the hypothalamic control of satiety in second-generation offspring, which were fed a control diet. METHODS: Progenitor rats were fed a high-fat or a control diet for 59 d until weaning. The first-generation and second-generation offspring were fed the control diet until 90 d of age. Body mass and adiposity index of the progenitors fed the high-fat diet and the second-generation offspring from progenitors fed the high-fat diet were evaluated as were the gene expression of DNA methyltransferase 3a, angiotensin-converting enzyme type 2, angiotensin II type 2 receptor, insulin and leptin signaling pathway (insulin receptor, leptin receptor, insulin receptor substrate 2, protein kinase B, signal transducer and transcriptional activator 3, pro-opiomelanocortin, and neuropeptide Agouti-related protein), superoxide dismutase activity, and the concentration of carbonyl protein and satiety-regulating neuropeptides, pro-opiomelanocortin and neuropeptide Agouti-related protein, in the hypothalamus. RESULTS: The progenitor group fed a high-fat diet showed increased insulin resistance and reduced insulin-secreting beta-cell function and reduced food intake, without changes in caloric intake. The second-generation offspring from progenitors fed a high-fat diet, compared with second-generation offspring from progenitors fed a control diet group, had decreased insulin-secreting beta-cell function and increased food and caloric intake, insulin resistance, body mass, and adiposity index. Furthermore, second-generation offspring from progenitors fed a high-fat diet had increased DNA methyltransferase 3a, neuropeptide Agouti-related protein, angiotensin II type 1 receptor, and nicotinamide adenine dinucleotide phosphate oxidase p47phox gene expression, superoxide dismutase activity, and neuropeptide Agouti-related protein concentration in the hypothalamus. In addition, there were reduced in gene expression of the insulin receptor, leptin receptor, insulin receptor substrate 2, pro-opiomelanocortin, angiotensin II type 2 receptor, angiotensin-converting enzyme type 2, and angiotensin-(1-7) receptor and pro-opiomelanocortin concentration in the second-generation offspring from progenitors fed the high-fat diet. CONCLUSIONS: Overall, progenitors fed a high-fat diet induced changes in the hypothalamic control of satiety of the second-generation offspring from progenitors fed the high-fat diet through intergenerational inheritance. These changes led to hyperphagia, alterations in the hypothalamic pathways of insulin, and leptin and adiposity index increase, favoring the occurrence of different cardiometabolic disorders in the second-generation offspring from progenitors fed the high-fat diet fed only with the control diet.

Assuntos

Resistência à Insulina , Neuropeptídeos , Ratos , Animais , Leptina/metabolismo , Insulina/metabolismo , Receptor de Insulina/genética , Receptor de Insulina/metabolismo , Dieta Hiperlipídica/efeitos adversos , Proteína Relacionada com Agouti/metabolismo , Proteínas Substratos do Receptor de Insulina/metabolismo , Receptor Tipo 2 de Angiotensina/metabolismo , Pró-Opiomelanocortina/genética , Pró-Opiomelanocortina/metabolismo , Receptores para Leptina/genética , DNA Metiltransferase 3A , Ratos Sprague-Dawley , Obesidade/genética , Obesidade/metabolismo , Hiperfagia/complicações , Hipotálamo/metabolismo , Neuropeptídeos/metabolismo , Superóxido Dismutase/metabolismo , Angiotensinas/metabolismo

RESUMO

Insulin is a hormone secreted by pancreatic ß cells. The concentration of glucose in circulation is proportional to the secretion of insulin by these cells. In target cells, insulin binds to its receptors and activates phosphatidylinositol-3-kinase/protein kinase B, inducing different mechanisms depending on the cell type. In the liver it activates the synthesis of glycogen, in adipose tissue and muscle it allows the capture of glucose, and in the hypothalamus, it regulates thermogenesis and appetite. Defects in insulin function [insulin resistance (IR)] are related to the development of neurodegenerative diseases in obese people. Furthermore, in obesity and diabetes, its role as an anorexigenic hormone in the hypothalamus is diminished during IR. Therefore, hyperphagia prevails, which aggravates hyper-glycemia and IR further, becoming a vicious circle in which the patient cannot regulate their need to eat. Uncontrolled calorie intake induces an increase in reactive oxygen species, overcoming cellular antioxidant defenses (oxidative stress). Reactive oxygen species activate stress-sensitive kinases, such as c-Jun N-terminal kinase and p38 mitogen-activated protein kinase, that induce phos-phorylation in serine residues in the insulin receptor, which blocks the insulin signaling pathway, continuing the mechanism of IR. The brain and pancreas are organs mainly affected by oxidative stress. The use of drugs that regulate food intake and improve glucose metabolism is the conventional therapy to improve the quality of life of these patients. Currently, the use of antioxidants that regulate oxidative stress has given good results because they reduce oxidative stress and inflammatory processes, and they also have fewer side effects than synthetic drugs.

