Search Results (3,038)

Background: Artificial intelligence (AI) is increasingly incorporated into nutrition research and practice; however, the extent of its clinical integration and impact on health outcomes remains unclear. This systematic review evaluated how AI-based systems have been implemented in human nutritional interventions and summarized reported outcomes. Methods: PubMed, Scopus, Google Scholar, SpringerLink, JMIR, and MDPI were searched from January 2020 to March 2025 (search completed in March 2025). Randomized controlled trials and prospective or retrospective cohort studies published in English or Spanish were included if they evaluated AI-driven nutritional interventions in human populations and reported health-related outcomes. Risk of bias was assessed using RoB 2 and ROBINS-I. A qualitative synthesis was performed. Results: Sixteen studies involving 10,863 participants were included. Most were randomized controlled trials targeting metabolic disorders, particularly type 2 diabetes and obesity. Eleven studies evaluated metabolic outcomes, including HbA1c, body weight, fat mass, lipid levels, and insulin resistance indices. Six studies assessed gastrointestinal symptom severity scores, and two examined quality-of-life or patient-reported outcomes. Several trials reported short-term improvements favoring AI-supported interventions in glycemic control, weight reduction, and symptom severity. However, effects were heterogeneous and often observed within multimodal programs, limiting attribution of outcomes solely to the AI component. Conclusions: AI integration in nutrition remains in an early phase of clinical implementation. Although preliminary findings suggest potential benefits, interpretation should be cautious given methodological heterogeneity and moderate-to-high risk of bias across studies. Larger, rigorously designed investigations are required to determine sustained clinical effectiveness. Full article

Diabetes complications may increase frailty rates among the elderly, leading to falls, immobility, dependency, hospitalizations, and death. The study aimed to assess any association between frailty status and glycaemic control among older adults with type 2 diabetes mellitus at Kenyatta National Hospital, Kenya. We conducted a cross-sectional study of 430 older individuals aged 60+ years with type 2 diabetes at a specialized diabetes clinic using a modified FRAIL scale. Mean age was 69.1 years; 65.7% were female and 76.2% completed primary school. Frailty prevalence was 3.8%, pre-frailty constituted 24.3%, and robust/non-frail comprised 71.9%. It was associated with age, social status, health knowledge, duration of DM, blood pressure, body mass index, high-density lipoprotein-C, and renal failure. Mean fasting plasma glucose (FPG) was 8.7 mmol/L, with 60% having FPG > 7 mmol/L; mean glycated haemoglobin (HbA1C) was 8.0%, with 41% having HbA1C > 8%. Glycaemic control was correlated with number of medications, blood pressure, and lipidaemia, but not age, sex, or social status. No correlation was found between frailty and glycaemic control: frailty versus FPG (r = 0.038, p = 0.459; χ² = 0.699, p = 0.705) and HbA1C (r = −0.009, p = 0.877; χ² = 0.046, p = 0.977). Low frailty prevalence was noted, with no association to glycaemic control. Our findings provide evidence for conducting frailty assessments in chronic disease care. Full article

