Paola Stiuso

Background/Objectives: The development of functional staple foods with improved metabolic properties represents a practical dietary strategy for the prevention of type 2 diabetes. This study investigated the effects of incorporating sprouted fenugreek (Trigonella foenum-graecum L.) into wheat-based flatbread (chapatti) on postprandial glycemic and insulinemic responses in healthy adults. Methodology: Wheat (cv. Galaxy 2013) and fenugreek seeds were germinated for up to 96 h and analyzed for nutritional composition and antioxidant activity. Composite flours containing 0%, 2.5%, 5%, and 7.5% sprouted fenugreek were formulated and evaluated for sensory acceptability. Eighteen healthy participants (18–25 years; BMI 21–22.5 kg/m²) consumed chapattis containing 7.5% sprouted fenugreek or white flour as a control in a randomized crossover design. Blood glucose and serum insulin were measured at 0, 30, 60, and 120 min postprandially. Results: Sprouting significantly increased protein, dietary fiber, and antioxidant capacity in both wheat and fenugreek (p < 0.001). Total phenolic content in wheat increased from 55.82 to 110.17 mg GAE/100 g after 96 h of germination, accompanied by a significant rise in DPPH radical scavenging activity. The formulation containing 7.5% sprouted fenugreek showed the highest sensory acceptability (7.52/9). Fenugreek-supplemented chapattis significantly reduced postprandial glucose and insulin responses (p < 0.05) compared with control. Conclusion: Incorporation of 7.5% sprouted fenugreek into wheat flatbread improves nutritional quality while attenuating glycemic and insulinemic responses, suggesting a practical dietary strategy for metabolic health and diabetes prevention.

The development of functional staple foods with improved metabolic properties represents a practical dietary strategy for the prevention of type 2 diabetes. This study investigated the effects of incorporating sprouted fenugreek (Trigonella foenum-graecum L.) into wheat-based flatbread (chapatti) on postprandial glycemic and insulinemic responses in healthy adults. Wheat (cv. Galaxy 2013) and fenugreek seeds were germinated for up to 96 h and analyzed for nutritional composition and antioxidant activity. Composite flours containing 0%, 2.5%, 5%, and 7.5% sprouted fenugreek were formulated and evaluated for sensory acceptability. Eighteen healthy participants (18–25 years; BMI 21–22.5 kg/m²) consumed chapattis containing 7.5% sprouted fenugreek or control white flour in a ran-domized crossover design. Blood glucose and serum insulin were measured at 0, 30, 60, and 120 min postprandially. Sprouting significantly increased protein, dietary fiber, and antioxidant capacity in both wheat and fenugreek (p < 0.001). Total phenolic content in wheat increased from 55.82 to 110.17 mg GAE/100 g after 96 h of germination, accompa-nied by a significant rise in DPPH radical scavenging activity. The formulation containing 7.5% sprouted fenugreek showed the highest sensory acceptability (7.52/9). Fenu-greek-supplemented chapattis significantly reduced postprandial glucose and insulin re-sponses (p < 0.05) compared with control. Incorporation of 7.5% sprouted fenugreek into wheat flatbread improves nutritional quality while attenuating glycemic and insulinemic responses, suggesting a practical dietary strategy for metabolic health and diabetes pre-vention.

Background: Humans are constantly exposed to environmental microplastic (MP) particles, which can be absorbed through the gut and exert adverse health effects. This study aimed to investigate the harmful effects of environmental polyethylene MPs (PE, 2.6 μm) on differentiated Caco‐2 (D‐Caco‐2) intestinal epithelial cells and to assess the protective potential of Limoncella apple polyphenol extract (LAPE). Methods: D‐Caco‐2 cells were exposed to PE, LAPE, or their combination. Cell viability and lipid peroxidation were evaluated using MTT and TBARS assays, respectively. The organization of F‐actin and alkaline phosphatase proteins was evaluated by immunofluorescence, whereas occludin and NF‐κB were evaluated by Western blot analysis. Results: PE reduced D‐Caco‐2 viability and impaired cell differentiation by increasing lipid peroxidation. In addition, PE destructured F‐actin organization and altered the expression of occludin, a tight‐junction protein. Conclusions: Our findings show that PE increases oxidative stress, triggering epithelial–mesenchymal transition and dedifferentiation in Caco‐2 cells. Interestingly, LAPE, owing to its antioxidant and anti‐inflammatory properties, counteracted the harmful effects of PE, suggesting its potential as a nutraceutical strategy to prevent MP‐induced damage in the gastrointestinal (GI) tract.

