Sucralose consumption alters microbiome and carbohydrate metabolism in mouse models. However, there are no conclusive studies in humans. Our goals were to examine the effect of sucralose consumption on the intestinal abundance of bacterial species belonging to Actinobacteria, Bacteroidetes, and Firmicutes and explore potential associations between microbiome profiles and glucose and insulin blood levels in healthy young adults. In this open-label clinical trial, volunteers randomly drank water, as a control (n = 20), or 48 mg sucralose (n = 20), every day for ten weeks. At the beginning and the end of the study, participants were subjected to an oral glucose tolerance test (OGTT) to measure serum glucose and insulin every 15 min for 3 h and provided fecal samples to assess gut microbiota using a quantitative polymerase chain reaction. Sucralose intake altered the abundance of Firmicutes without affecting Actinobacteria or Bacteroidetes. Two-way ANOVA revealed that volunteers drinking sucralose for ten weeks showed a 3-fold increase in Blautia coccoides and a 0.66-fold decrease in Lactobacillus acidophilus compared to the controls. Sucralose consumption increased serum insulin and the area under the glucose curve compared to water. Long-term sucralose ingestion induces gut dysbiosis associated with altered insulin and glucose levels during an OGTT.

Background: Non-nutritive sweeteners (NNS) are widely consumed by humans due to their apparent innocuity, especially sucralose. However, several studies link sucralose consumption to weight gain and metabolic derangements, although data are still contradictory. Objective: To determine the effect of acute and chronic consumption of sucralose on insulin and glucose profiles in young healthy adults. Material and methods: This was a randomized, parallel, double-blind, placebo-controlled trial conducted in healthy young adults from 18 to 35 years old, without insulin resistance. A hundred thirty seven participants were randomized into three groups: a) volunteers receiving 48 mg sucralose, b) volunteers receiving 96 mg sucralose, and c) controls receiving water as placebo. All participants underwent a 3-h oral glucose tolerance test (OGTT) preceded by consuming sucralose or placebo 15 min before glucose load, at two time points: week zero (Wk0) and week ten (Wk10). Serum insulin and glucose were measured every 15 min during both OGTTs. Results: Compared to Wk0, consumption of sucralose for 10 weeks provoked 1) increased insulin concentrations at 0 min (7.5 ± 3.4 vs 8.8 ± 4.1 μIU/mL; p = 0.01), 30 min (91.3 ± 56.2 vs 110.1 ± 49.4 μIU/mL; p = 0.05), 105 min (47.7 ± 24.4 vs 64.3 ± 48.2 μIU/mL; p = 0.04) and 120 min (44.8 ± 22.1 vs 63.1 ± 47.8 μIU/mL; p = 0.01) in the 48 mg sucralose group; 2) increased blood glucose at − 15 min (87.9 ± 4.6 vs 91.4 ± 5.4 mg/dL; p = 0.003), 0 min (88.7 ± 4 vs 91.3 ± 6 mg/dL; p = 0.04) and 120 min (95.2 ± 23.7 vs 106.9 ± 19.5 mg/dL; p = 0.009) in the 48 mg sucralose group; 3) increased area under the curve (AUC) of insulin in both 48 and 96 mg sucralose groups (9262 vs 11,398; p = 0.02 and 6962 vs 8394; p = 0.12, respectively); and 4) reduced Matsuda index in the 48 mg sucralose group (6.04 ± 3.19 vs 4.86 ± 2.13; p = 0.01). Conclusions: These data show that chronic consumption of sucralose can affect insulin and glucose responses in non-insulin resistant healthy young adults with normal body mass index (between 18.5 and 24.9 kg/m²), however, the effects are not consistent with dose; further research is required. Clinical trial registry: NCT03703141.

Background: A diet containing non-caloric sweeteners (NCS) could reduce calorie intake; conversely, some animal studies suggest that NCS consumption may increase functional gastrointestinal disorder symptoms (FGDs). This study aimed to compare the effect of consuming a diet containing NCS (c-NCS) versus a non-caloric sweetener-free diet (NCS-f) on FGDs. Methods: We conducted a randomized, controlled, parallel-group study using two different diets for five weeks: the c-NCS diet contained 50–100 mg/day NCS, whereas the NCS-f diet had less than 10 mg/day NCS. At the beginning of the study (PreTx) and at the end (PostTx), we assessed FGDs, dietary intake, and NCS consumption. Results: The percentage of participants with diarrhea (PreTx = 19% vs. PstTx = 56%; p = 0.02), post-prandial discomfort (PreTx = 9% vs. PstTx = 39%; p = 0.02), constipation (PreTx = 30% vs. PostTx = 56%; p < 0.01), and burning (PreTx = 13% vs. PostTx = 33%; p < 0.01) increased in the c-NCS diet group. Conversely, abdominal pain (PreTx = 15% vs. PostTx = 3%; p = 0.04), post-prandial discomfort (PreTx = 26% vs. PostTx = 6%; p = 0.02), burning (PreTx = 15% vs. PostTx = 0%; p = 0.02), early satiety (PreTx = 18% vs. PostTx = 3%; p < 0.01), and epigastric pain (PreTx = 38% vs. PostTx = 3%; p < 0.01) decreased in the NCS-f diet group. Conclusion: A c-NCS diet is associated with increased FGDs, including diarrhea, post-prandial discomfort, constipation, and burning or retrosternal pain. The NCS-f diet also decreased FGDs, as well as abdominal pain, post-prandial discomfort, burning or retrosternal pain, early satiety, and epigastric pain.

