Periprandial changes of the sympathetic–parasympathetic balance related to perceived satiety in humans

Food intake regulation involves various central and peripheral mechanisms. In this study the relevance of physiological responses reflecting the autonomic nervous system were evaluated in relation to perceived satiety. Subjects were exposed to a lunch-induced hunger-satiety shift, while profiling diverse sensory, physiological, and biochemical characteristics at 15 min intervals. Sensory ratings comprised questionnaires with visual analogues scales about their feeling of satiety, desire to eat, fullness, and hunger. Physiological characteristics included heart rate, heart rate variability, and blood pressure, while biochemical markers such as cortisol levels and α-amylase activity were monitored in saliva. The four sensory ratings correlated with heart rate and salivary α-amylase suggesting a higher sympathetic tone during satiety. Furthermore, heart rate variability was associated with age and waist-to-hip ratio and cortisol levels negatively correlated with body mass index. Finally, neither chewing nor swallowing contributed to a heart rate increase at food consumption, but orosensory stimulation, as tested with modified sham feeding, caused a partial increase of heart rate. In conclusion, after meal ingestion critical physiological alterations reveal a elevated sympathetic tone, which is a potential measure of satiety

Assessing established BMI variants for a role in nighttime eating behavior in robustly phenotyped Southwestern American Indians

BACKGROUND/OBJECTIVES: Nighttime eating (NE) behavior has a genetic component and predicts weight gain. We hypothesized that some genetic variants, which affect NE would also show an effect on body mass index (BMI). We aimed to determine which known BMI variants associate with NE in Southwestern American Indians (SWAIs), who are at elevated risk for obesity. METHODS: Known BMI variants from the GIANT-UK Biobank meta-analysis (N = 700,000) were analysed in SWAIs characterized for NE during an inpatient 3-day protocol. Variants were analysed for association with NE using whole-genome sequence data from 50 SWAIs (23 cases and 27 controls) and selected variants were genotyped in an additional 32 SWAIs (13 NE cases and 19 controls). Variants associated with NE in a meta-analysis of the two SWAI samples were further analysed for association with nightly caloric intake and functionality in hypothalamus, pituitary, and adrenal tissues. RESULTS: Variants were identified where the allele that associated with increased BMI in the GIANT-UK Biobank meta-analysis (P ≤ 1 × 10-8) also had a P < 0.01 for increased NE in the SWAI meta-analysis. These variants were captured by six tagSNPs. Comparison of the nightly calorie intake by genotype and eQTL data from relevant tissues highlighted rs3753612 upstream of HCRTR1. CONCLUSIONS: Our strategy led to the HCRTR1 locus, which has previously been linked to sleep regulation and feeding. Although this is an intriguing candidate gene for NE, further studies in larger samples and different populations are required to validate the role of HCRTR1 in NE

Síndrome do comer noturno: aspectos conceituais, epidemiológicos, diagnósticos e terapêuticos Night eating syndrome: conceptual, epidemiological, diagnostic and therapeutic aspects

O comportamento e o padrão alimentar são complexos, envolvendo aspectos metabólicos, fisiológicos e ambientais, e apresentando ritmicidade circadiana, herdada e espécie específica, sendo a humana essencialmente diurna. Este estudo tem como objetivo descrever a Síndrome do Comer Noturno, caracterizada por um atraso circadiano do padrão alimentar, mediado por alterações neuroendócrinas ao estresse. Procedeu-se à revisão da bibliografia existente, a partir do exame de artigos publicados pela literatura internacional nas bases de dados dos sites Pubmed, Lilacs, Sirus, referentes ao período de 1955 até as últimas publicações em 2007. Realizou-se um levantamento bibliográfico usando os seguintes descritores: night eating syndrome, sleep, circadian rhythm, appetite, nocturnal eating. Foram localizados 74 artigos e destes foram selecionados 26, cujo tema central era a Síndrome do Comer Noturno. Apesar dos estudos realizados, ainda existe longo percurso a ser percorrido para compreender a gênese da Síndrome do Comer Noturno e as relações intrínsecas desta com outros processos fisiopatogênicos. Tendo em conta que esta síndrome está vinculada ao controle da fome e da saciedade e à dessincronização entre o ritmo alimentar e o ritmo sono/vigília, a compreensão do seu processo gênico poderá demonstrar o impacto da dessincronização dos ritmos circadianos da alimentação no processo saúde-doença, e auxiliar a compreensão de fatores implicados no índice crescente de obesidade da sociedade moderna.<br>Behavior and eating patterns are complex, involve metabolic, physiological and environmental aspects and have inherited and species-specific circadian rhythmicity, with humans being essentially diurnal. The aim of this study is to describe the night eating syndrome, characterized by a delay of the circadian eating patterns and mediated by neuroendocrine stress. A review of the literature found in the Pubmed, Lilacs and Sirus databases published between 1955 and 2007 was done. The keywords used were: night eating syndrome, sleep, circadian rhythm, appetite, nocturnal eating. A total of 74 articles were found of which 26 were selected, whose central theme was the night eating syndrome. Despite all the studies done, there is still long way to go to understand the genesis of the night eating syndrome and its intrinsic relation with other physiological and pathogenic processes. Given that this syndrome is linked to the control of hunger and satiety and to the desynchronization between the eating rhythm and sleep / wake rhythm, understanding its genetic process can reveal the impact that the desynchronization of circadian eating rhythms has on the health-disease process and help understand the factors involved in the rising rates of obesity in modern society