Ulcerative colitis (UC) is a chronic inflammatory disease that affects the colon, triggering persistent inflammation and ulceration, resulting in a severe impact on patients’ quality of life. Currently, the standard diagnostic methods for UC include invasive procedures such as colonoscopy and the use of non-specific inflammatory markers like C-reactive protein, which can be inconvenient or painful and lack specificity. This underscores the need for non-invasive and highly specific biomarkers for UC. MicroRNAs (miRNAs) are small non-coding RNAs, typically 22 nucleotides in length, which are well described as gene expression regulators. Several studies have reported their differential expression in various pathological conditions, including UC. Due to their role in gene regulation and stability in biological fluids, miRNAs present a promising opportunity as biomarkers. This systematic review explores the potential use of miRNAs as diagnostic biomarkers to distinguish between active and inactive ulcerative colitis. Following PRISMA guidelines and based on inclusion and exclusion criteria, seven studies, encompassing a total of 514 participants (181 with active UC and 116 with inactive UC), were included. Multiple miRNAs exhibiting differential expression between active and inactive UC were identified. Most notably, miR-21, miR-126, miR-146b-5p, and miR-223 exhibited consistent upregulation in active UC, suggesting their potential as diagnostic biomarkers. Supporting these findings is the fact that these miRNAs are involved in inflammatory pathways, further highlighting their relevance to the pathogenesis of UC. This review emphasizes the need for further validation studies with larger cohorts to confirm the utility of miRNAs as diagnostic tools for UC disease activity differentiation, which could enhance non-invasive disease monitoring and inform therapeutic decision-making. Future research should also evaluate the prognostic potential of these miRNAs for predicting treatment responses and long-term disease outcomes.

Background: Ulcerative colitis (UC) is a chronic inflammatory disease that affects the colon, triggering persistent inflammation and ulceration, resulting in a severe impact on patients' quality of life. Currently, the standard diagnostic methods for UC include invasive procedures such as colonoscopy and the use of non-specific inflammatory markers like C-reactive protein, which can be inconvenient or painful and lack specificity. This underscores the need for non-invasive and highly specific biomarkers for UC. MicroRNAs (miRNAs) are small non-coding RNAs, typically 22 nucleotides in length, which are well described as gene expression regulators. Several studies have reported their differential expression in various pathological conditions, including UC. Due to their role in gene regulation and stability in biological fluids, miRNAs present a promising opportunity as biomarkers. This systematic review explores the potential use of miRNAs as diagnostic biomarkers to distinguish between active and inactive ulcerative colitis. Methods: Following PRISMA guidelines and based on inclusion and exclusion criteria, seven studies, encompassing a total of 514 participants (181 with active UC and 116 with inactive UC), were included. Results: Multiple miRNAs exhibiting differential expression between active and inactive UC were identified. Most notably, miR-21, miR-126, miR-146b-5p, and miR-223 exhibited consistent upregulation in active UC, suggesting their potential as diagnostic biomarkers. Supporting these findings is the fact that these miRNAs are involved in inflammatory pathways, further highlighting their relevance to the pathogenesis of UC. Conclusions: This review emphasizes the need for further validation studies with larger cohorts to confirm the utility of miRNAs as diagnostic tools in UC, which could enhance non-invasive disease monitoring and inform therapeutic decision-making.

Unresolved inflammation, due to unfavorable imbalances between pro‐inflammatory and pro‐resolving mediators, leads to chronic inflammatory pathologies that are often sex‐biased and regulated by sex hormones, including inflammatory bowel disease. Lipid mediators (LM) produced from polyunsaturated fatty acids by various lipoxygenases (LOX) and cyclooxygenases govern all stages of inflammation, i.e., the initiation and progression by pro‐inflammatory eicosanoids and its resolution by specialized pro‐resolving mediators (SPM). Here, we reveal sex‐specific differences in murine experimental colitis with male preponderance, which was abolished by sex hormone deprivation using gonadectomy, and this correlated to the levels of inflammation‐relevant mediators in the colon. Oral dextran sodium sulfate administration caused more severe colon inflammation in male CD‐1 mice than in female counterparts during the acute phase. Colitis in males yielded higher colonic cytokine/chemokine levels but lower 12−/15‐LOX‐derived LM including SPM compared to female animals in the resolving phase. Sex hormone deprivation in male mice by orchidectomy ameliorated colitis and impaired pro‐inflammatory cytokine/chemokine levels but elevated 12−/15‐LOX products including SPM, thus abolishing the observed sex differences. Conversely, ovariectomy impaired the levels of those LM that dominated in females and that were increased in males after gonadectomy. Our findings suggest that male sex hormones promote the development of colitis connected to the biosynthesis of inflammatory cytokines, chemokines, and certain LM, especially pro‐resolving 12−/15‐LOX products that appear to be suppressed in the male colon due to androgens.

