Current diabetes reviews最新文献

Aims: Preclinical Evaluation of Fisetin in the Management of Diabetic Foot Ulcer in Wistar Rats.

Introduction: Diabetic foot ulcer (DFU) is a complication of diabetes mellitus, often leading to non-traumatic amputations and significantly impacting patient morbidity. Globally, the prevalence of DFU ranges from 9.1 to 26.1 million annually. A 2022 meta-analysis revealed that 6.3% of diabetic adults (33 million) are affected by DFUs. The current treatments primarily focus on topical treatments, neglecting the underlying metabolic conditions.

Objective: To investigate the wound healing efficacy of the phytoconstituent fisetin, administered orally, in managing DFU in diabetic neuropathic Wistar rats.

Method: This study investigates the therapeutic potential of a phytoconstituent fisetin, in the management of wound healing in STZ-NAD induced diabetic animal model with surgically induced wounds after indication of neuropathy. Fisetin was administered orally at doses of 5, 10, and 15 mg/kg for 30 days following the induction of foot ulcers, Various parameters were measured, including blood glucose levels, HbA1c, lipid profile, pro-inflammatory cytokines, antioxidant activity, MDA, and histopathological analysis of wound healing.

Result: Fisetin, particularly at 15 mg/kg, significantly modulates blood glucose level, HbA1c, lipid profile, and pro-inflammatory cytokines, further enhancing antioxidant activity, while reducing MDA, indicating a reduction in oxidative stress. Histopathological analysis demonstrated enhanced wound healing by increased fibroblast proliferation and collagen formation, as well as restoration of the epithelial layer. Fisetin also exhibited potential in enhancing re-epithelization, enhancing pro-angiogenic markers, diminishing inflammation, and reducing wound size.

Conclusion: Fisetin demonstrates promising potential in managing DFU by modulating metabolic conditions, reducing blood glucose, oxidative stress, and inflammation, and promoting wound healing. Future studies should focus on unraveling the detailed molecular pathways involved in fisetin's action, along with clinical trials to validate its efficacy in DFU patients.

Type 2 diabetes mellitus (T2DM) remains one of the most prevalent chronic metabolic disorders globally, presenting an ongoing challenge in terms of prevention and management. The majority of existing therapeutic strategies focus primarily on glycemic control. However, the role of inflammation in the pathogenesis of the disease is being recognized increasingly, which has brought to light a critical gap in our understanding of diabetes treatment in the context of anti-inflammatory therapeutics. Inflammatory reactions are essential to the development and progression of T2DM. The NLRP3 inflammasome, along with its downstream inflammatory factors, is a key mediator of these responses. Recent data underscore the significance of Interleukin- 1β (IL-1β) in instigating and sustaining inflammation-related organ dysfunction in T2DM. Consequently, factors governing NLRP3 activation and IL-1β expression emerge as potential therapeutic targets. Here, we aim to examine one such therapeutic agent, colchicine, which can potentially manage inflammation associated with T2DM. As an anti-inflammatory medicine, colchicine can inhibit the assembly and activation of the NLRP3 inflammasome via various mechanisms, thereby mitigating inflammation. In this context, the study discusses the mechanisms that link metabolic disorders with the onset of chronic inflammation, evaluates clinical studies and trials that investigate the efficacy and safety of colchicine, as well as discusses its benefits and limitations as an anti-inflammatory therapy in T2DM. The goal is to provide a clear framework for understanding the role of colchicine in the therapeutic landscape of T2DM, potentially leading to novel approaches for managing the disease.

Introduction: Type 2 Diabetes Mellitus (T2DM) is the most prevalent form of hyperglycemia, often coexisting with Non-Alcoholic Fatty Liver Disease (NAFLD), as both share disrupted glucose and lipid metabolic pathways. The study aimed to explore the antidiabetic and hepatoprotective potential of active phytoconstituents from Tinospora cordifolia, Phyllanthus niruri, and Picrorhiza kurroa, focusing on their interaction with GPR120 and GPR 40 receptors through network pharmacology and molecular docking approaches.

Method: A combined extract of T. cordifolia, P. niruri, and P. kurroa was prepared following the Ayurvedic pharmacopoeia standards. Phytoconstituents were identified using High-Performance Thin-Layer Chromatographic (HPTLC) and mass spectroscopy. Network pharmacology analysis predicted mechanisms of action involving PI3-kinase, Protein Kinase C, and PI3K-Akt signaling pathways, targeting GPR120 and GPR40. Molecular docking was conducted for 31 identified compounds, and pharmacokinetic (ADMET) properties of the key hits were evaluated.

Results: Molecular docking identified six compounds with strong binding affinities to GPR 120 and 40. Among these, ferulic acid, caffeic acid, and cinnamic acid exhibited significant binding to GPR40 with docking scores of -10.68, -9.991, and -7.580 kcal/mol, respectively. Similarly, veronicoside, malic acid, and corilagin demonstrated strong interaction with GPR120, with docking scores of -8.95, -7.32, and -9.21 kcal/mol. The combined extract contained cinnamic acid and corilagin as major phytoconstituents, supported by favourable ADMET properties. The analysis highlighted their role in modulating glucose and lipid metabolism via key signaling pathways, corroborating their antidiabetic and hepatoprotective potential.

