Current diabetes reviews最新文献

{"title":"\"NADPH Oxidases: Central Regulators of Redox Signalling and Cellular Homeostasis\".","authors":"Namra Aziz, Ankita Wal, Inshrah Alvi, Sakshi Tiwari, Ritu Rani Yadav, Aayush Sharma, Abida Khan, Roshni Tandey","doi":"10.2174/0115733998441886260601113636","DOIUrl":"https://doi.org/10.2174/0115733998441886260601113636","url":null,"abstract":"<p><strong>Introduction: </strong>The seven isoforms of the NADPH oxidase (NOX) family-NOX1-5, DUOX1, and DUOX2-are multidomain enzymes that require distinct regulatory subunits for activation. These enzymes are major sources of reactive oxygen species (ROS), particularly the superoxide anion (O2·-), which exerts both cytotoxic and signalling effects. NADPH acts as a critical electron donor, maintaining cellular redox homeostasis and supporting anabolic metabolism. Dysregulated NOX activity has been linked to metabolic reprogramming in cancer and oxidative stress-induced complications in diabetes mellitus.</p><p><strong>Methods: </strong>A focused systematic literature analysis was conducted using PubMed, Scopus, Web of Science, and Google Scholar databases (up to March 2025). Studies exploring NOX isoform regulation, ROS generation, NADPH-driven redox metabolism, and NOX-related signalling in cancer and diabetes were critically reviewed.</p><p><strong>Results: </strong>Aberrant activation of the NOX1, NOX2, and NOX4 isoforms is strongly associated with oncogenic PI3K/Akt and MAPK signalling cascades, promoting metabolic reprogramming and antioxidant dependency in tumour cells. In diabetes, chronic hyperglycemia induces persistent NOX activation, leading to excessive ROS production and contributing to microvascular complications such as retinopathy, nephropathy, and neuropathy.</p><p><strong>Discussion: </strong>NOX enzymes act as redox integrators that couple metabolic state to cellular signalling. Their dysregulation drives divergent yet overlapping pathogenic outcomes in cancer and diabetes. Selective NOX inhibition may normalize redox tone, restore metabolic flexibility, and enhance therapeutic responses. Understanding NOX isoform-specific regulation offers opportunities for biomarker development and combination therapy design.</p><p><strong>Conclusion: </strong>NOX1, NOX2, and NOX4 are key regulators of oxidative metabolism in cancer and diabetes. Targeting these isoforms represents a promising translational approach to modulate redox imbalance, suppress tumour progression, and mitigate diabetic microvascular complications.</p>","PeriodicalId":10825,"journal":{"name":"Current diabetes reviews","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acrylamide Exposure and Glycemic Dysregulation: A Population-Based Study.","authors":"Shuang Chen, Wenxuan Bian, Yuncai Zhou, Xianyong Yin, Tao Yang","doi":"10.2174/0115733998471547260803120141","DOIUrl":"https://doi.org/10.2174/0115733998471547260803120141","url":null,"abstract":"<p><strong>Introduction: </strong>Acrylamide has been shown to induce oxidative stress and β-cell toxicity in animal studies; however, population-based evidence remains limited and inconsistent. Therefore, this study aimed to evaluate the associations between acrylamide (AA) hemoglobin biomarkers and the risk of prediabetes and diabetes in the US population.</p><p><strong>Methods: </strong>Data were obtained from the 2013-2016 National Health and Nutrition Examination Survey (NHANES). Participants were classified into diabetes, prediabetes, and healthy control groups by their glycometabolic status. The associations between prediabetes and diabetes with AA biomarkers, specifically hemoglobin adducts of acrylamide (HbAA), glycidamide (HbGA), the Hb- GA/HbAA ratio, and their combined levels (HbAA + HbGA), were investigated using multivariate logistic regression and restricted cubic spline models.</p><p><strong>Results: </strong>The fully adjusted logistic regression analyses indicated that participants in the highest HbGA quartile had a significantly elevated risk of prediabetes (odd ratio [OR] = 2.47, 95% confidence interval [CI]: 1.52-4.02, P = 0.007; Ptrend = 0.005) and diabetes (OR = 2.46, 95% CI: 1.27-4.73, P = 0.019; Ptrend = 0.043). The HbGA/HbAA ratio showed a positive correlation with prediabetes (OR = 2.10, 95% CI: 1.05-4.20, P = 0.042; Ptrend = 0.024) and diabetes (OR = 5.58, 95% CI: 2.10-14.79, P = 0.008; Ptrend < 0.001). In contrast, HbAA levels were not significantly associated with either prediabetes (OR = 1.49, 95% CI: 0.86-2.61, P = 0.116; Ptrend = 0.088) or diabetes (OR = 0.92, 95% CI: 0.47-1.81, P = 0.744; Ptrend = 0.351).