Peripheral Neuropathy Research Articles

The Application of Kinesin Inhibitors in Medical Issues.

Kinesins are a group of motor proteins in charge of several crucial functions in the cell. These proteins often bind to microtubules and perform their functions using the energy produced by ATP hydrolysis. One function of mitotic kinesin, a subclass of kinesin that is expressed during cell division at the mitotic phase, is to create the mitotic spindle. Uncontrolled cell growth is one trait of cancerous cells. Traditional anticancer medications still used in clinics include taxanes (paclitaxel) and vinca alkaloids (vincristine, vinblastine), which interfere with microtubule dynamics. However, because non-dividing cells like post-mitotic neurons contain microtubules, unwanted side effects like peripheral neuropathy are frequently found in patients taking these medications. More than ten members of the mitotic kinesin family play distinct or complementary roles during mitosis. The mitotic kinesin family's KSP, or Eg5, is regarded as its most dramatic target protein. The current work systematically reviews the use of kinesin inhibitors in the medical field. The challenges of KSP and the practical solutions are also examined, and the outcomes of the previous works are reported. The significant gaps and shortcomings of the related works are also highlighted, which can be an onset topic for future works.

The effects of multisensory exercises on balance control in people with diabetic peripheral neuropathy: a narrative review

AbstractThis study aimed to examine the impact of multisensory exercises on balance control in people with diabetic peripheral neuropathy (DPN). Articles on multisensory balance training for individuals with DPN were discovered in MEDLINE, Scopus and Web of Science databases through targeted key words. Moreover, this review examined the impact of multisensory balance training in isolation or in conjunction with other exercises, using outcome measures that assess balance attributes. A narrative review encompassed seven research studies as corroborating evidence. Six randomised controlled trials (RCTs) and one non‐RCT were eligible, including 212 participants. The results supported our assumption that multisensory exercise could enhance balance in people with DPN. This review suggests that multisensory exercises could aid in enhancing balance control in individuals with DPN. Nevertheless, additional research is needed to identify the most beneficial multisensory exercises for enhancing balance in individuals with varying levels of DPN severity and disability.

Synergistic effect of Wharton's jelly-derived mesenchymal stem cells and insulin on Schwann cell proliferation in Charcot-Marie-Tooth disease type 1A treatment

Charcot-Marie-Tooth disease type 1A (CMT1A) is a demyelinating disease caused by PMP22 duplication and an exceedingly rare hereditary peripheral neuropathy, with an incidence of 1 in 2500. Currently, no cure exists for CMT1A; however, various therapeutic approaches are under development. Considering the known therapeutic effects of mesenchymal stem cells (MSCs) and the relation of blood sugar levels with nerve damage in CMT, this study aimed to confirm the therapeutic effects of MSCs and insulin on CMT, using both in-vitro and in-vivo models. CMT1A in-vitro models were exposed to Wharton's jelly-derived MSCs (WJ-MSCs) or insulin, and the resulting proliferation changes were measured. CMT1A mice were treated with WJ-MSCs or insulin, and their phenotypic changes were observed. We observed improvements in myelination of Schwann cells in vitro and motor function in vivo. Insulin also showed therapeutic efficacy by promoting Schwann cell proliferation. Furthermore, combination therapy using insulin and WJ-MSCs was more effective than WJ-MSCs or insulin alone. Insulin promoted the proliferation of Schwann cells and WJ-MSCs through activation of the ATK and PI3K-MAPK signaling pathways. Overall, this study is the first to confirm the therapeutic efficacy of WJ-MSCs and insulin in CMT1A, and their synergistic effect without causing insulin resistance.

The role of novel inflammation-associated biomarkers in diabetic peripheral neuropathy

The role of novel inflammation-associated biomarkers in diabetic peripheral neuropathy

Risk factors associated with overactive bladder severity in patients with type 2 diabetes.