Inflammatory Bowel Disease (IBD), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory condition of the gastrointestinal tract that significantly impacts nutritional status. Malnutrition is a frequent complication, resulting from reduced nutrient intake, malabsorption, and increased metabolic demands due to chronic inflammation. A comprehensive nutritional assessment encompassing anthropometric, biochemical, and dietary evaluations is crucial for informing personalized interventions. Several nutritional approaches have been explored to modulate inflammation and the gut microbiota, yielding promising results. The Mediterranean, anti-inflammatory, and low-FODMAP diets have shown potential benefits in symptom control. In contrast, diets high in ultra-processed foods and saturated fats are associated with worsened disease activity. Additionally, stool consistency, assessed using the Bristol Stool Scale, serves as a practical indicator for dietary adjustments, helping to regulate fiber intake and hydration strategies. When dietary modifications alone are insufficient, nutritional support becomes a critical component of IBD management. Enteral nutrition (EN) is preferred whenever possible because it maintains gut integrity and modulates immune responses. It has demonstrated efficacy in reducing postoperative complications and improving disease control. In cases where EN is not feasible, such as in intestinal obstruction, severe malabsorption, or high-output fistulas, parenteral nutrition (PN) is required. The choice between peripheral and central administration depends on treatment duration and osmolarity considerations. Despite growing evidence supporting nutritional interventions, further research is needed to establish standardized guidelines that optimize dietary and nutritional support strategies in managing IBD.

Background: Accumulating evidence has proposed phase angle (PhA) as a marker for assessing cellular integrity and nutritional status in ulcerative colitis (UC) patients; the aim of the study was to evaluate the efficacy of PhA in assessing nutritional status in patients with UC, investigating its potential as a biomarker of disease activity. Methods: We conducted a cross-sectional study in patients with UC and healthy controls. We determined PhA by electrical bioimpedance and categorized participants through bioelectrical impedance analysis. They were classified as normal PhA > 6.1° and low PhA < 6.1° in men and normal PhA > 5.6° and low PhA < 5.6° in women. Results: PhA was significantly lower in UC patients than in controls (5.8 ± 0.8 vs. 6.6 ± 0.7°; p < 0.001). Among UC patients, participants with low PhA showed a decrease in lean, dry mass (LDM) (p < 0.001), total body water (p = 0.008), and intracellular water (p = 0.005), accompanied by an increase in extracellular water (p = 0.001) compared to UC patients with normal PhA. Conclusions: PhA significantly decreases in UC patients compared to healthy controls and is even more reduced when UC is active. A cut-off point of <6.1 for men and <5.6 for women could be suitable for nutritional diagnosis in patients with UC, but it still needs to be validated.

Non-nutritive sweeteners (NNSs) provide a sweet taste to foods and beverages without significantly adding calories. Still, their consumption has been linked to modifications in adult’s and children’s gut microbiota and the disruption of blood glucose control. Human milk microbiota are paramount in establishing infants’ gut microbiota, but very little is known about whether the consumption of sweeteners can alter it. To address this question, we sequenced DNA extracted colostrum samples from a group of mothers, who had different levels of NNS consumption, using the Ion Torrent Platform. Our results show that the “core” of colostrum microbiota, composed of the genera Bifidobacterium, Blautia, Cutibacteium, Staphylococcus, and Streptococcus, remains practically unchanged with the consumption of NNS during pregnancy, but specific genera display significant alterations, such as Staphylococcus and Streptococcus. A significant increase in the unclassified archaea Methanobrevibacter spp. was observed as the consumption frequency of NNS increased. The increase in the abundance of this archaea has been previously linked to obesity in Mexican children. NNS consumption during pregnancy could be related to changes in colostrum microbiota and may affect infants’ gut microbiota seeding and their future health.