RESUMO

Introducción: La lipodistrofia congénita de Berardinelli-Seip es un síndrome genético autosómico recesivo, caracterizado por la ausencia generalizada del tejido adiposo, el déficit de leptina y las alteraciones metabólicas incluidas la resistencia a la insulina, la esteatohepatitis y la hipertrigliceridemia. Objetivo: Definir los diferentes espectros clínicos y fisiopatológicos del síndrome y su relación con el fenotipo definiendo las estrategias terapéuticas actuales. Métodos: Se realizó una búsqueda bibliográfica no sistemática en las bases de datos Science Direct, EMBASE, LILACS, Redalyc, SciELO y PubMed. Los criterios de inclusión fueron publicaciones en inglés, portugués o español, en las que el título y las palabras clave, abordaban el tema planteado con una vigencia de 10 años. Se obtuvieron 50 artículos relacionados con el síndrome, de los cuales 30 fueron seleccionados para su revisión. Conclusiones: El diagnóstico de la enfermedad es principalmente clínico. Se establece en presencia de tres criterios mayores o la combinación de dos mayores con dos menores y/o por la identificación de variantes patogénicas por medio del estudio genético y molecular. La dieta y el ejercicio conjuntamente con la administración de la metreleptina son pilares fundamentales en el manejo de estos pacientes. El reconocimiento temprano del síndrome es esencial para prevenir las complicaciones, y brindar asesoría genética y reproductiva a los pacientes y familiares(AU)

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Introduction: Berardinelli-Seip congenital lipodystrophy is an autosomal recessive genetic syndrome, characterized by the general absence of adipose tissue, leptin deficiency and metabolic alterations including insulin resistance, steatohepatitis and hypertriglyceridemia. Objective: To present the different clinical and pathophysiological spectra of the syndrome, its relationship with the phenotype, defining the current therapeutic strategies. Methods: A non-systematic bibliographic search was carried out in Science Direct, EMBASE, LILACS, Redalyc, SciELO and PubMed databases. The inclusion criteria were publications in English, Portuguese and Spanish, in which the title and keywords included information pertinent to the stated objective with a periodicity of 10 years, 50 articles were retrieved, and 30 of them were selected. Conclusions: The diagnosis of the disease is mainly clinical. It is established in the presence of three major criteria or the combination of two major and two minor criteria and/or by the identification of pathogenic variants through genetic and molecular studies. Diet and exercise together with the administration of metreleptin are fundamental pillars in the management of these patients. Early recognition of the syndrome is essential to prevent complications, allowing genetic and reproductive counseling to be provided to patients and their families(AU)

Assuntos

Humanos , Síndrome Metabólica/prevenção & controle , Lipodistrofia Generalizada Congênita/fisiopatologia , Resistência à Insulina , Literatura de Revisão como Assunto , Bases de Dados Bibliográficas , Estratégias de Saúde

RESUMO

Nicotine is an endocrine disruptor and imprinting factor during breastfeeding that can cause food intake imbalance in the adulthood. As nicotine affects the intestinal microbiota, altering the composition of the bacterial communities and short-chain fatty acids (SCFAs) synthesis in a sex-dependent manner, we hypothesized that nicotine could program the gut-brain axis, consequently modifying the eating pattern of adult male and female rats in a model of maternal nicotine exposure (MNE) during breastfeeding. Lactating Wistar rat dams received minipumps that release 6 mg/kg/day of nicotine (MNE group) or saline for 14 days. The progeny received standard diet from weaning until euthanasia (26 weeks of age). We measured: in vivo electrical activity of the vagus nerve; c-Fos expression in the nucleus tractus solitarius, gastrointestinal peptides receptors, intestinal brain-derived neurotrophic factor (BDNF), SCFAs and microbiota. MNE females showed hyperphagia despite normal adiposity, while MNE males had unchanged food intake, despite obesity. Adult MNE offspring showed decreased Bacteroidetes and increased Firmicutes, Actinobacteria and Proteobacteria. MNE females had lower fecal acetate while MNE males showed higher vagus nerve activity. In summary nicotine exposure through the milk induces long-term intestinal dysbiosis, which may affect eating patterns of adult offspring in a sex-dependent manner.

Assuntos

Eixo Encéfalo-Intestino/efeitos dos fármacos , Comportamento Alimentar/fisiologia , Nicotina/toxicidade , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Animais , Disbiose/induzido quimicamente , Disbiose/microbiologia , Feminino , Lactação/fisiologia , Masculino , Gravidez , Ratos , Ratos Wistar

RESUMO

This article aims to understand the hyperphagic experience in the obesity of patients in the French and Brazilian contexts. Using the critical phenomenological method, twenty subjects were interviewed in health services in Paris and in Fortaleza. We note an objectification and expropriation of the body often experienced in the hyperphagic experience in obesity. We highlight the emphasis on health in the French context and on form and aesthetics in the Brazilian context. In Fortaleza, there seems to be a more evidenced discrimination in relation to obesity and a pathological discourse, whereas in Paris this pathologization is viewed from a critical position regarding the treatments. We conclude that the hyperphagic experience in obesity reveals a subject who is often lost in his/her way of being and having a body, and that clinical work must involve the re-appropriation of this body and the recovery of the condition of the autonomous subject.