</p><p><strong>Discussion: </strong>The divergent patterns observed for HbAA and the HbGA/HbAA ratio may reflect a shift from exogenous exposure to intrinsic metabolic capacity across different stages of disease progression.</p><p><strong>Conclusion: </strong>Higher HbGA levels and elevated HbGA/HbAA ratios were associated with an increased prevalence of prediabetes and diabetes. Further research is needed to clarify the causal role of acrylamide exposure in abnormal glucose metabolism.</p>","PeriodicalId":10825,"journal":{"name":"Current diabetes reviews","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating Micronutrients with Nanoparticle- Based Delivery for Diabetic Foot Ulcer Management: Emerging Therapeutic Paradigms.","authors":"Krishnendu Adhikary, Krishnendu Ganguly, Subhajit Mahanty, Surajit Majumder, Abhinaba Gupta, Rajkumar Maiti","doi":"10.2174/0115733998437466260529162016","DOIUrl":"https://doi.org/10.2174/0115733998437466260529162016","url":null,"abstract":"<p><p>Diabetic foot ulcers (DFUs) are a serious diabetic complication leading to high rates of morbidity, amputation risks, and economic burdens on the treatment facilities. The present review continues our exploration of the novel paradigm of combining micronutrients with nanoparticles to address diabetes-related DFUs effectively. We performed a detailed examination of published studies to discuss our views on the ever-increasing utilization of essential micronutrients like zinc, selenium, and vitamins A, C, D, and E to modulate oxidative stress levels, stimulate the secretion of vascular endothelial growth factors, and aid in tissue repair mechanisms. This detailed scrutiny was carried out in parallel to analyze various nanoparticle-based systems to specifically address their bioavailability, stability, deliverability, and efficiency in carrying out wound repair in DFUs. Both micronutrients and nanoparticles have shown substantial activity to increase antioxidant mechanisms, boost the immunomodulatory system, and accelerate tissue repair mechanisms in DFUs. Both methods utilize advanced delivery mechanisms to precisely deliver drugs to the affected areas reliably. Novel delivery methods with micronutrients in DFUs showed a therapeutic integration approach to quicken the healing time to DFUs in faster re-epithelialization, decrease microbial counts, increase extracellular matrix remodeling, and improve healing rates in clinical settings. There is a need for further clinical development to stabilize formulations of combining micronutrients with delivering nanoparticles to serve clinical needs effectively in DFUs. There is a great potential influence in applying this novel multipurpose approach to treat DFUs effectively to increase healing rates and minimize risks of complications in diabetic clients.</p>","PeriodicalId":10825,"journal":{"name":"Current diabetes reviews","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Diabetes on the Transcriptomic Profile of the Endocrine Pancreas: A Systematic Review.","authors":"Maria Eduarda Picolo Gomes, Verônyca Gonçalves Paula, Vinícius Soares Barco, Débora Cristina Damasceno, Giovana Vesentini","doi":"10.2174/0115733998452583260504045518","DOIUrl":"https://doi.org/10.2174/0115733998452583260504045518","url":null,"abstract":"<p><strong>Introduction: </strong>Type 2 Diabetes Mellitus (T2DM) is characterized by progressive pancreatic beta-cell dysfunction and insulin resistance. Although transcriptomic approaches have improved the understanding of molecular mechanisms underlying T2DM, evidence specifically addressing gene expression changes in the endocrine pancreas remains limited and fragmented across experimental and clinical studies.</p><p><strong>Aim: </strong>To systematically review the experimental and clinical evidence on the effects of diabetes on the transcriptomic profile of the endocrine pancreas.