Background/Objectives: Sphingosine-1-phosphate (S1P) is implicated in glycemic control. However, its circulating levels and clinical significance in type 2 diabetes mellitus (T2DM) remain controversial. We assessed plasma S1P levels in T2DM patients, its associations with metabolic parameters and complications, and explored its biomarker potential and non-linear (U-/J-shaped) relationships. Methods: This cross-sectional study enrolled 140 patients with T2DM and 63 matching healthy controls. Plasma S1P was measured by competitive ELISA. Statistical analyses included comparisons, correlation, ROC analysis, multivariable logistic regression, and quadratic/spline regression for U-shaped relationships. Results: Plasma S1P was significantly elevated in T2DM patients [1256.7 (149.4–1510.0) ng/mL] compared to controls [1075.1 (202.0–1510.0) ng/mL; p < 0.001]. S1P correlated positively with age, disease duration, HbA1c, insulin resistance, TyG index, triglycerides, systolic blood pressure, and negatively with HDL-C. Patients with complications had higher S1P than those without (p = 0.001), with progressive increases from retinopathy to nephropathy to mixed complications. Insulin-treated patients exhibited the highest S1P levels (p < 0.001). ROC analysis showed moderate diagnostic accuracy (AUC = 0.724). S1P is an independent associated factor with complications (OR = 1.18 per 100 ng/mL, p = 0.003). Non-linear analysis revealed a U-shaped relationship with HDL-C (optimal S1P: 1100–1350 ng/mL) and a J-shaped relationship with complication risk (threshold ~1250 ng/mL). Conclusions: Plasma S1P is elevated in T2DM and correlates with disease severity, glycemic control, insulin resistance, and complications. S1P demonstrates moderate biomarker potential and exhibits non-linear U-/J-shaped relationships with metabolic parameters, suggesting an optimal therapeutic window of 1100–1280 ng/mL. These findings support S1P as a marker of cumulative disease burden and a potential therapeutic target. Full article

Diabetic retinopathy (DR) is a common cause of vision loss in diabetes, and it often progresses without early symptoms. DR reflects injury of the retinal neurovascular unit (NVU), which includes neurons, Müller glia, astrocytes, endothelial cells, pericytes, and immune cells. Chronic hyperglycemia drives oxidative stress, advanced glycation end products–receptor for advanced glycation end products (AGE–RAGE) signaling, mitochondrial injury, and low-grade inflammation. These changes disrupt endothelial junctions, promote leukostasis, weaken pericyte support, increase basement membrane thickening, and lead to capillary dropout and hypoxia. Hypoxia-related signaling increases anti-vascular endothelial growth factor (VEGF) activity, which raises vascular leakage and supports neovascular disease. Glial stress and microglial activation add cytokines and reactive oxygen species, and neural dysfunction can appear early and can weaken neurovascular coupling. Modern diabetes care changes the short-term risk landscape because potent therapies can lower HbA1c quickly. Large and rapid HbA1c reductions can trigger early worsening of diabetic retinopathy (EWDR), mainly in patients with high baseline HbA1c and moderate-to-severe baseline DR. Semaglutide’s retinopathy complication signal in SUSTAIN-6 fits an EWDR-like pattern that tracks with rapid glycemic improvement in vulnerable eyes. In parallel, surgery adds acute stress, inflammation, glucose swings, hemodynamic shifts, and medication interruptions. These factors can worsen microvascular instability during recovery. Current perioperative guidelines and regulatory recommendations describe glucose targets and medication safety considerations, including preoperative interruption of SGLT2 inhibitors to reduce euglycemic ketoacidosis risk; however, the retina-specific implications of these measures remain indirect. This review summarizes current evidence linking NVU biology, EWDR risk, and perioperative diabetes-related factors. It discusses how these factors may interact in patients with diabetes and how they may influence retinal outcomes. The review is intended to synthesize current evidence and mechanistic interpretations rather than to provide formal clinical practice recommendations. Full article

Background: Diabetes mellitus is a metabolic disturbance characterized by chronic hyperglycemia, which stems from defective secretion and/or action of insulin. D-Limonene has been studied for the confirmation of its antidiabetic and antioxidant effects. This paper aims to investigate the antidiabetic and antioxidants effects of D-Limonene in an experimental model of DM1. Methods: Female Wistar rats (180–250g) received streptozotocin (STZ, 45 mg/kg) intraperitoneally. Animals with capillary glycemia ≥ 250 mg/dL were considered diabetic. D-Limonene at oral doses of 12.5 mg/kg, 25 mg/kg and 50 mg/kg was administered during 28-day treatment. Water and food intake, weight gain and capillary glycemia were evaluated. At the end of the treatment, the following biochemical parameters were assessed: serum glucose, HbA1c, urea, creatinine, AST, ALT, GGT, ALP and albumin. The oxidative stress markers were determined in plasma, erythrocytes, and aortic homogenates: malondialdehyde, nitrite, myeloperoxidase, superoxide dismutase and catalase. Results: D-Limonene (25 and 50 mg/kg) significantly reduced serum glucose, HbA1c, AST, ALT, GGT and ALP when compared to DC, as well as plasma MDA and nitrite concentrations. Interestingly, D-Limonene (25 and 50 mg/kg) decreased both plasma and aortic myeloperoxidase activities, as well as increased both erythrocytic and aortic catalase activities. Conclusions: These findings, besides a marked D-Limonene-induced hypoglycemic effect, pave the way for further studies comprising a multi-target treatment by providing benefits on hepatic and vascular complications related to the diabetic condition. Full article