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Este artigo tem como objetivo compreender a experiência hiperfágica na obesidade de pacientes nos contextos francês e brasileiro. Utilizando o método fenomenológico crítico, 20 sujeitos foram entrevistados em serviços de saúde de Paris e de Fortaleza. São evidenciadas a objetificação e a desapropriação do corpo frequentemente vividas na experiência hiperfágica na obesidade. No contexto francês, destaca-se a ênfase na saúde e, no contexto brasileiro, a forma corporal e a estética. Em Fortaleza parece haver uma discriminação em relação à obesidade mais evidenciada e um discurso em direção à patologização dessa experiência, enquanto que em Paris essa patologização é revestida por uma posição crítica em relação aos tratamentos. Conclui-se que a experiência hiperfágica na obesidade revela um sujeito, muitas vezes, perdido em seu modo de ser e de ter um corpo e que o trabalho clínico deve envolver a reapropriação desse corpo e a recuperação de sua condição de sujeito autônomo.

Assuntos

Psicopatologia , Hiperfagia , Transtornos da Alimentação e da Ingestão de Alimentos

RESUMO

Literature shows that gestational and/or lactational exposure to hypercaloric diets induces long term effects on eating behavior and the involvement of neurochemical mechanisms. We hypothesized that the effects of hypercaloric diets in early development phases can precede an overweight or an obesity status. The aim of the present study was to evaluate the impact of gestational and lactational exposure to cafeteria diet on eating behavior and neurochemical parameters, BDNF signaling, epigenetic and astrocyte marks in the hippocampus and olfactory bulb during the weaning phase. Pregnant female rats were randomized between standard and cafeteria diet, the respective diet was maintained through the lactational period. The framework of feeding pattern, meal, and its microstructure, was observed in postnatal day 20. Exposure to cafeteria diet increased the number of meals, associated with a lower first inter-meal interval and higher consumption in both genders, without any changes in body weight. Diet exposure also reduced the number of grooming, a behavior typically found at the end of meals. Hypercaloric diet exposure reduced BDNF levels in the olfactory bulb and hippocampus from rats of both sexes and increased the content of the TrkB receptor in hippocampi. It was observed an increase in HDAC5 levels, an epigenetic mark. Still, early exposure to the hypercaloric diet reduced hippocampal GFAP and PPARγ levels, without any effect on NeuN content, indicating that alterations in astrocytes can precede those neuronal outcomes. Our results showed that changes in interrelated neurochemical signaling, BDNF, and astrocyte marks, induced by hypercaloric diet in early stages of development may be related to impairment in the temporal distribution of eating pattern and consequent amounts of consumed food during the weaning phase.

Assuntos

Astrócitos/metabolismo , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Dieta , Comportamento Alimentar/fisiologia , Transdução de Sinais/fisiologia , Animais , Ingestão de Energia/fisiologia , Feminino , Proteína Glial Fibrilar Ácida/metabolismo , Masculino , PPAR gama/metabolismo , Gravidez , Ratos , Ratos Wistar , Receptor trkB/metabolismo , Desmame

RESUMO

RESUMO Objetivo Avaliar os tipos de comportamentos alimentares em indivíduos com obesidade e correlacionar com a adesão ao tratamento proposto. Métodos Estudo transversal desenvolvido em instituição de cardiologia em indivíduos com obesidade. Os tipos de comportamentos alimentares foram analisados pela escala The Three Factor Eating Questionnaire - R21 (TFEQ-21) - versão traduzida e adaptada para brasileiros. Nela são abordadas três subescalas: restrição cognitiva (RC), alimentação emocional (AE) e descontrole alimentar (DA). A adesão ao tratamento nutricional foi verificada pelo instrumento desenvolvido pela instituição, baseado nas principais diretrizes de doenças crônicas. Resultados Analisaram-se 100 indivíduos, com maior prevalência do sexo feminino (68%). Em relação à adesão, somente 25% apresentam boa aderência (escore > 60%). Foi possível identificar a relação entre o IMC e a RC; quanto maior o IMC, menor foi a intensidade da RC (p = 0,02). Observou-se correlação positiva entre a RC e adesão ao consumo de gorduras (p = 0,02) e fibra alimentar (p = 0,004). A subescala AE apresentou correlação negativa com a adesão ao consumo de gorduras (p = 0,03) e correlação positiva com a DA (p < 0,01). Conclusões O tipo de comportamento alimentar mais frequente na amostra foi a restrição cognitiva, que não foi correlacionada com o escore total de adesão. A AE foi associada com maior consumo de gorduras, similar ao encontrado em estudos nacionais e internacionais. Nota-se uma lacuna de estudos que relacionam o comportamento alimentar com a adesão ao tratamento nutricional.