Ulcerative colitis (UC), an inflammatory bowel disease (IBD), may increase the risk of colorectal cancer (CRC) by activating chronic proinflammatory pathways. The goal of this study was to find serum prediction biomarkers in UC to CRC development by combining low-density miRNA microarray and biocomputational approaches. The UC and CRC miRNA expression profiles were compared by low-density miRNA microarray, finding five upregulated miRNAs specific to UC progression to CRC (hsa-let-7d-5p, hsa-miR-16-5p, hsa-miR-145-5p, hsa-miR-223-5p, and hsa-miR-331-3p). The circRNA/miRNA/mRNA competitive endogenous RNA (ceRNA) network analysis showed that the candidate miRNAs were connected to well-known colitis-associated CRC ACVR2A, SOCS1, IGF2BP1, FAM126A, and CCDC85C mRNAs, and circ-SHPRH circRNA. SST and SCARA5 genes regulated by hsa-let-7d-5p, hsa-miR-145-5p, and hsa-miR-331-3p were linked to a poor survival prognosis in a CRC patient dataset from The Cancer Genome Atlas (TCGA). Lastly, our mRNA and miRNA candidates were validated by comparing their expression to differentially expressed mRNAs and miRNAs from colitis-associated CRC tissue databases. A high level of hsa-miR-331-3p and a parallel reduction in SOCS1 mRNA were found in tissue and serum. We propose hsa-miR-331-3p and possibly hsa-let-7d-5p as novel serum biomarkers for predicting UC progression to CRC. More clinical sample analysis is required for further validation.

Inflammatory bowel conditions can involve nearly all organ systems and induce pathological processes through increased oxidative stress, lipid peroxidation and disruption of the immune response. Patients with inflammatory bowel disease (IBD) are at high risk of having extra-intestinal manifestations, for example, in the hepatobiliary system. In 30% of patients with IBD, the blood values of liver enzymes, such as AST and ALT, are increased. Moreover, treatments for inflammatory bowel diseases may cause liver toxicity. Apple polyphenol extracts are widely acknowledged for their potential antioxidant effects, which help prevent damage from oxidative stress, reduce inflammation, provide protection to the liver, and enhance lipid metabolism. The aim of this study was to investigate whether the polyphenol apple extract from Malus domestica cv. ‘Limoncella’ (LAPE) may be an effective intervention for the treatment of IBD-induced hepatotoxicity. The LAPE was administrated in vivo by oral gavage (3–300 mg/kg) once a day for 3 consecutive days, starting 24 h after the induction of dinitro-benzenesulfonic acid (DNBS) colitis in mice. The results showed that LAPE significantly attenuated histological bowel injury, myeloperoxidase activity, tumor necrosis factor and interleukin (IL-1β) expressions. Furthermore, LAPE significantly improved the serum lipid peroxidation and liver injury in DNBS-induced colitis, as well as reduced the nuclear transcription factor-kappaB activation. In conclusion, these results suggest that LAPE, through its antioxidant and anti-inflammatory properties, could prevent liver damage induced by inflammatory bowel disease.

Polycaprolactone nanofibers are used as scaffolds in the field of tissue engineering for tissue regeneration or drug delivery. Polycaprolactone (PCL) is a biodegradable hydrophobic polyester used to obtain implantable nanostructures, which are clinically applicable due to their biological safety. Polydatin (PD), a glycosidic precursor of resveratrol, is known for its antioxidant, antitumor, antiosteoporotic, and bone regeneration activities. We aimed to use the osteogenic capacity of polydatin to create a biomimetic innovative and patented scaffold consisting of PCL-PD for bone tissue engineering. Both osteosarcoma cells (Saos-2) and mesenchymal stem cells (MSCs) were used to test the in vitro cytocompatibility of the PD-PCL scaffold. Reverse-phase (RP) HPLC was used to evaluate the timing release of PD from the PCL-PD nanofibers and the MTT assay, scanning electron microscopy, and alkaline phosphatase (ALP) activity were used to evaluate the proliferation, adhesion, and cellular differentiation in both osteosarcoma and human mesenchymal stem cells (MSCs) seeded on PD-PCL nanofibers. The proliferation of osteosarcoma cells (Saos-2) on the PD-PCL scaffold decreased when compared to cells grown on PLC nanofibers, whereas the proliferation of MSCs was comparable in both PCL and PD-PCL nanofibers. Noteworthy, after 14 days, the ALP activity was higher in both Saos-2 cells and MSCs cultivated on PD-PCL than on empty scaffolds. Moreover, the same cells showed a spindle-shaped morphology after 14 days when grown on PD-PCL as shown by SEM. In conclusion, we provide evidence that nanofibers appropriately coated with PD support the adhesion and promote the osteogenic differentiation of both human osteosarcoma cells and MSCs.