Background: The Middle East and North Africa (MENA) region faces a high cardiovascular disease (CVD) burden alongside endemic serum 25(OH)D (vitamin D) deficiency. This systematic review examines the relationship between vitamin D deficiency and CVD risk factors in MENA populations. Methods: PubMed, Cochrane Library, and Scopus were searched from inception to 18 October 2024, for observational studies in the MENA region examining vitamin D deficiency and cardiovascular risk factors in adults. Independent data extraction was conducted. Study quality was appraised using the Joanna Briggs Institute tool and the Newcastle–Ottawa Scale, with risk of bias visualized using Robvis. Weighted mean differences in cholesterol, body mass index (BMI), and HbA1c between those with and without vitamin D deficiency were computed with random-effects meta-analysis. The protocol was registered in PROSPERO (ID: CRD42025615188) and funded by the Royal College of Surgeons in Ireland—Medical University of Bahrain. Results: Seventeen studies from nine MENA countries were included, predominantly cross-sectional, involving community-based and disease-specific cohorts. Vitamin D deficiency was highly prevalent and consistently associated with higher adiposity and central obesity. Several studies reported significant links between deficiency and poor glycemic control, particularly in obese and prediabetic groups. Meta-analysis demonstrated significantly higher total cholesterol (MD = 0.32; 95% CI = 0.11 to 0.52, p < 0.001), BMI (MD = 1.81; 95% CI = 0.68 to 2.94, p < 0.001), and HbA1c levels (MD = 0.31; 95% CI = 0.06 to 0.57, p = 0.02) in vitamin D deficient individuals, with notable heterogeneity. Conclusions: Vitamin D deficiency is highly prevalent in the MENA region and consistently associated with adiposity-related risk factors. Despite heterogeneity, findings underscore the need for public health strategies and further research to clarify causal pathways and population-specific interventions. Full article

Conventional diabetes therapy primarily targets HbA1c using a standardized, stepwise approach, often neglecting individual clinical and diagnostic phenotypes. In this second part of our discussion, we present an alternative strategy. After phenotyping the patient, we initiate a targeted pharmacological combination therapy tailored to the individual’s underlying pathophysiology, alongside lifestyle modifications. Sulfonylureas are completely avoided in this approach. Instead, medications are selected based on their alignment with the patient’s phenotype and absence of contraindications. Early insulin therapy, for example, is particularly effective in patients with β-cell-dysfunction-driven diabetes, whereas GLP-1-supported weight reduction and glitazone therapy are more suitable for insulin-resistance-driven diabetes. For monitoring and determining when temporary therapy intensification may be necessary, we rely on a combination of functional biomarkers (intact proinsulin, adiponectin, hsCRP, and leptin) and conventional clinical parameters (HbA1c, BMI, lipids, blood pressure). Using this personalized strategy, we have consistently achieved long-term glycemic control—often maintaining normal HbA1c levels for up to 15 years in our patients so far. Full article

