Circadian rhythms integrate a finely tuned network of biological processes recurring every 24 h, intricately coordinating the machinery of all cells. This self-regulating system plays a pivotal role in synchronizing physiological and behavioral responses, ensuring an adaptive metabolism within the environmental milieu, including dietary and physical activity habits. The systemic integration of circadian homeostasis involves a balance of biological rhythms, each synchronically linked to the central circadian clock. Central to this orchestration is the temporal dimension of nutrient and food intake, an aspect closely interwoven with the neuroendocrine circuit, gut physiology, and resident microbiota. Indeed, the timing of meals exerts a profound influence on cell cycle regulation through genomic and epigenetic processes, particularly those involving gene expression, DNA methylation and repair, and non-coding RNA activity. These (epi)genomic interactions involve a dynamic interface between circadian rhythms, nutrition, and the gut microbiota, shaping the metabolic and immune landscape of the host. This research endeavors to illustrate the intricate (epi)genetic interplay that modulates the synchronization of circadian rhythms, nutritional signaling, and the gut microbiota, unravelling the repercussions on metabolic health while suggesting the potential benefits of feed circadian realignment as a non-invasive therapeutic strategy for systemic metabolic modulation via gut microbiota. This exploration delves into the interconnections that underscore the significance of temporal eating patterns, offering insights regarding circadian rhythms, gut microbiota, and chrono-nutrition interactions with (epi)genomic phenomena, thereby influencing diverse aspects of metabolic, well-being, and quality of life outcomes.

Gut microbiota encompasses the set of microorganisms that colonize the gastrointestinal tract with mutual relationships that are key for host homeostasis. Increasing evidence supports cross intercommunication between the intestinal microbiome and the eubiosis–dysbiosis binomial, indicating a networking role of gut bacteria as potential metabolic health surrogate markers. The abundance and diversity of the fecal microbial community are already recognized to be associated with several disorders, such as obesity, cardiometabolic events, gastrointestinal alterations, and mental diseases, which suggests that intestinal microbes may be a valuable tool as causal or as consequence biomarkers. In this context, the fecal microbiota could also be used as an adequate and informative proxy of the nutritional composition of the food intake and about the adherence to dietary patterns, such as the Mediterranean or Western diets, by displaying specific fecal microbiome signatures. The aim of this review was to discuss the potential use of gut microbial composition as a putative biomarker of food intake and to screen the sensitivity value of fecal microbiota in the evaluation of dietary interventions as a reliable and precise alternative to subjective questionnaires.

A promising strategy to improve the gut microbiome in hypertension is to target the gut microbiota. This study evaluated the effects of a potential nutraceutical product composed of three strains of Limosilactobacillus (L.) fermentum, quercetin, and resveratrol on the intestinal microbiome of healthy and hypertensive subjects. The nutraceutical product consisting of strains of L. fermentum 139, 263 and 296, fructooligosaccharides (200 mg), quercetin (160 mg), and resveratrol (150 mg) (LfQR) was added to the in vitro fecal fermentation process occurring for 48 h. Fecal samples of healthy and hypertensive subjects were allocated into four groups: (i) healthy controls (CTL); (ii) healthy controls with the addition of LfQR (CTL + LfQR); (iii) hypertensive (HTN) subjects; and (iv) hypertensive subjects with the addition of LfQR (HTN + LfQR). The diversity and composition of the fecal microbiota and the production of microbial metabolites were evaluated. CTL and HTN groups exhibited a distinct gut microbiota composition, as shown by the β-diversity assessment. The addition of the potentially nutraceutical-modulated β-diversity was similar between CTL and HTN groups, suggesting a similar gut microbiome composition after nutraceutical addition. The addition of the nutraceutical product increased the relative abundance of Enterobacteriaceae in the CTL group and that of Lachnospiraceae in the HTN group. The nutraceutical media showed higher levels of sugars (maltose, fructose, and glucose), lactic acid, ethanol, succinic acid, and acetic acid compared to the CTL and HTN media. Although the results are heterogeneous between healthy and hypertensive fermentation media, it was demonstrated that the nutraceutical formulation can modulate the intestinal microbiota and its metabolic activity.