The prevalence of overactive bladder (OAB) is known to be higher in patients with type 2 diabetes (T2DM) however there are not many studies about specific risk factors contributing to its progression among diabetes mellitus (DM) patients, so this study aimed to investigate the risk factors specific to DM that influence the progression of OAB in Syrian population. This cross-sectional study was carried out at five endocrinology centers situated in four Syrian provinces: Damascus, Aleppo, Homs, Hama, and Latakia. The study comprised patients who were diagnosed with both T2DM and OAB and had visited these centers from March 2020 and February 2024. The Arabic version of the OAB Symptom Score (OABSS) scale was used to categorize the participants based on the severity score into two groups: the mild OAB group and the moderate-severe OAB group. A logistic analysis was conducted to assess the risk factors associated with the progression of OAB among patients with diabetes. Among the 186 patients diagnosed with both DM and OAB, significant distinctions were found between the two groups concerning the severity of OAB, age, duration of diabetes, symptomatic diabetic peripheral neuropathy (DPN), and ankle reflex (p < 0.05). Furthermore, a multivariate analysis revealed that age (odds ratio [OR] 1.07, 95% confidence interval [CI] 0.68-1.58), duration of diabetes (OR 2.14, 95% CI 1.75-3.74), and symptomatic DPN (OR 2.47, 95% CI 1.17-3.54) independently acted as risk factors for the advancement of OAB. The progression of OAB in Syrian patients with diabetes is closely associated with the severity of DM. Factors such as age, duration of diabetes, and symptomatic DPN are independent predictors of the severity of OAB. Patients who experience symptomatic DPN are at an increased risk of developing OAB.

Predictive Factors of Chemotherapy-Induced Peripheral Neuropathy in Breast Cancer: A Decision Tree Model Approach

PURPOSE Chemotherapy-induced peripheral neuropathy (CIPN) poses a substantial challenge in breast cancer (BC) chemotherapy, affecting the patient's quality of life. Recent studies have focused on exploring predictors and patterns of CIPN occurrence. We aimed to develop a prediction model for CIPN occurrence using a classification and regression tree (CART) algorithm. METHODS In this prospective study of 170 patients with BC undergoing chemotherapy, patient-reported adaptation of the Common Terminology Criteria for Adverse Events version 4.0 was used to assess CIPN occurrence. Multivariable analysis using the CART model was tuned using 10-fold cross-validation to identify baseline predictors for CIPN throughout chemotherapy. A receiver operating characteristic curve analysis was conducted for the CART model. A multivariable logistic regression was conducted from the variables included in the CART model to assess the strength and direction of the association. RESULTS The prevalence of CIPN was 64.7% (n = 110). The most decisive predictor of CIPN occurrence in the CART model was the subject's C-reactive protein (CRP) level. CRP level &gt;3.91 mg/dL, BMI &gt;21.85 kg/m 2 , and a marital status of unmarried have predicted a probability of 100% in CIPN occurrence. The CART model showed an accuracy of 65.9%, sensitivity of 51.7%, specificity of 73.2%, and an area under the curve of 0.705. A CRP level of &gt;3.91 mg/dL and a neutrophil-to-lymphocyte ratio (NLR) of &gt;2.82 are significantly associated with the occurrence of CIPN (odds ratio [OR], 2.01 [95% CI, 1.01 to 4.01]; P = .046, OR, 2.09 [95%, CI, 1.02 to 4.24]; P = .042, respectively). CONCLUSION Baseline CRP, NLR, BMI level, and marital status are significant predictors of CIPN occurrence throughout chemotherapy. Our CART model was better at ruling out individuals who would not experience CIPN. The CART model may provide insight into the future development of individualized patient care and prevention strategies.