</p><p><strong>Methods: </strong>A comprehensive literature search was conducted in PubMed (MEDLINE), EMBASE, Web of Science, and CINAHL from database inception to December 9, 2024. Data extraction included study design, population, interventions, outcomes, and risk of bias. Two studies met the eligibility criteria. Due to methodological heterogeneity and qualitative outcomes, meta-analysis was not feasible.</p><p><strong>Results: </strong>In Wistar rats fed a high-fat-high-fructose diet, diabetes was associated with downregulation of GCG, INS1, RBP4, PPY, and PYY and upregulation of PDX1, SLC2A2, and INS1 in islet cells. In humans, diabetic individuals showed reduced GPRC5C expression, independent of sex.</p><p><strong>Discussion: </strong>Transcriptomic alterations in the endocrine pancreas have indicated dysfunctions in insulin synthesis, glycemic homeostasis, and β-cell maintenance in type 2 diabetes models.</p><p><strong>Conclusion: </strong>Pancreatic beta-cell dysfunction in T2DM may be linked to alterations in the expression of key genes involved in the development, maturation, maintenance, and function of the endocrine pancreas. This review provides insights into the molecular mechanisms of T2DM in pancreatic islets in animal and clinical models and highlights potential candidate biomarkers for future translational research.</p>","PeriodicalId":10825,"journal":{"name":"Current diabetes reviews","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148807845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms and Current Therapeutic Targets of Podocyte Damage in Diabetic Kidney Disease.","authors":"Bilge Karatoy Erdem","doi":"10.2174/0115733998492007260723100211","DOIUrl":"https://doi.org/10.2174/0115733998492007260723100211","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetic Kidney Disease (DKD) is a leading cause of end-stage kidney disease, and podocyte injury is a pivotal driver of albuminuria, glomerulosclerosis, and progressive loss of kidney function.</p><p><strong>Methods: </strong>A targeted narrative search of PubMed/MEDLINE, Scopus, and Web of Science was performed, primarily covering 2015-2025 and supplemented by seminal earlier studies. Inclusion criteria prioritized human studies, randomized and translational studies, and mechanistic work directly addressing podocyte injury or podocyte-relevant therapeutic effects in DKD. Studies with limited mechanistic or translational relevance were excluded or deprioritized.</p><p><strong>Results: </strong>Diabetic metabolic and hemodynamic stress activates AGE/PKC/RAAS signaling and downstream TGF-β/Smad, NF-κB, PI3K/Akt/mTOR, TRPC6-Ca2+, and mitochondrial stress pathways. These pathways converge on slit diaphragm disruption, actin cytoskeletal remodeling, impaired autophagy, ER stress, apoptosis, detachment, and progressive podocyte depletion. Current standard-of-care therapies, including RAAS blockade, SGLT2 inhibitors, GLP-1 receptor agonists, and finerenone, provide partial podocyte-relevant renoprotection, whereas endothelin receptor antagonists, anti-TGF-β/CTGF approaches, JAK/STAT inhibitors, TRPC6 blockade, redox-targeted therapies, RNA-based strategies, and extracellular vesicle approaches remain at different stages of clinical readiness.</p><p><strong>Discussion: </strong>The available evidence supports a layered model in which systemic metabolic and hemodynamic therapies reduce upstream stress, while emerging podocyte-directed strategies aim to stabilize cytoskeletal, slit diaphragm, inflammatory, fibrotic, calcium, and organelle-stress pathways. Combination therapy is biologically plausible but should be guided by albuminuria, eGFR, cardiometabolic phenotype, tolerability, and validated podocyte-related biomarkers.</p><p><strong>Conclusion: </strong>A podocyte-centered framework that links mechanisms, biomarkers, evidence tiering, and patient stratification may improve translation of targeted and combination strategies. However, clinical implementation requires stronger biomarker validation, optimized human-relevant models, and long-term safety and outcome data.