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ABSTRACT Objective To analyze the types of eating behavior in individuals with obesity and correlated with adherence to the adopted treatment. Methods Cross-sectional study developed at the institution of cardiology in individuals with obesity. The types of eating behavior were analyzed using the scale The Three-Factor Eating Questionnaire - R21 (TFEQ-21) - translated and adapted for Brazilians. Three subscales are addressed: cognitive restriction (CR), emotional eating (EE), and uncontrolled eating (UE). Adherence to nutritional treatment was verified by the instrument developed by the institution, based on the main guidelines for chronic diseases. Results We analyzed 100 individuals, with a higher prevalence of females (68%). Regarding adherence, only 25% have good adherence (score > 60%). It was possible to identify the relationship between the BMI and the CR, the higher or lower the BMI was the intensity of the CR (p = 0.02) There was a positive correlation between CR and adherence to fat (p = 0.02) and dietary fiber (p = 0.004). The EE subscale showed a negative correlation with adherence to fat consumption (p = 0.03) and a positive correlation with UE (p < 0.01). Conclusions The most frequent type of eating behavior in the sample was cognitive restriction and was not correlated with the total adherence score. AE was associated with greater consumption of fats, like national and international studies. There is a gap in studies that relate to eating behavior with adherence to nutritional treatment.

Assuntos

Hiperfagia , Transtornos da Alimentação e da Ingestão de Alimentos , Comportamento Alimentar , Cooperação e Adesão ao Tratamento , Obesidade

RESUMO

OBJECTIVE: Regulation of food intake and energy balance depends on a group of hypothalamic neurons that release anorexigenic melanocortins encoded by the Pomc gene. Although the physiological importance of central melanocortins is well appreciated, the genetic program that defines the functional identity of melanocortin neurons and assures high levels of hypothalamic Pomc expression is only beginning to be understood. This study assessed whether the transcriptional regulator PRDM12, identified as a highly expressed gene in adult mouse POMC neurons, plays an important role in the identity and function of melanocortin neurons. METHODS: We first determined the cellular distribution of PRDM12 in the developing hypothalamus. Then we studied mutant mice with constitutively inactivated Prdm12 to evaluate possible changes in hypothalamic Pomc expression. In addition, we characterized conditional mutant mice specifically lacking Prdm12 in ISL1-positive or POMC neurons during development. Finally, we measured food intake, body weight progression up to 16 weeks of age, adiposity, and glucose tolerance in adult mice lacking Prdm12 selectively from POMC neurons. RESULTS: PRDM12 co-expressed with POMC in mouse hypothalamic neurons from early development to adulthood. Mice lacking Prdm12 displayed greatly reduced Pomc expression in the developing hypothalamus. Selective ablation of Prdm12 from ISL1 neurons prevented hypothalamic Pomc expression. The conditional ablation of Prdm12 limited to POMC neurons greatly reduced Pomc expression in the developing hypothalamus and in adult mice led to increased food intake, adiposity, and obesity. CONCLUSIONS: Altogether, our results demonstrate that PRDM12 plays an essential role in the early establishment of hypothalamic melanocortin neuron identity and the maintenance of high expression levels of Pomc. Its absence in adult mice greatly impairs Pomc expression and leads to increased food intake, adiposity, and obesity.

Assuntos

Adiposidade , Peso Corporal , Proteínas de Transporte/metabolismo , Ingestão de Alimentos , Hipotálamo/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Pró-Opiomelanocortina/genética , Animais , Proteínas de Transporte/genética , Feminino , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Proteínas do Tecido Nervoso/genética , Gravidez , Pró-Opiomelanocortina/metabolismo

RESUMO

Objective: Evaluate the impact of the cafeteria diet during lactation and/or post-lactation on physiological parameters and anxiety in the offspring of Wistar rats. Methods: Male offspring of Wistar rats (n = 60) were randomized into four groups: Control (C), Lactation Cafeteria (LC), Post-lactation Cafeteria (PC) and Total Cafeteria (TC). Later in adult life the animals were submitted to the behavioral (elevated plus-maze and open field) and biological (body weight, consumption and food preference, glycemia, total cholesterol, LDL cholesterol, HDL cholesterol, VLDL cholesterol, triglycerides, total proteins, urea, creatinine, bilirubin, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, serum protein, and oxidative stress) evaluations. The data were submitted to ANOVA, followed by the Newman-Keuls test (p < 0.05). Results: Animals treated with the cafeteria diet presented greater weight measurements compared to the control group. Triglyceride levels were higher in the PC group than in the other groups. MDA levels were higher in the PC and TC group than CL and C. The animals of the PC and TC groups presented higher levels of anxiety compared to the C and LC groups. No significant differences due to diet were observed in the locomotor and exploratory behaviors. Conclusions: The cafeteria diet ingestion was capable of triggering biological and behavioral alterations in rats.