Diabetic Peripheral Neuropathy and Glycemia Risk Index in Type 2 Diabetes: A Cross-Sectional Study

Diabetic Peripheral Neuropathy and Glycemia Risk Index in Type 2 Diabetes: A Cross-Sectional Study

Hydrogen sulfide alleviates neural degeneration probably by reducing oxidative stress and aldose reductase expression

AbstractWe investigated the potential role of hydrogen sulfide (H2S) as a novel therapy for diabetic peripheral neuropathy in diabetic rats. A single dose of streptozotocin (60 mg/kg) was applied to the rats for the diabetic rat models. Sodium bisulfide (50 μmol/kg/d) was injected intraperitoneally daily for 2 weeks as H2S treatment. Electromyogram, haematoxylin eosin staining, transmission electron microscopy, western blotting and enzyme‐linked immunosorbent assay were then performed. H2S treatment did not affect body weights, blood glucose levels or liver function of diabetic rats, while the creatine levels of the H2S‐treated diabetic rats decreased compared with the diabetic control rats. H2S treatment for 2 weeks did not affect the sciatic nerve conduction velocity of the diabetic rats. However, H2S treatment relieved neurons loss and cell atrophy of dorsal root ganglion, and axon degeneration of sciatic nerve in diabetic rats. Serum super oxide dismutase (SOD) levels and SOD2 levels in the sciatic nerve of diabetic rats were lower than the non‐diabetic rats but were restored after H2S treatment. Serum and sciatic nerve homogenate malondialdehyde and aldose reductase expression were higher in diabetic rats but decreased significantly after H2S treatment. Our study revealed that H2S alleviates neural degeneration in diabetic rats probably by reducing oxidative stress and downregulating aldose reductase expression.

Prevalence and predictors of chemotherapy-induced peripheral neuropathy among female breast cancer patients undergoing chemotherapy in Lagos

Prevalence and predictors of chemotherapy-induced peripheral neuropathy among female breast cancer patients undergoing chemotherapy in Lagos

Cardiovascular Autonomic Dysfunction Before and After Chemotherapy in Cancer Patients.

Complications that occur during cancer therapy have emerged as a major contributor to the poor quality of life experienced by cancer patients as they live longer due to improved treatments. Many studies have investigated chemotherapy-induced peripheral neuropathy, but few have investigated the autonomic nervous system. Cardiovascular autonomic dysfunction (CAD) contributes to the distressing symptoms experienced by cancer patients, and it is also related to poor treatment outcomes. CAD has a multifactorial etiology in patients with cancer: it can be caused by the cancer itself, chemotherapy or radiation therapy, or other comorbidities. Its symptoms are nonspecific, and they include orthostatic hypotension, resting tachycardia, dizziness, chest tightness, and exertional dyspnea. It is important to suspect CAD and perform therapeutic interventions in a clinical context, because a patient who is more frail is less like to endure the treatment process. The quality of life of patients receiving active cancer treatments can be improved by evaluating the risk of CAD before and after chemotherapy, and combining both nonpharmacological and pharmacological management. Here we review the prevalence, pathogenesis, diagnosis, and treatment of CAD, which is the most common and a sometimes serious symptom in cancer patients.

Relationship between autonomic and peripheral neuropathies and cardiovascular outcomes in diabetes

This review explores the complex relationship between diabetic neuropathy and cardiovascular disease (CVD). Neuropathy, a common complication of type 1 and type 2 diabetes, is divided into autonomic and peripheral types, each impacting cardiovascular health. Cardiovascular autonomic neuropathy, a form of autonomic neuropathy, is associated with various CVD complications, including arrhythmias, impaired nocturnal blood pressure regulation, and increased mortality. The prevalence of cardiovascular autonomic neuropathy varies depending on the type and duration of diabetes and is influenced by factors like glycemic control and metabolic stress. Peripheral polyneuropathy, which is often linked to diabetic foot disease, is also correlated with elevated CVD risk; research suggests shared pathophysiological mechanisms between peripheral neuropathy and cardiovascular conditions. Screening for neuropathies using tools like the Michigan Neuropathy Screening Instrument and heart rate variability analyses can facilitate early detection of CVD risk. Additionally, emerging technologies, like deep learning models, have demonstrated promise in detecting early cardiovascular patterns associated with autonomic neuropathy through electrocardiogram analysis. These findings underscore the value of integrating novel diagnostic approaches for early intervention. As CVD represents a leading cause of death among patients with diabetes, this article emphasizes the need for thorough assessment and proactive management of neuropathy to mitigate cardiovascular risk. The review recommends a multidisciplinary approach to diabetes care, including early screening, accurate risk stratification, and targeted therapeutic strategies to prevent or slow the progression of CVD in patients with autonomic and peripheral neuropathies. Further research is warranted to clarify the optimal intervention strategies for reducing CVD risk in these populations.

