Non-celiac gluten sensitivity (NCGS) is a clinical entity characterized by the absence of celiac disease and wheat allergy in patients that trigger reproducible symptomatic responses to gluten-containing foods consumption. Due to the lack of sensitive and reproducible biomarkers for NCGS diagnosis, placebo-controlled gluten challenges must be carried out for its diagnosis. The gluten challenges can be either double- or single-blind, for research or clinical practice purposes, respectively. For improving our understanding about the magnitude and relevance of NCGS in different populations, epidemiological studies based on self-report have been carried out. However, the gluten challenge-based prevalence of NCGS remains to be estimated. Since NCGS was recently recognized as a clinical entity, more studies are needed to delve into NCGS pathogenesis, for instance, the molecular interactions between the suspected cereal grain components that trigger NCGS, such as fermentable oligo-, di-, monosaccharides, and polyols (FODMAPs) and amylase and trypsin inhibitors, and the immune system remains to be elucidated. Although still under debate, NCGS patients can be susceptible to only one or more than one of the NCGS triggers. The treatment of NCGS involves the dietary restriction of the suspected triggers of the disease, but there is controversial data about the effectiveness of different dietary interventions such as the gluten-free diet and low-FODMAP diet. Certainly, our understanding of NCGS is improving quickly due to the constant availability of new scientific information on this topic. Thus, the aim of the present narrative review is to present an up-to-date overview on NCGS from epidemiology to current therapy.

Chickpea (Cicer arietinum L.) peptides have shown in vitro potential to inhibit the angiotensin I-converting enzyme (ACE-I). However, the potential molecular interactions between chickpea peptides (CP) and ACE-I as well as their ADMET (absorption/distribution/metabolism/excretion/toxicity) characteristics remain unknown. Thus, our aim was to study the in silico interactions of CP with ACE-I and the CP ADMET characteristics. Legumin and provicilin sequences were submitted to in silico analysis to search for ACE-I inhibitory peptides. Simulated enzymatic hydrolysis was performed using the BIOPEP-UWM database, and the ACE-I inhibitory peptides generated (EC50 ≤ 200 μM) were selected to perform molecular docking and ADMET analysis. After hydrolysis, 59 out of 381 peptides with ACE-I inhibitory potential were released. Based on A and B parameters, the legumin peptides showed better ACE-I inhibitory potential than the provicilin ones. CP mainly interact with residues from pocket S1 (Ala354/Glu384) and S2 (His353/His513) through hydrogen bonds (distances < 3.0 Å) and hydrophobic interactions (binding energy from −5.7 to −9.2 kcal/mol). Through ADMET analysis, CP showed optimal values for inhibiting ACE-I in vivo. ACE-I inhibitory peptides from legumin and provicilin can bind strongly and tightly to the active site of ACE-I. Further studies to evaluate in vivo the antihypertensive effects of CP are warranted.

The relationship between sleep, glial cells, and the endocannabinoid system represents a multifaceted regulatory network with profound implications for neuroinflammation and cognitive function. The molecular underpinnings of sleep modulation by the endocannabinoid system and its influence on glial cell activity are discussed, shedding light on the reciprocal relationships that govern these processes. Emphasis is placed on understanding the role of glial cells in mediating neuroinflammatory responses and their modulation by sleep patterns. Additionally, this review examines how the endocannabinoid system interfaces with glia-immune signaling to regulate inflammatory cascades within the central nervous system. Notably, the cognitive consequences of disrupted sleep, neuroinflammation, and glial dysfunction are addressed, encompassing implications for neurodegenerative disorders, mood disturbances, and cognitive decline. Insights into the bidirectional modulation of cognitive function by the endocannabinoid system in the context of sleep and glial activity are explored, providing a comprehensive perspective on the potential mechanisms underlying cognitive impairments associated with sleep disturbances. Furthermore, this review examines potential therapeutic avenues targeting the endocannabinoid system to mitigate neuroinflammation, restore glial homeostasis, and normalize sleep patterns. The identification of novel therapeutic targets within this intricate regulatory network holds promise for addressing conditions characterized by disrupted sleep, neuroinflammation, and cognitive dysfunction. This work aims to examine the complexities of neural regulation and identify potential avenues for therapeutic intervention.

Background: Alcalase-treated amaranth proteins generate angiotensin-1-converting enzyme (ACE-1) inhibitory peptides, which could be useful for functional foods development. Our aim was to evaluate the technological, sensory, and antihypertensive properties of pasta enriched with an amaranth hydrolysate. Methods: Pasta with 11% (A; control), 15% (B), and 20% (C) of protein content were formulated. Pastas B and C were supplemented with an alcalase-treated amaranth protein concentrate. Cooking time, cooking lost, color, and texture were assessed. An untrained panel (n = 30) evaluated sensory attributes. The antihypertensive effect was evaluated in hypertensive rats. Results: The hydrolysate IC50 was 0.014 mg/mL. Optimum cooking time and cooking loss decreased in products B and C vs. A (p < 0.05). The L* values decreased in pasta C. Firmness increased in pasta C vs. A (p < 0.05). Adhesiveness was different among groups (p < 0.05). Pasta A had the highest acceptability (p < 0.05). The products B and C, and captopril (positive control) showed antihypertensive properties after 3 h of supplementation (p < 0.05). This effect remained after 7 h, 8 h, or 9 h. Conclusions: The addition of amaranth hydrolysates to pasta negatively impacts on the overall acceptability and, to a lesser extent, on pasta taste. However, it is possible to maintain the antihypertensive properties of the supplemented pasta under physiological conditions.

Gluten-related disorders (GRDs) are increasing around the world, but their magnitude and relevance remain unknown in most Latin American countries. Thus, an online survey was conducted to estimate the prevalence of GRDs as well as adherence to a gluten-free diet (GFD) in Paraguayan adult population. There were 1058 individuals surveyed using a validated questionnaire (response rate of 93.9%). The self-reported prevalence rates were as follows (95% CI): gluten sensitivity (GS), 10.30% (8.53–12.29); non-celiac GS (NCGS), 5.19% (3.94–6.71); physician-diagnosed celiac disease (PD-CD), 3.11% (2.15–4.35); wheat allergy (WA), 2.07% (1.30–3.13); and adherence to GFD, 15.69% (13.55–18.02). Excluding CD, more women than men met the criteria for GRDs, adverse food reactions, and GFD (p < 0.05). Eight respondents reported the coexistence of NCGS with PD-CD and/or WA. Most cases on a GFD indicated medical/dietitian advice for following the diet (68.07%). Non-self-reported GS individuals indicated weight control (46.4%) and the notion that the GFD is healthier (20.2%) as the main motivations for following the diet. GRDs are not uncommon in Paraguayan adult population. It seems that there is awareness about GRDs and the GFD, but training about the diagnosis of GRDs is desirable because of the informed overlapping diagnoses of CD or WA with NCGS. Future studies involving face-to-face interviews are necessary.