Assuntos

Ansiedade/metabolismo , Dieta/efeitos adversos , Peroxidação de Lipídeos , Animais , Ansiedade/etiologia , Comportamento Animal , Peso Corporal , Ingestão de Alimentos , Feminino , Preferências Alimentares , Lactação , Masculino , Ratos Wistar

RESUMO

OBJECTIVES: To evaluate salivary biomarkers that elucidate the molecular mechanisms by which in utero opioid exposure exerts sex-specific effects on select hypothalamic and reward genes driving hyperphagia, a hallmark symptom of infants suffering from neonatal opioid withdrawal syndrome (NOWS). STUDY DESIGN: We prospectively collected saliva from 50 newborns born at ≥34 weeks of gestational age with prenatal opioid exposure and 50 sex- and gestational age-matched infants without exposure. Saliva underwent transcriptomic analysis for 4 select genes involved in homeostatic and hedonic feeding regulation (neuropeptide Y2 receptor [NPY2R], proopiomelanocortin [POMC], leptin receptor [LEPR], dopamine type 2 receptor [DRD2]). Normalized gene expression data were stratified based on sex and correlated with feeding volume on day of life 7 and length of stay in infants with NOWS requiring pharmacotherapy. RESULTS: Expression of DRD2, a hedonistic/reward regulator, was significantly higher in male newborns compared with female newborns with NOWS (Δ threshold cycle 10.8 ± 3.8 vs 13.9 ± 3.7, P = .01). In NOWS requiring pharmacotherapy expression of leptin receptor, an appetite suppressor, was higher in male subjects than female subjects (Δ threshold cycle 8.4 ± 2.5 vs 12.4 ± 5.1, P = .05), DRD2 expression significantly correlated with intake volume on day of life 7 (r = 0.58, P = .02), and expression of NPY2R, an appetite regulator, negatively correlated with length of stay (r = -0.24, P = .05). CONCLUSIONS: Prenatal opioid exposure exerts sex-dependent effects on hypothalamic feeding regulatory genes with clinical correlations. Neonatal salivary gene expression analyses may predict hyperphagia, severity of withdrawal state, and length of stay in infants with NOWS.

Assuntos

Analgésicos Opioides/efeitos adversos , Expressão Gênica , Hiperfagia/etiologia , Síndrome de Abstinência Neonatal/genética , Saliva/química , Estudos de Casos e Controles , Feminino , Perfilação da Expressão Gênica , Marcadores Genéticos , Humanos , Recém-Nascido , Masculino , Síndrome de Abstinência Neonatal/complicações , Projetos Piloto , Pró-Opiomelanocortina/genética , Estudos Prospectivos , Receptores de Dopamina D2/genética , Receptores para Leptina/genética , Receptores de Neuropeptídeo Y/genética , Índice de Gravidade de Doença , Fatores Sexuais

RESUMO

Abstract Background: Obesity is a multifactorial disease and a serious public health problem. Some of the associated factors are modifiable and, among them, the diet is highlighted. Objective: To evaluate the association of dietary patterns of schoolchildren with obesity and body adiposity. Methods: A cross-sectional study was carried out with 378 children aged 8 and 9 years, enrolled in urban schools in the city of Viçosa, Minas Gerais, Brazil. A semi-structured questionnaire was applied to the children and their caregivers on sociodemographic characteristics and life habits. Three 24-hour food recalls were used to identify dietary patterns; the Principal Component Analysis was employed. Weight and height were measured for the calculation of the body mass index (BMI) of the children and their mothers, waist circumference and neck circumference. Body composition was also evaluated through dual-energy X-ray absorptiometry (DXA). For all performed tests, the level of significance was set at 5%. Results: Five dietary patterns (DP) were identified: "unhealthy", "snacks", "traditional", "industrialized" and "healthy". There was an association between excess weight (prevalence ratio [PR]: 1.38, 95% confidence interval [95%CI]: 1.02 to 1.87) and body fat (PR: 1.32, 95%CI : 1.07 to 1.64) with industrialized DP. There was an association between excess body fat (PR: 1.31, 95%CI: 1.01 to 1.74) and lower adherence to traditional DP. The other patterns were not associated with obesity and body adiposity. Conclusion: Children with excess weight and body adiposity showed greater adherence to the industrialized DP and lower adherence to the traditional DP. We suggest that early assessments of dietary habits should be undertaken for monitoring and modifying these habits when necessary.

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Resumo Fundamentos: A obesidade é uma doença multifatorial e um grave problema de saúde pública. Alguns dos fatores associados são modificáveis; dentre eles destaca-se a alimentação. Objetivo: Avaliar a associação dos padrões alimentares de escolares com a obesidade e adiposidade corporal. Métodos: Estudo transversal, com 378 crianças de 8 e 9 anos, matriculadas em escolas urbanas no município de Viçosa, Minas Gerais (MG), Brasil. Foi aplicado um questionário semiestruturado com as crianças e seus responsáveis sobre características sociodemográficas e hábitos de vida. Utilizaram-se três recordatórios 24 horas para identificar os padrões alimentares; a Análise de Componentes Principais foi empregada. Foram aferidos peso e estatura para o cálculo do índice de massa corporal (IMC) das crianças e de suas mães, perímetro da cintura e perímetro do pescoço A composição corporal também foi avaliada, por meio de absorciometria por dupla emissão de raios X (DXA, do inglês dual energy X-ray absorptiometry). Para todos os testes realizados, o nível de significância adotado foi de 5%. Resultados: Foram identificados cinco padrões alimentares (PA): "não saudável", "lanche", "tradicional", "industrializado" e "saudável". Houve associação entre o excesso de peso (razão de prevalência [RP]: 1,38; intervalo de confiança de 95% [IC95%]: 1,02 a 1,87) e gordura corporal (RP: 1,32; IC95%: 1,07 a 1,64) com o PA industrializado. Foi encontrada associação entre o excesso de gordura corporal (RP: 1,31; IC95%: 1,01 a 1,74) e a menor adesão ao PA tradicional. Os demais padrões não estiveram associados a obesidade e adiposidade corporal. Conclusão: As crianças com excesso de peso e de adiposidade corporal apresentaram maior adesão ao PA industrializado e menor adesão ao PA tradicional. Sugerimos que avaliações precoces dos hábitos alimentares devam ser realizadas para monitoramento e modificação destes, quando necessário.