</p>","PeriodicalId":10825,"journal":{"name":"Current diabetes reviews","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improvement in Tight Glycemic Control in Adults with Type 1 Diabetes Using the MiniMed™ 780G Hybrid Closed-Loop System: A Real-World Evaluation.","authors":"Jose Atencia Goñi, Amaya Morales Jaurrieta, Blanca Farache Suberviola, Victor Andia Melero, Ana Isabel Castellanos Rodríguez, Maravillas Bescos Pérez, Olga González Albarrán","doi":"10.2174/0115733998500238260720112301","DOIUrl":"https://doi.org/10.2174/0115733998500238260720112301","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction/objective: &lt;/strong&gt;Hybrid Closed-Loop (HCL) systems improve glycemic control in patients with Type 1 Diabetes Mellitus (T1D). An increasing body of evidence supports the utility of time within a tight range (TITR, 70-140 mg/dL) as a marker of near normoglycemia. The primary objective was to evaluate changes in TITR (70-140 mg/dL) at 3 months following initiation of the MiniMed™ 780G system in adults with T1D in routine clinical practice. Secondary objectives included: (i) assessment of changes in TIR, mean glucose, GMI, CV, TAR, TBR, and total daily insulin dose at 14 days and 3 months post-initiation; (ii) characterization of the temporal trajectory of glycemic improvement from baseline to 3 months; and (iii) an exploratory comparison of glycemic outcomes between patients previously treated with MDI and those previously treated with CSII.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This single-center, retrospective, consecutive cohort study included 23 adults with T1D who initiated the MiniMed™ 780G system between September and December 2024. Glycemic data were collected for 14 days before HCL initiation, the first 14 days after initiation, and at 3 months. The outcomes included TIR, TITR, GMI, glucose variability (CV), time above and below the range, and insulin requirements. Exploratory analyses compared the outcomes of patients previously administered multiple daily injections (MDI, n=4) and those receiving continuous subcutaneous insulin infusion (CSII, n=19).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;At 3 months, TIR and TITR improved by 13.0% and 12.2%, respectively (both p&lt;0.001). Mean glucose fell by 16.7 mg/dL, GMI by 0.38%, and CV by 3.41%. Time below range decreased despite a significant increase in total daily insulin dose (from 0.25 to 0.58 IU/kg, p&lt;0.001). Improvements were achieved within the first 14 days and remained stable thereafter. Patients transitioning from MDI had poorer baseline glycemic control but showed greater relative improvements in this exploratory analysis; however, between-group differences were not statistically significant, given the exploratory nature of this analysis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;These results are consistent with previously published real-world evidence on the MiniMed™ 780G system and support TITR as a sensitive metric for capturing the benefits of advanced HCL therapy. The early onset and sustained nature of glycemic improvement, along with the absence of increased hypoglycemia, suggests that aggressive system settings may safely optimize glycemic outcomes in routine clinical practice. These findings should be interpreted in the context of the single-center design and limited sample size.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;MiniMed™ 780G use was associated with early and sustained improvements in glycemic control, particularly in TITR, without increasing hypoglycemia. These findings support the effectiveness of this system for safely achieving near normoglycemia in real-world clinic","PeriodicalId":10825,"journal":{"name":"Current diabetes reviews","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetes and the Nervous System: Linking Peripheral Neuropathy to Central Neurodegeneration.","authors":"Md Mahmudul Hoque, Shamima Akter, Jawad Ul Karim Mahir, Nadia Afrin, Shakila Jahan Shimu, Farzana Mahzabin Auny, Shazid Md Sharker, Mohammad Mohabbulla Mohib, Mohammad Borhan Uddin, Mohammad Sarif Mohiuddin, Mayank Choubey","doi":"10.2174/0115733998440886260306085847","DOIUrl":"https://doi.org/10.2174/0115733998440886260306085847","url":null,"abstract":"<p><p>Diabetes mellitus affects both the peripheral and central nervous systems, giving rise to