An Integrative Review of the Effectiveness of Duloxetine Use in Cancer Patients Receiving Chemotherapy

Purpose: The objective of this Integrative Review of Literature (IRL) was to assess the efficacy of duloxetine in the management of chemotherapy-induced peripheral neuropathy (CIPN) among cancer patients. Peripheral neuropathy associated with chemotherapy manifests as symptoms such as tingling, burning, numbness, weakness, or pain in the hands and feet. The detrimental and, in some cases, debilitating impact of CIPN on individuals undergoing cancer treatment underscores the significance of investigating the effectiveness of duloxetine as part of the treatment plan for this condition. Procedure: A comprehensive literature search was performed to identify peer-reviewed journal articles on the effectiveness and safety of the use of duloxetine for the treatment of CIPN. The search was conducted using two electronic databases: CINHAL and PubMed. Additional supplemental sources, including the American Cancer Society, American Society of Clinical Oncology, Google Scholar, and Medline, were used to compile additional information for review. Results: The strengths and weaknesses of each article were reviewed utilizing the Johns Hopkins Research Appraisal tool. A data synthesis review exhibited good to high-quality articles with a range of evidence, including Level I, Level II, and Level III. Research yielded positive outcomes in reducing pain, increasing quality of life, and reducing the severity of symptoms for both physical and mental health with Duloxetine treatment. Results showed effectiveness and tolerability in the treatment of CIPN. Adding Duloxetine to the CIPN treatment plan positively impacted pain management and enhanced quality of life (QoL). Conclusion: Studies revealed that Duloxetine, as a pharmacologic intervention, resulted in a reduction in pain and an improvement in the quality of life (QoL) for patients experiencing chemotherapy-induced peripheral neuropathy (CIPN). Duloxetine demonstrated enhanced effectiveness, safety, and tolerability in its outcomes. Notably, the American Society of Clinical Oncology has designated Duloxetine as the standard of care for CIPN. Given its status as the standard of care, there is a higher likelihood of favorable considerations for Duloxetine by insurance companies.

Phase II Trial of Enfortumab Vedotin in Patients With Previously Treated Advanced Head and Neck Cancer.

Despite advances in immunotherapy, unresectable recurrent/metastatic head and neck cancer (HNC) carries a poor prognosis, and effective treatments are needed. As nectin-4 is widely expressed in HNC, enfortumab vedotin (EV), a nectin-4-directed antibody-drug conjugate, was explored in HNC in EV-202 (ClinicalTrials.gov identifier: NCT04225117). This open-label, multicohort, phase II study evaluated intravenous EV 1.25 mg/kg on days 1, 8, and 15 of each 28-day cycle. In the HNC cohort, eligible patients had recurrent/metastatic HNC and had received platinum-based therapy for locally advanced/metastatic disease and a PD-1/PD-L1 inhibitor. The primary end point was investigator-assessed confirmed objective response rate (ORR) per RECIST version 1.1. Secondary end points were investigator-assessed duration of response (DOR), disease control rate (DCR), and progression-free survival (PFS); overall survival (OS); and safety. The primary analysis included 46 patients; all received EV (median follow-up, 9.3 months). Most patients (52.2%) had ≥3 previous lines of systemic therapy in the metastatic setting. Confirmed ORR was 23.9%, DCR was 56.5%, and median DOR was not reached (median DOR was 9.4 months at a later data cutoff [median follow-up, 11.3 months]). Median PFS and OS were 3.9 and 6.0 months, respectively. Treatment-related adverse events (TRAEs) occurring in >20% of patients were alopecia (28.3%), fatigue (26.1%), and peripheral sensory neuropathy (23.9%). Sixteen patients (34.8%) experienced grade ≥3 TRAEs; anemia and decreased neutrophil count occurred in ≥1 patient (both n = 2; 4.3%). EV demonstrated antitumor activity in heavily pretreated HNC. Safety was consistent with the known safety profile of EV; no new safety signals were identified. These data support further evaluation of EV for advanced HNC not amenable to definitive local therapy.