Conclusion: his study identifies cinnamic acid and corilagin as promising candidates for natural therapeutics targeting T2DM and NAFLD. The translational potential of T. cordifolia, P. niruri, and P. kurroaprovide further experimental validation to confirm their clinical efficacy in modulating metabolic pathways.

Diabetic wounds are a class of chronic wounds that exhibit significant healing abnormalities due to dysregulated cytokines, growth factors, and unique cellular expressions, currently affecting an estimated 9.1-26.1 million people per year globally. Matrix metalloproteinases (MMPs), angiogenic factors, and inflammatory mediators remain the key determinants for managing diabetic wounds. Vascular endothelial growth factor (VEGF) is one of the most prominent types of growth factors induced during angiogenesis in general and cell proliferation pathways. Chronic hyperglycemia, neuropathy, and inflammation associated with diabetes disorders affect cellular responses, blood circulation, and immunological systems impair normal wound healing. This reduced effectiveness of current management strategies is reflected in the high number of delayed wounds among diabetic patients due to escalated oxidative stress and impaired signaling pathways, which prevent healing, calling for new therapies. MMPs are essential for tissue remodeling, but excess levels of MMPs predispose tissues to matrix degradation and interruption in cell signaling leading thereby prolonging inflammation seen in diabetic wounds. Efficient wound healing requires a balanced relationship regarding matrix metalloproteinases and tissue inhibitors of metalloproteinases (TIMPs). New regenerative solutions, such as stem cells, platelet-rich plasma (PRP), gene therapies, and MMP inhibitors that can re-establish angiogenesis; decrease inflammation; and stimulate growth factor signaling, suggest promising strategies for improved diabetic wound healing. Hyperbaric oxygen therapy allows tissue regeneration and reduces the area of ulceration, bringing other benefits. In the future, therapeutics should focus on multifunctional and responsive strategies that include anti-inflammatory agents, cytokine modulators, and stem cell treatments that exhibit superior efficacy in comparison to conventional therapies when assessed clinically. Novel advanced combination strategies represent a realistic route to targeted therapies that meet clinical needs and have the potential capability for utilizing mechanistic insights, both creative in their implementation of recently developed techniques as well as applied on a broader scale through the evidence-based management across diabetic wounds offering better outcomes and quality of life amongst increasing diabetic commonalities.

Introduction/objective: Kidney diseases cause high morbidity and mortality worldwide. This study investigated the mechanistic effects of Fisetin (FIS) on nephrotoxicity, kidney injury, and nephropathy induced by drugs, toxic chemicals, diabetes, lupus, diet, ureteral obstruction, and ischemic situations.

Methods: To identify pertinent articles published before Oct 1, 2024, a comprehensive electronic search was performed across several databases, including MEDLINE/PubMed, Embase, Cochrane Library, Web of Science, and Scopus. After establishing clear inclusion and exclusion criteria, studies that met the research objectives were selected. Data were extracted and analyzed, documenting study characteristics, methodologies, and biological mechanisms.

Results: Antioxidant benefits were evident with increased levels of endogenous antioxidant enzymes and NQO1, alongside reduced oxidative stress markers such as 8-OHdG and MDA. Enhanced mitochondrial function, including improved respiration, ATP synthesis, and antioxidant capacity, further supported cellular resilience. Anti-inflammatory effects were marked by reduced pro-inflammatory cytokines, macrophage and neutrophil infiltration, and inhibited pathways like NF-κB and MAPK. Anti-apoptotic actions included decreased levels of pro-apoptotic proteins. FIS also reduced fibrotic markers and pathways such as TGF-β/SMAD, mitigating excessive ECM buildup. Additionally, modulation of metabolic pathways was observed, including decreased glucose and lipid profiles and improved insulin sensitivity. Kidney function and structural integrity were preserved with reduced levels of nephrotoxic agents.

Conclusion: Preclinical studies revealed that FIS demonstrates promising protective effects against kidney toxicity, renal injury, diabetes, and lupus-induced nephropathy. However, more clinical studies are needed in this field to determine effective and safe doses.

Diabetes mellitus represents a spectrum of chronic metabolic disorders characterized by elevated blood glucose levels (hyperglycemia), largely due to insulin deficiency or resistance. Type 2 diabetes mellitus (T2DM) is the most prevalent form, accounting for over 90% of diabetes cases globally. Its rising prevalence is a global concern, with projections indicating 783 million cases by 2045. T2DM leads to severe complications, including macrovascular diseases like cardiovascular events and microvascular issues such as retinopathy and neuropathy. Despite extensive research, the molecular mechanisms underlying T2DM are not fully understood. However, advancements in omics technologies, including genomics, proteomics, and metabolomics, have revolutionized diabetes research, notably in the following areas: ▪ The advent of single-cell sequencing has revealed cellular heterogeneity and dynamic changes during T2DM progression, paving the way for precision medicine approaches in diabetes research. ▪ Liquid chromatography-mass spectrometry (LC-MS)-based proteomics and metabolomics approaches have transformed T2DM research by enabling the discovery of early detection biomarkers, providing insights into key disease mechanisms and metabolic pathways, and facilitating the identification of novel therapeutic targets. Despite challenges, integrating multi-omics data holds promise for unravelling the complex molecular networks involved in T2DM. This review explores recent advancements in omics research, its impact on T2DM, and future directions in the field.