Assuntos

Humanos , Masculino , Feminino , Criança , Comportamento Alimentar , Obesidade Infantil/epidemiologia , Fatores Socioeconômicos , População Urbana , Constituição Corporal , Brasil/epidemiologia , Estudos Transversais

RESUMO

RESUMEN El síndrome de Prader-Willi (SPW) es un trastorno genético, que afecta el neurodesarrollo que, a pesar de su baja frecuencia, merece ser considerado como un trastorno de relevancia clínica al ser la causa más frecuente de obesidad de origen genético. Las manifestaciones clínicas que derivan de SPW tienen origen en la desregulación hipotalámica, por lo que al comprender la trascendencia e implicación de ésta se entenderá la amplia gama de manifestaciones que pueden presentarse con severidad variable y cuyas complicaciones a su vez afectan la salud y socialización a largo plazo lo que influye sobre la calidad de vida de los pacientes con SPW. El diagnóstico preciso permite distinguir este síndrome de otros trastornos genéticos y de otras patologías que afectan la función hipotalámica a la vez que posibilita estimar la gravedad de las manifestaciones y el riesgo de repetición en una misma familia. Por ello, esta revisión se presenta con el objetivo de describir las manifestaciones clínicas del síndrome de Prader-Willi que orienten la sospecha clínica, las similitudes que comparte éste con otros trastornos, así como dar a conocer las técnicas de diagnóstico disponibles que favorecen el abordaje de los pacientes y facilitar su manejo integral oportunamente.

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ABSTRACT Prader-Willi syndrome (PWS) is a genetic disorder that affects neurodevelopment, which, despite its low frequency, deserves to be consideredaclinically relevant disorder since it is themost frequent cause of genetically derived obesity. The clinical manifestations that derive from SPW correlate to those from a hypothalamic dysregulation, so that, understanding the importance and implication of the hypothalamic involvement, the wide range of manifestations that can present with variable severity and whose complications in turn affect the health can be understood. and long-term socialization affecting the quality of life of patients with PWS. An accurate diagnosis can discriminate this syndrome from other genetic disorders and from non-genetic pathologies that affect hypothalamic function, while also allowing to estimate the severity in a specific patient and the risk of repetition in other family members. Therefore, the present descriptive review is aimed to describe the clinical manifestations of Prader-Willi syndrome to guide the clinical diagnosis; the signs and symptoms that can differentiate this syndrome from other disorders, as well as presenting a description of the actual diagnostic techniques that can allow a prompt and precise diagnosis, and thus, translate in a comprehensive and timely approach of the patients with PWS.

RESUMO

Introducción: Dentro de la problemática del diagnóstico, tratamiento y pronóstico de patologías en infantes; la pobre educación respecto a cómo se desarrollan y el conocimiento carente en relación a las enfermedades metabólicas, conlleva a este fenómeno, al no ser identificado por padres o tutores del infante, llegando a ser factor de riesgo para el desarrollo de estas enfermedades y sus complicaciones que llegan a ser fatales. Objetivo: Conocer la edad, género y etiología en la cual se presenta mayormente la Diabetes Mellitus Tipo I dentro de la población seleccionada. Identificar los factores predisponentes para su desarrollo, sintomatología inicial y complicaciones más frecuentes. Metodología: Se realizó un estudio descriptivo, de corte transversal, en base a expedientes de pacientes que han sido tratados respecto a esta patología. Se consideró una población total de 51 pacientes con antecedentes de Diabetes Mellitus tipo I tomando muestra de 49 casos. Resultados: El género femenino con 27 casos presentándose con incidencia máxima de 14 años respecto al género masculino con 22 casos con pico de edad a los 16 años. La principal etiología fue autoinmunitario representándose en 79% de los casos. Obesidad presente en el 12%, contrastado con pacientes que no presentaban factor de riesgo (75%). Respecto a síntomas iniciales, la hiperfagia fue la más frecuente, seguido de polidipsia, pérdida de peso y poliuria. La principal complicación fue cetoacidosis con 35% de frecuencia Conclusión: En la población pediátrica con Diabetes Mellitus tipo I en Honduras predomina la etiología autoinmune, desarrollandose mayormente en el género femenino.