Daphnetin Protects Schwann Cells Against High-Glucose-Induced Oxidative Injury by Modulating the Nuclear Factor Erythroid 2-Related Factor 2/Glutamate–Cysteine Ligase Catalytic Subunit Signaling Pathway

Diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus, is primarily characterized by damage to Schwann cells caused by oxidative stress under hyperglycemic conditions. Recently, we demonstrated the ability of coumarin-rich Ficus formosana Maxim. to alleviate DPN in ovariectomized diabetic mice. However, the underlying mechanisms remain unclear. In this study, we established an in vitro DPN model using RSC96 Schwann cells exposed to high glucose levels. Daphnetin, a natural coumarin found abundantly in Ficus formosana Maxim., was co-incubated with Schwann cells in a high-glucose medium to investigate its protective effects against DPN. The free radical scavenging capacity of daphnetin was evaluated, along with assessments of cell viability, apoptosis, H2O2 levels, and the expression of proteins by the nuclear factor erythroid 2-related factor 2 (Nrf2)/glutamate–cysteine ligase catalytic subunit (GCLC) pathway in RSC96 Schwann cells. The results showed that daphnetin was non-toxic within the tested concentration range of 6.25 μM to 50 μM in RSC96 Schwann cells. Moreover, daphnetin significantly improved cell viability, exhibited strong antioxidant activity, reduced H2O2 levels, and regulated the Nrf2/GCLC pathway protein expressions in RSC96 cells cultured in high-glucose medium. Additionally, daphnetin influenced apoptosis-related proteins by decreasing the expression levels of Bax and Caspase 3, while increasing the Bcl-2 expression level in high-glucose-treated RSC96 cells. These findings suggest that daphnetin may alleviate oxidative stress induced by high glucose levels through activation of the Nrf2/GCLC pathway and inhibition of Schwann cell apoptosis, underscoring its potential as a therapeutic agent for DPN.

P66shc deficiency attenuates high glucose-induced autophagy dysfunction in Schwann cells.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Lesión bilateral de ligamento cruzado craneal y neuropatía periférica en un canino Golden Retriever con hipotiroidismo: Reporte de caso

The case of a 6 -year -old female Golden Retriever is presented. She was limping in the left posterior limb. A 4/4 grade lameness, pain by palpating the knee, and a negative drawer test, but positive tibial compression was identified. No proprioceptive deficit or signs compatible with lesions joints in X-rays images were found. There was no response to treatment with Meloxicam and Tramadol and because a suspicion of partial rupture of the cranial cruciate ligament, the transposition of tibial tuberosity (TTT) procedure was chosen. The patient returned with lameness in the right hind limb right nine months later and after ruling out other causes of limp, the TTT was successfully performed in the affected limb. However, 18 months later he developed signs of peripheral neuropathy. Metabolic, infectious and hormonal profile analyses revealed increased serum alkaline phosphatase, decreased thyroxine (free T4) and thyroid-stimulating hormone (TSH) values within normal ranges according to the reference laboratory. Based on the patient's history and laboratory findings, the diagnosis was hypothyroidism, and the decision was made to supplement the patient with sodium levothyroxine. Remission of the nervous symptoms was observed 45 days after treatment.