Diabetes mellitus is a major risk factor for chronic kidney disease (CKD) and accelerates kidney function decline, leading to end-stage renal disease. In addition, patients with CKD are at elevated risk of developing cardiovascular disease with its manifestations as coronary artery disease, heart failure, arrhythmias, and sudden cardiac death through the cardiorenal connection. An online regional and international expert panel of cardiologists, nephrologists, and diabetologists convened in November 2021 to obtain a broad perspective on the intersection of diabetes mellitus, CKD, and cardiovascular disease and identified treatment gaps that can help address the unmet needs of the patients in the Middle East region. The current review article summarizes the epidemiology, pathophysiology, diagnosis, and treatment options of CKD in diabetes and discusses the currently available treatment options to reduce morbidity and mortality in this high-risk population. The panel discussed the roles of clinical specialties and how to simplify the patient journey.

Wound healing is a complex process involving various cellular and molecular events aimed at restoring tissue integrity. Growth factors play a pivotal role in orchestrating these events by regulating cell migration, proliferation, differentiation, and extracellular matrix synthesis. Several growth factors have been identified as crucial mediators of wound healing, including PDGF, TGF-β, VEGF, FGF, and EGF. PDGF is released by platelets upon injury and stimulates the migration and proliferation of fibroblasts and smooth muscle cells, promoting the formation of granulation tissue. TGF-β regulates various aspects of wound healing, including inflammation, collagen deposition, and tissue remodeling. VEGF promotes angiogenesis, facilitating the formation of new blood vessels to supply oxygen and nutrients to the healing tissue. FGF stimulates fibroblast proliferation and angiogenesis, contributing to tissue regeneration. EGF promotes the migration and proliferation of epithelial cells, aiding in the re-epithelialization of the wound. These growth factors act in a coordinated manner to promote each phase of wound healing, including hemostasis, inflammation, proliferation, and remodeling. Dysregulation of growth factor expression or signaling can impair the healing process, leading to chronic wounds or excessive scar formation. Understanding the roles of growth factors in wound healing has led to the development of therapeutic strategies aimed at enhancing wound repair.

Background: Hypoglycemia is a complication that can disrupt the continuity of therapy for Type 2 Diabetes Mellitus (T2DM) patients. Therefore, ambulatory T2DM patients need supportive treatment to ensure the safety of their medication. Currently, health workers lack a standardized reference for assessing the risk of hypoglycemia in these patients. Therefore, this study aimed to determine, validate, and develop a prediction score of risk factors influencing hypoglycemia in T2DM patients.

Methods: The psychometric properties method was used in this study design, including item development, content validity, criterion validity, and construct validity. During the process of item development, Focus Group Discussions (FGDs) with experts were used. Known predictors were then validated through panelists' content assessment. Risk factors for hypoglycemia from item development and content validation were tested for criterion and construct validation using a case-- control method.

Results: Eight significant predictors caused hypoglycemia, including insulin use, SU use, insulin-- SU combination use, CKD, diabetic neuropathy, uncontrolled blood glucose, >5-year DM duration, and history of severe hypoglycemia, and the total score of risk factors was 24. The categories were defined as follows: scores of 0-8 as low-risk, 9-16 as moderate-risk, and 17-24 as high-risk. There was a positive linear relationship between the total score and risk category (p<0.05; r²: 0.959).

Conclusion: This risk factor and score prediction model can be used by health workers in clinical practice to predict the risk of ambulatory hypoglycemia in T2DM patients because it meets content, criterion, and construct validity.

Background: Eriobotrya japonica Lindl, also known as loquat, is a subtropical fruit tree widely used in traditional Chinese medicine for thousands of years to treat many diseases such as asthma and chronic cough. Traditional healers also use it for weight reduction. In our present study, we validated the impact of E. japonica leaf extract on body weight, glycemic control, and lipid profile.

Methods: The anti-obesity, anti-diabetic, and antihyperlipidemic effects of E. japonica leaf extract were screened in high-fat diet-fed rats. After treatment with different E. japonica leaf extract concentrations, body weight, blood glucose levels, HBA1c, and lipid profile were determined.

Results: The high-fat diet group treated with Loquat leaf extract >= 200 mg/ml/kg showed significant weight loss and a beneficial lipid marker profile. However, the glycemic markers were not significantly different.

Conclusion: The findings demonstrate that E. japonica leaf extract at doses of ≥200 mg/kg significantly reduces body weight and improves lipid markers in HFD-fed rats. However, glycemic markers such as blood glucose and HbA1c were not significantly affected. These results highlight the potential of E. japonica as a natural weight loss and lipid control aid, warranting further investigation into its mechanisms and clinical applicability.