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Introduction: Inside the problematic of the diagnosis, treatment and prognosis of infant pathology, the poor education respect to how they develop and the lack of knowledge in relationship to the metabolic diseases, that entrails to this phenomenon, not being identificated by parents nor tutors of the infant, leading up as a risk factor to the development of these diseases and their complications that can be fatal. Objective: Know the age, genre and ethiology in which Diabetes Mellitus Type I is mostly presented inside the selected population. Identify the predisposing factors for its developing, initial symptomatology and most frequent complications. Results: The feminine gender with 27 cases presenting itself with a peak of incidence at 14 years compared with the male gender with 22 cases and a peak of incidence at 16 years. The most frequent etiology in both genre was autoimmune, representing 79% of the cases. Obesity was present in the 12%, in contrast with patients that didn't presented any risk factor (75%). In respect of initial symptoms; hyperphagia was the most frequent, followed up by polydipsia weight loss and polyuria. The principal complication was ketoacidosis with a 35% frequency. Conclusion: In the pediatric population with type I Diabetes Mellitus in Honduras, autoimmune etiology predominates, mostly developing in the feminine genre.

RESUMO

OBJECTIVE: We investigated the effect of intermittent food restriction (IFR) cycles on hypothalamic expression of lipogenic proteins and induction of overeating. METHODS: Female Wistar rats were distributed in three groups: free access to feed (control, C), 2 d feed restriction at 50% of C intake followed by 3 d (restricted 3, R3) or 5 d (restricted 5, R5) ad libitum feeding. After 6 wk, the rats were submitted to euthanasia and collected the hypothalamus and blood. The deposits of retroperitoneal, mesenteric, and gonadal fat were weighed. The expression of the mRNA for sterol regulatory element binding protein (SREBP) 1c and 2 and acetyl-CoA carboxylase in the hypothalamus were determined by real-time polymerase chain reaction, and glucose and triacylglycerol were evaluated by a commercial kit. Body mass and food intake were measured daily. RESULTS: IFR promoted increased expression of SREBP-2 in both treated groups and, in R5, increased expression of SREBP-1c. The serum triacylglycerol, mesenteric deposit, and total fat content were higher in R3. Neither of the treatment intervals altered the expression of the mRNA of acetyl-CoA carboxylase enzyme but induced hyperglycemia and higher food intake immediately after food restriction. CONCLUSION: IFR affected the expression of SREBP-1c in R5 and SREBP-2 in the hypothalamus and caused overeating immediately after fasting in both groups. We suggest that hypothalamic and peripheral alterations, coupled with compulsive eating behavior in the ad libitum period, indicate risks for diabetes mellitus and recovery of body mass after interruption of IFR.

Assuntos

Restrição Calórica/efeitos adversos , Ingestão de Alimentos/genética , Jejum/efeitos adversos , Hiperfagia/metabolismo , Proteínas de Ligação a Elemento Regulador de Esterol/metabolismo , Acetil-CoA Carboxilase/metabolismo , Animais , Feminino , Hiperfagia/etiologia , Hipotálamo/metabolismo , RNA Mensageiro/metabolismo , Ratos , Ratos Wistar

RESUMO

The growth and body composition of Leporinus obtusidens juveniles (32.0 ± 8.0 g; 137.3 ± 11.9 mm) were evaluated under food deprivation followed by refeeding. Fish were stocked in 130-L tanks (15 fish tank-1), maintained at 26.6 ± 0.3 C, and fed commercial feed (42% crude protein). Four feeding regimes (days fed to apparent satiation × days without food) were evaluated: control (144F:0D), 1D (1F:1D), 6D (6F:6D) or 12D (12F:12D). The greatest increase in weight and growth rates was observed in control. Fish in 1D, 6D or 12D grew to 73, 64 and 65% in weight of fish in control treatment, respectively. Total daily food intake was lower in 12D (1.02 ± 0.06 g) compared to control (1.28 ± 0.02 g). Water content of body composition was higher in control, but other parameters were not significantly different. Leporinus obtusidens showed partial compensatory growth, and the pattern of productive performance and final body composition could be adjusted to lipostatic model, since during food deprivation energy reserves are mobilized to maintain metabolism, resulting in weight loss, whereas during refeeding nutrients are used for restoration of energy reserves, slowing growth.

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O crescimento e a composição corporal de juvenis de Leporinus obtusidens (32,0 ± 8,0 g; 137,3 ± 11,9 mm) foram avaliados em condição de privação alimentar seguida por realimentação. Os peixes foram estocados em tanques de 130-L (15 peixes tanque-1), mantidos em 26,6 ± 0,3 C e alimentados com ração comercial (42% de proteína bruta). Quatro regimes de alimentação (dias de alimentação até a saciedade × dias sem alimentação) foram avaliados: controle (144F:0D), 1D (1F:1D), 6D (6F:6D) ou 12D (12F:12D). O maior crescimento em ganho em peso e taxa de crescimento foi no controle. Os peixes dos tratamentos 1D, 6D e 12D cresceram 73, 64 e 65% do peso dos peixes do tratamento controle, respectivamente. O consumo alimentar diário total foi menor em 12D (1,02 ± 0,06 g) quando comparado ao controle (1,28 ± 0,02 g). A umidade da composição corporal dos peixes foi maior no controle, mas os demais parâmetros não foram significativamente diferentes. Leporinus obtusidens apresentou crescimento compensatório parcial, e seu padrão de desempenho produtivo e a composição corporal final poderiam ser ajustados ao modelo lipostático, no qual se prevê que durante a privação alimentar, as reservas energéticas são mobilizadas para a manutenção do metabolismo, resultando em perda de peso, enquanto na realimentação a alocação dos nutrientes é utilizada na restauração das reservas energéticas, diminuindo a velocidade de crescimento.