Background/Objective: In recent years, epidemiological and clinical evidence has suggested an association between the use of second-generation antipsychotics (SGAs) and hyperglycemic complications: notably, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). However, the role of first-generation antipsychotics (FGAs) remains less well understood. To conduct a systematic review of evidence established in case reports (CRs) on adverse drug reactions, specifically DKA and HHS, associated with the use of both FGAs and SGAs in order to identify patterns that may inform clinical awareness and future research. Methods: Pertinent bibliographic databases (MEDLINE, EMBASE, PsycINFO and the Cochrane Central Register of Controlled Trials (CENTRAL)) were searched using index phrases and keywords up until 17 October 2025. Eligible CRs discussed exposure to at least one US FDA-approved antipsychotic drug (APD) and assessed either DKA or HHS. Results: A total of 151 CRs were included in the systematic review (DKA, n = 121; HHS, n = 28; both conditions, n = 2). Patients aged 30 to 39 years accounted for the highest number of emergencies (n = 49, 32.5%), which occurred mostly in males (n = 108, 71.5%). The most common mental health diagnosis was schizophrenia (n = 77, 51%), followed by bipolar disorder (n = 26, 17.2%). Olanzapine was associated with the highest number of DKA cases (n = 53, 43.1%), followed by clozapine (n = 24, 19.5%). The average blood glucose at presentation was 842.8 mg/dL for DKA patients and 1252.8 mg/dL for HHS patients. The average hemoglobin A1c levels (HbA1c) were 11.5% and 12%, respectively, for these two conditions. Of the 12 reported fatalities, treatment with olanzapine was noted in four DKA cases and in one HHS case. Conclusion: This analysis provides additional evidence of an association between the use of atypical APDs and DKA or HHS. Clinicians should continue to monitor metabolic risk factors for these conditions, as well as educating patients about the prevention of acute diabetic complications. Full article

The diagnosis of type 2 diabetes using classical clinical and laboratory biomarkers (HbA1c, glucose, lipids, BMI, and blood pressure) is a classification by symptoms and does not provide insight into the underlying pathophysiological disorders (insulin resistance, β-cell dysfunction, visceral adipose tissue hormonal secretion, and chronic systemic inflammation). A better understanding of these disorders may help in the selection of appropriate and potentially more successful personalized therapeutic interventions. Based on extensive clinical trial experience, a method for individual phenotyping and consecutive personalized diabetes therapy has been developed in our practice, which we have been using for more than 15 years and would like to share for discussion and debate. In this Part 1, the pathophysiological background and diagnostic approach to phenotyping is described. A consecutive Part 2 will present the translation of the phenotyping result into a personalized diabetes therapy, and another consecutive Part 3 will provide more comprehensive real-world patient observations when practicing this concept. This article is intended as a discussion/concept paper and does not present unpublished patient-level outcome data or formal effectiveness analyses. Prospective validation studies are needed to evaluate the clinical utility of this phenotype-based framework. Full article

Hydrophobic carbon quantum dots (hbCQDs) with tunable photoluminescence were synthesized via a solvothermal approach and further hybridized with Rhodamine B (RhB) to extend emission into the visible range. The hbCQDs exhibit quasi-spherical morphology with an average particle size of 8 nm and predominantly disordered graphitic structure, as confirmed by TEM and XRD analyses. FTIR and XPS characterizations reveal surface functional groups including C–N, C=O/C–O, and S–H, which govern the photoluminescence properties. Pure hbCQDs display blue emission at 453 nm under excitation, with a quantum yield (QY) of 6.2%. Incorporation of RhB leads to dual-emission behavior: the surface-state emission remains in the blue region, while molecular-state emission from RhB appears in the orange-red region. The 0.2 mL RhB–CQD composite exhibits optimal properties, including a QY of 13% and a production yield of 82%, emitting white light under 365 nm UV excitation. Increasing RhB loading to 0.4 mL results in a shift in emission peaks and a reduced QY (<9%), with weaker orange fluorescence. These findings demonstrate that controlled RhB hybridization effectively tunes the emission spectrum of hbCQDs, offering a simple and reproducible strategy to achieve dual-color and white-light emission. The optimized hbCQDs/RhB composites hold significant potential for applications in hydrophobic media-compatible organic optoelectronics, light-emitting devices, and bioimaging. Full article