Cerebral palsy (CP) is a non-progressive neurological condition associated with neuroinflammation, motor impairments, and gastrointestinal dysfunction mediated by the gut–brain axis. Preserving the intestinal epithelial barrier integrity may represent a therapeutic strategy, and quercetin is a bioactive compound with potential intestinal protective effects. This study investigated the effects of neonatal quercetin treatment on morphometric parameters, oxidative stress markers, and epithelial barrier gene expression in an experimental CP model. Wistar rats were distributed into four groups according to health status and treatment with a vehicle (V) or quercetin (Q, 10 mg/kg, intraperitoneally): healthy control (CV and CQ) and CP (CPV and CPQ) (n = 10/group). Intestinal morphology, oxidative stress markers, and gene expression (occludin, zonulin, and mucin 2) were evaluated. CP animals showed segment-specific alterations, with structural impairment predominantly in the ileum and increased oxidative damage in the jejunum. Quercetin attenuated oxidative stress markers and modulated antioxidant enzyme activity in CP, increased jejunal tight-junction gene expression in both healthy and CP groups, and enhanced MUC2 expression only in healthy animals, without fully reversing CP-induced morphological changes. In conclusion, neonatal quercetin modulates oxidative stress and epithelial barrier-related gene expression, supporting its potential as an adjuvant strategy for intestinal barrier protection in experimental CP.

Objetivo: Avaliar o consumo de macro e micronutrientes em idosos diabéticos atendidos no Núcleo de Atenção ao Idoso da Universidade Federal de Pernambuco (NAI/UFPE). Métodos: Estudo transversal com idosos saudáveis (n=66) e com diabetes (n=55) do NAI/UFPE. Obteve-se dados de prontuários e/ou questionários de frequência alimentar. Análise dietética realizada através do DietWin Professional 2008 e para estatística utilizou-se teste t-Student, admitindo-se nível de significância para p<0,05. Resultados: Os resultados mostraram a prevalência do sexo feminino em ambos os grupos (73,8% no grupo saudável e 86,6% no grupo de idosos com diabetes), sendo idosos saudáveis com média de idade de 72,5 ± 6,2 anos, e grupo com diabetes com média de idade de 61,8 ± 5,0 anos (p<0,05). O excesso de peso prevaleceu no grupo com diabetes (67%) quando comparado ao grupo saudável (49,2%; p<0,027). A ingestão calórica dos pacientes com diabetes foi maior (1257,94 kcal) em relação aos indivíduos saudáveis (970,81 kcal; p=0,01). O mesmo ocorreu para consumo de sódio (1810,12 mg x 592,92 mg), cálcio (721,44 mg x 286,23 mg), zinco (8,73 mg x 6,26 mg), magnésio (266,22 mg x 128,60 mg), vitamina A (442,35 µg x 131,83 µg) e E (4,59 mg x 1,45 mg) (p<0,01 para todas as variáveis). Por outro lado, observou-se consumo inferior de potássio (1580,83 mg x 2349,23 mg; p<0,01) e proteína (9% x 17%; p<0,01). Conclusão: Foi identificado um padrão alimentar hipercalórico nos idosos com diabetes, acompanhado de excesso de sódio, cálcio, magnésio e zinco, com reduzido consumo proteico e de potássio.

The consumption of a high-fat high-fructose diet partly resemble the western dietary patterns, which is closely associated with excessive body adiposity and metabolic disorders, such as obesity and type 2 diabetes. Moreover, this unhealthy regime produces unfavourable changes on the faecal microbiota, potentially interfering with microorganisms postbiotic function, such as spermidine, a natural polyamine that has been involved in the control of weight gain. The study aimed to analyse the repercussions of spermidine supplementation on somatic measurements, metabolic markers, and the faecal microbiota profile of rats fed a diet rich in fat and fructose. Indeed, Wistar males with oral administration of spermidine (20 mg/kg/day) for 6 weeks were evaluated for food and energy intake, biochemical markers, and faecal microbiota signatures. The daily use of spermidine decreased weight gain (), reduced feed efficiency (), and attenuated visceral fat deposition (), although no effect on energy intake, hepatic weight, triglyceride and glucose index and atherogenic indexes. Similarly, the consumption of spermidine partially restored the presence of microbial species, notably Akkermansia muciniphila. Elevated concentrations of this species were linked to a decrease in triglycerides (), indicating that the supplementation of spermidine might contribute to managing energy fuel homeostasis in association with an obesogenic diet.