Assuntos

Animais , Caraciformes/crescimento & desenvolvimento , Caraciformes/fisiologia , Hiperfagia , Jejum/fisiologia

RESUMO

The growth and body composition of Leporinus obtusidens juveniles (32.0 ± 8.0 g; 137.3 ± 11.9 mm) were evaluated under food deprivation followed by refeeding. Fish were stocked in 130-L tanks (15 fish tank-1), maintained at 26.6 ± 0.3 C, and fed commercial feed (42% crude protein). Four feeding regimes (days fed to apparent satiation × days without food) were evaluated: control (144F:0D), 1D (1F:1D), 6D (6F:6D) or 12D (12F:12D). The greatest increase in weight and growth rates was observed in control. Fish in 1D, 6D or 12D grew to 73, 64 and 65% in weight of fish in control treatment, respectively. Total daily food intake was lower in 12D (1.02 ± 0.06 g) compared to control (1.28 ± 0.02 g). Water content of body composition was higher in control, but other parameters were not significantly different. Leporinus obtusidens showed partial compensatory growth, and the pattern of productive performance and final body composition could be adjusted to lipostatic model, since during food deprivation energy reserves are mobilized to maintain metabolism, resulting in weight loss, whereas during refeeding nutrients are used for restoration of energy reserves, slowing growth.(AU)

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O crescimento e a composição corporal de juvenis de Leporinus obtusidens (32,0 ± 8,0 g; 137,3 ± 11,9 mm) foram avaliados em condição de privação alimentar seguida por realimentação. Os peixes foram estocados em tanques de 130-L (15 peixes tanque-1), mantidos em 26,6 ± 0,3 C e alimentados com ração comercial (42% de proteína bruta). Quatro regimes de alimentação (dias de alimentação até a saciedade × dias sem alimentação) foram avaliados: controle (144F:0D), 1D (1F:1D), 6D (6F:6D) ou 12D (12F:12D). O maior crescimento em ganho em peso e taxa de crescimento foi no controle. Os peixes dos tratamentos 1D, 6D e 12D cresceram 73, 64 e 65% do peso dos peixes do tratamento controle, respectivamente. O consumo alimentar diário total foi menor em 12D (1,02 ± 0,06 g) quando comparado ao controle (1,28 ± 0,02 g). A umidade da composição corporal dos peixes foi maior no controle, mas os demais parâmetros não foram significativamente diferentes. Leporinus obtusidens apresentou crescimento compensatório parcial, e seu padrão de desempenho produtivo e a composição corporal final poderiam ser ajustados ao modelo lipostático, no qual se prevê que durante a privação alimentar, as reservas energéticas são mobilizadas para a manutenção do metabolismo, resultando em perda de peso, enquanto na realimentação a alocação dos nutrientes é utilizada na restauração das reservas energéticas, diminuindo a velocidade de crescimento.(AU)

Assuntos

Animais , Caraciformes/crescimento & desenvolvimento , Caraciformes/fisiologia , Jejum/fisiologia , Hiperfagia

RESUMO

We have investigated early programming of body mass in order to understand the multifactorial etiology of obesity. Considering that the renin-angiotensin system (RAS) is expressed and functional in the white adipose tissue (WAT) and modulates its development, we reasoned whether early transitory inhibition of angiotensin-I converting enzyme activity after birth could modify late body mass development. Therefore, newborn Wistar rats were treated with enalapril (10 mg/kg of body mass) or saline, starting at the first day of life until the age of 16 days. Between days ninetieth and hundred and eightieth, a group of these animals received high fat diet (HFD). Molecular, biochemical, histological, and physiological data were collected. Enalapril treated animals presented hyperphagia, overweight, and increased serum level of triglycerides, total cholesterol and leptin, in adult life. Body composition analyses revealed higher fat mass with increased adipocyte size in these animals. Molecular analyses revealed that enalapril treatment increases neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) gene expression in hypothalamus, fatty acid synthase (FAS), and hormone-sensitive lipase (HSL) gene expression in retroperitoneal WAT, and decreases peroxixome proliferators-activated receptor (PPAR)γ, PPARα, uncoupling protein (UCP)2, and UCP3 gene expression in WAT. The results of the current study indicate that enalapril administration during early postnatal development increases body mass, adiposity and serum lipids in adulthood associated with enhanced food intake and decreased metabolic activity in WAT, predisposing to obesity in adulthood.