In this study, the chemical composition of highland barley (HB), microwave fluidization HB (HB-1), extrusion and puffing HB (HB-2), and ultrafine pulverization HB (HB-3) were investigated based on untargeted metabolomics. In addition, RNA-seq transcriptomics, real-time polymerase chain reaction (qRT-PCR) and Western blot (WB) analysis were used to investigate the lipid metabolism mechanism of HB-1, induced by a high fat and cholesterol diet (HFCD). The results indicated that a total of 1292 metabolites were detected and classified into 78 distinct classes in the untargeted metabolomics analysis including fatty acyls, carboxylic acids and derivatives, glycerophospholipids, organooxygen compounds, prenol lipids, and so on. HB-1, HB-2, and HB-3 all increased the levels of amino acids and their derivatives, phenols, and carboxylic acid and its derivatives compared with HB. Furthermore, RNA-seq transcriptomic results indicated that HB-1 significantly modulated key genes of Cyp2c38, Cyp2b13, and Cyp2b9 related to steroid hormone biosynthesis and CD36, Plin4, and Fabp4 related to the PPAR signaling pathway, which played key roles in lipid metabolism. Moreover, qRT-PCR and WB results indicated that HB-1 obviously enhanced ADIPOQ expression level, while it reduced SCD-1, CD36, Fabp4, and SREBP-1c expression levels, suggesting that the alleviation of lipid metabolic dysregulation by HB-1 in hyperlipidemia mice might be mediated via participating in the PPARγ pathway. This study provided essential theoretical insights for the development and utilization of HB. Full article

Background/Objectives: Vitamin D plays an important role in glucose metabolism, lipid regulation, and inflammatory processes, and has been implicated in cardiometabolic health. However, its associations with specific metabolic biomarkers remain inconsistent, particularly in older adults. This study aimed to examine whether vitamin D deficiency is differentially associated with multiple metabolic biomarkers in a nationally representative sample of older adults. Methods: This cross-sectional study used data from the 2024 Korea National Health and Nutrition Examination Survey, including 1806 adults aged ≥65 years. Vitamin D deficiency was defined as serum 25-hydroxyvitamin D levels < 20 ng/mL. Metabolic biomarkers included fasting glucose, glycated hemoglobin (HbA1c), triglycerides, C-reactive protein (CRP), high-density lipoprotein cholesterol (HDL-C), waist circumference, and body mass index (BMI). Complex sample linear regression analyses were performed with sequential adjustment for sociodemographic factors, health behaviors, and comorbidities. Results: In unadjusted analyses, vitamin D deficiency was associated with adverse metabolic profiles, including higher fasting glucose, HbA1c, triglycerides, waist circumference, and CRP levels, and lower HDL-C levels. After adjustment for sociodemographic factors, health behaviors, and comorbidities, significant associations remained for HbA1c (β = 0.10, p = 0.034), triglycerides (β = 0.10, p = 0.003), and waist circumference (β = 1.21, p = 0.040). No significant associations were observed for fasting glucose, HDL-C, CRP, or BMI. Conclusions: Vitamin D deficiency was independently associated with poorer long-term glycemic status, hypertriglyceridemia, and central adiposity in older adults, but not with other metabolic markers after adjustment. These findings suggest that the metabolic correlates of vitamin D deficiency may be domain-specific rather than generalized. Longitudinal and interventional studies are needed to clarify causality and underlying mechanisms. Full article