a spectrum of neurological complications that extend far beyond the traditional focus on diabetic peripheral neuropathy (DPN). Chronic hyperglycemia disrupts cellular homeostasis through increased formation of advanced glycation end-products, activation of inflammatory pathways, mitochondrial dysfunction, oxidative stress, and impaired neurovascular regulation. These disturbances converge to drive axonal degeneration, demyelination, synaptic injury, and progressive cognitive decline. Emerging evidence also highlights a critical role for gut dysbiosis and intestinal barrier dysfunction, which facilitate microbial translocation and systemic inflammation, ultimately disrupting the blood-brain barrier and amplifying neuroimmune injury. This narrative review synthesizes current mechanistic, clinical, and translational insights into how metabolic, inflammatory, vascular, and microbial pathways interact to produce diabetes-associated neurodegeneration. We summarize key molecular drivers-including mitochondrial ROS overproduction, microglial and astrocytic activation, endothelial dysfunction, and insulin resistance-while also describing their contributions to DPN, autonomic neuropathy, and diabetes-related cognitive impairment. We further integrate evidence from emerging therapeutic domains, including mitochondrial stabilizers, anti-inflammatory strategies, gut-microbiome modulation, and neurovascular-targeted interventions. Despite advances in understanding, disease-modifying therapies remain limited, and diagnostic tools for early detection are underutilized. Bridging these gaps will require longitudinal human studies, improved biomarkers, and integrative therapeutic approaches that target multiple convergent pathways. A deeper understanding of cross-talk among metabolic, immune, vascular, and microbial systems may enable earlier intervention and more effective strategies to mitigate the neurological burden of diabetes.</p>","PeriodicalId":10825,"journal":{"name":"Current diabetes reviews","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Making Donor Cells Invisible: A Leap Forward in the Fight Against Type 1 Diabetes.","authors":"Dinesh Kumar, Neeraj Choudhary","doi":"10.2174/0115733998463022260403041455","DOIUrl":"https://doi.org/10.2174/0115733998463022260403041455","url":null,"abstract":"","PeriodicalId":10825,"journal":{"name":"Current diabetes reviews","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing Diabetes Treatment Through NanoPhytotherapeutics: Uncovering the Therapeutic Promise of Syzygium Cumini, Pterocarpus Santalinus, and Momordica Cymbalaria.","authors":"Sowmika Sagi, Sravya Bojjala, Kesavulu Muppuru Muni, Mariadoss Arokia Vijaya Anand","doi":"10.2174/0115733998470934260630070603","DOIUrl":"https://doi.org/10.2174/0115733998470934260630070603","url":null,"abstract":"<p><strong>Background: </strong>Diabetes mellitus is among the most critical health issues all over the world, marked by persistent hyperglycemia, oxidative stress, inflammation, and the lack of insulin activity. The synthetic antidiabetic drugs that are on the market have a very short lifespan of use because of the side effects and failure to control metabolic dysregulation. The multi-targeted therapeutic advantages of phytochemicals present in medicinal plants are limited by low aqueous solubility, chemical instability, rapid metabolism, and low oral bioavailability. To address these restrictions, nano-phytotherapeutics have become a viable option to improve pharmacokinetics, increase tissue-specific delivery, and enable controlled release of bioactive compounds.</p><p><strong>Objective: </strong>The aim is to provide an overview of the therapeutic potential of three antidiabetic medicinal plants, Syzygium cumini, Pterocarpus santalinus, and Momordica cymbalaria, considering their major phytoconstituents and their mode of action. These three plants were selected because of their phytochemical diversity and complementary therapeutic potential, as well as their experimentally demonstrated antidiabetic activities and growing relevance in nanotechnology-based delivery systems. Anthocyanins, ellagic acid, pterostilbene, and cucurbitacins are some of the bioactive compounds with potent antihyperglycemic, antioxidant, and anti-inflammatory effects, making them promising candidates for nano-enabled formulations.</p><p><strong>Method: </strong>Compared to traditional plant extracts, a comparative study of polymeric nanoparticles, lipid-based nanocarriers, nanoemulsions, and green-synthesized metal nanoparticles has shown significant improvements in solubility, stability, bioavailability, and glycemic control. The present review provides a comprehensive, plant-specific, and carrier-oriented overview of current research, with particular emphasis on formulation relevance, mechanistic foundations, and translational limitations.</p><p><strong>Results: </strong>Although promising preclinical findings have been reported, several barriers to clinical translation remain unresolved, including the lack of long-term toxicological data, inconsistencies in phytochemical composition and preparation methods, and regulatory challenges specific to nano-herbal therapeutics. Furthermore, most existing studies are predominantly limited to in vitro and animal models, with a substantial lack of well-designed clinical studies and direct human validation.</p><p><strong>Conclusion: </strong>Stimuli-responsive nano-herbal therapeutics should be the focus of future research on rationally designed polyherbal nanoformulations, nanocarriers, AI-assisted optimization of formulation, and comprehensive pharmacokinetic and safety evaluations. These advancements may accelerate the development of long-term diabetes treatment with biocompatible nano-phytotherapeutics.</p>","PeriodicalId":10825,"journal":{"name":"Current diabetes reviews","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low Glycemic Index Diets on Glycemic and Lipid Control Across Diverse Populations: A Systematic Review and Meta-Analysis.","authors":"Xihan Sun, Shuang Meng, Wenting Peng, Huangkun Li, Hongwang Dong, Ge Song, Wentao Qi","doi":"10.2174/0115733998470495260601104543","DOIUrl":"https://doi.org/10.2174/0115733998470495260601104543","url":null,"abstract":"<p><strong>Background: </strong>Although low-Glycemic-Index (low-GI) diets are proposed to improve glucose balance and lipid metabolism, findings from Randomized Controlled Trials (RCTs) remain inconsistent.</p><p><strong>Objective: </strong>To comprehensively evaluate the overall effects of low-GI diets on glycemic and lipid profiles across diverse populations and to identify potential differences in outcomes among subgroups.</p><p><strong>Methods: </strong>This systematic review and meta-analysis, conducted following PRISMA guidelines, searched PubMed, Embase, Cochrane Library, and Web of Science through April 2025. Weighted Mean Difference (WMD) with 95% Confidence Interval (CI) was calculated. Subgroup and sensitivity analyses explored heterogeneity and robustness.</p><p><strong>Results: </strong>Twenty-five RCTs involving 1,973 participants (12-75 years) were included. Low-GI diets significantly reduced fasting blood glucose (FBG; -0.19 mmol/L, p = 0.04), glycated hemoglobin (HbA1c; -0.22%, p < 0.01), and low-density lipoprotein cholesterol (LDL-C; -0.15 mmol/L, p < 0.01) compared with control diets. Although not statistically significant, low-GI diets tended to increase High-Density Lipoprotein Cholesterol (HDL-C) and reduce Fasting Insulin (FI), Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), Triglycerides (TG), and Total Cholesterol (TC). Subgroup analyses revealed stronger benefits in Type 2 Diabetes Mellitus (T2DM), individuals with baseline FBG ≥ 6.1 mmol/L, trials with intervention duration ≥ 12 weeks, and people in the Asia-Pacific region. Sensitivity analyses provided confirmation of the reliability of these outcomes.</p><p><strong>Conclusions: </strong>Low-GI diets improve glycemic control and modestly lower LDL-C, particularly in metabolically high-risk populations and with sustained intervention. These results highlight low-- GI diets as a practical nutritional strategy for metabolic health, while suggesting that baseline glucose status, intervention length, and population characteristics influence their effectiveness.</p>","PeriodicalId":10825,"journal":{"name":"Current diabetes reviews","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}