Introduction: Oxidative stress and inflammation are major factors linked to obesity and metabolic dysfunction, leading to a significantly higher risk of related diseases. Atorvastatin and liraglutide possess lipid-lowering, antioxidant, and anti-inflammatory effects that could synergistically improve obesity-related perturbations through modulation of the Nrf2/HO-1 signaling pathway. Methodology: We assessed liraglutide’s pharmacological potential in extending atorvastatin’s benefit on obesity, hyperlipidemia, and fatty liver in rats fed a high-fat diet (HFD) for 12 weeks. We specifically evaluated the effects of liraglutide treatment on atorvastatin-induced anti-inflammatory and antioxidant mechanisms, with a particular focus on Nrf2/HO 1 modulation in adipose and hepatic tissue. In silico analyses, including molecular docking and AlphaFold- Multimer modeling, evaluated the binding affinities of atorvastatin and liraglutide to Nrf2 and HO 1. Results: Compared to ND, the HFD-fed rats had a significantly higher final body weight (362.4 ± 12.7 g vs. 245.6 ± 9.8 g in ND, p < 0.05). There was a marked increase in serum total cholesterol (178.6 ± 9.2 mg/dL vs. 98.3 ± 6.4), fasting glucose (340.1 ± 8.2 mg/dL vs. 82.3 ± 3.1), HbA1c (7.8 ± 0.3 vs. 4.5 ± 0.2), and hepatic COX-2 expression (99.9 ± 6.3 vs 19.6 ± 2.4). The oxidative stress markers were also disturbed, as indicated by SOD (42.5 ± 3.1 vs. 95.2 ± 4.6 U/mg protein), GSH (18.3 ± 1.5 vs. 42.7 ± 2.8 nmol/mg), and p62 (0.005 ± 0.001 vs. 0.125 ± 0.01). Atorvastatin lowered cholesterol (121.2 ± 7.5 mg/dL), COX-2 (61.3 ± 3.3), and body weight (301.7 ± 11.5 g) compared to HFD. Meanwhile, liraglutide caused a greater reduction in body weight (268.5 ± 10.3 g), glucose (112.5 ± 6.7 mg/dL), and COX-2 (42.2 ± 2.9) than atorvastatin. The combination therapy produced the most significant effects, returning body weight (253.6 ± 9.1 g) to baseline, normalizing glucose and lipids, reducing COX-2 to 22.9 ± 2.0, and reactivating the Nrf2/HO-1 pathway, as shown by increased HO-1 expression and the restoration of p62 levels (0.078 ± 0.004). In silico analyses suggest that atorvastatin favorably binds to Nrf2 and HO-1, while liraglutide interacts with structurally relevant interfaces on these proteins, providing a mechanistic basis for their complementary antioxidant and cytoprotective effects. Conclusions: Our findings support targeting the Nrf2/HO-1 signaling pathway as a potential therapy for reversing hyperlipidemia and preventing mediators of inflammation and oxidative stress damage in the liver tissue. The evidence of increased efficacy observed with the combined atorvastatin and liraglutide supports a potential novel understanding of the complementary effects of atorvastatin and liraglutide. This finding requires further investigation to elucidate the combination’s therapeutic advantages in treating metabolic disorder scenarios. Full article

Background/Objectives: Viral respiratory tract infections (VRTIs) in patients with diabetes mellitus (DM) are characterized by a severity gap rather than an infection gap. This review synthesizes evidence from the 2023–2026 respiratory seasons to provide a post-pandemic framework for managing the synergistic metabolic and viral threats in this population. Materials and Methods: A scoping review of literature from PubMed, Scopus, and Embase (2023–2026) was conducted, focusing on clinical outcomes and mechanistic interactions between DM and emerging respiratory pathogens. Results: Recent data identify human Metapneumovirus (hMPV) and adenovirus as significant threats to diabetic hosts, with mortality risks equivalent to seasonal influenza (HR 1.00 for hMPV vs. influenza). The two-hit model combines a baseline of innate immune paralysis, characterized by impaired neutrophil chemo-taxis and mechanical SP-D dysfunction, with a cellular signaling environment primed for cytokine overreaction by epigenetic metabolic memory. The stress hyperglycemia ratio (SHR) has emerged as a promising predictor of mortality compared to absolute glucose or HbA1c, with a proposed threshold of ≥1.14 identifying patients at 3.5-fold increased risk for mechanical ventilation. Precision management should consider the prudent suspension of SGLT2 inhibitors to mitigate euglycemic DKA risks and considering the early use of GLP-1 receptor agonists for their hypothesized pulmonary anti-inflammatory properties. Conclusions: Closing the mortality gap may require a shift from generic viral care to a precision model that treats metabolic susceptibility with high clinical priority alongside the treatment of the viral pathogen. Full article