Neuroprotective effect of chelidonic acid through oxidative stress reduction in paclitaxel-induced peripheral neuropathy in rats.

The present study evaluated the effect of chelidonic acid on paclitaxel-induced neuropathy in male Wistar rats. Neuropathy was induced by administering paclitaxel (2mg/kg, i.p.) on 0, 2, 4, and 6days of the protocol. Chelidonic acid treatment (at doses of 10, 20, and 40mg/kg orally, for 21days) was initiated simultaneously with paclitaxel administration. After completion of the protocol, mechanical allodynia, hyperalgesia, and thermal hyperalgesia were measured. Additionally, nerve conduction velocity was assessed. The study investigated inflammatory cytokines, oxidative stress, and histological changes in the sciatic nerve. Furthermore, the Nrf2 was measured, and the protein expression of pAMPK and HIF-1α was assessed using western blotting. The results showed that chelidonic acid significantly normalized mechanical allodynia, hyperalgesia, and thermal hyperalgesia. It also led to a significant improvement in motor and sensory nerve conduction velocity and reduced oxidative stress compared with paclitaxel alone. Inflammatory markers such as TNF-alpha, IL-6, and IL-1β concentrations, as well as nitric oxide and C-reactive protein, were significantly decreased in the chelidonic acid-treated group. Histopathological examination revealed reduced neuronal damage, demyelination, and leukocyte infiltration with chelidonic acid treatment. Chelidonic acid treatment also resulted in a considerable rise in Nrf2 levels (p < 0.001) and increased protein expression of pAMPK in the sciatic nerve. Conversely, HIF-1α expression was significantly declined in the chelidonic acid treatment. Overall, the findings suggest that chelidonic acid treatment attenuates paclitaxel-induced neuropathic pain.

Ulnar Compression Neuropathy Secondary to Ganglion Cyst at the Elbow Joint: A Case Report

Ulnar neuropathy is a common peripheral neuropathy, with cubital tunnel compression being the second most frequent upper extremity compression syndrome. Ganglion cysts, though rare, can contribute to ulnar nerve compression in the cubital tunnel. Here, we present a case of a 62-year-old farmer with longstanding diabetes and dyslipidemia who experienced progressive pain and numbness in his medial fingers, exacerbated by elbow flexion. Initially misdiagnosed and treated for Hansen’s disease. Clinico-radiological evaluation revealed a multiloculated cystic lesion in the posteromedial aspect of his left elbow, compressing the ulnar nerve. Surgical excision of the ganglion cyst alleviated symptoms, though residual motor deficits persisted postoperatively. This case underscores the importance of considering ganglion cysts in the differential diagnosis of cubital tunnel syndrome, highlighting the diagnostic challenges and therapeutic considerations in managing this rare etiology.

Molecular Insights and Pharmacotherapy of Diabetic Neuropathy

Background: Diabetes mellitus is a chronic disorder of energy metabolism caused by lack or decrease in the effectiveness of insulin, and is characterised by an abnormally elevated blood glucose concentrations and the development of macrovascular, microvascular and/or neuropathic complications. Diabetic neuropathy (DN) is one of the most debilitating outcomes of diabetes mellitus, and may cause pain, decreased mobility as well as amputation. Diabetes can damage the peripheral nervous system (PNS), through the induction of de-myelination in neurones, precipitated by chronic hyperglycaemia-induced oxidative stress, and causing a condition that involves the upper and lower limbs. Objective: The study discussed the risk factors for insulin resistance and pre-diabetes, type II diabetes mellitus and vascular complications, cellular and molecular basis of DN, physiopathological mechanisms, and the pharmacological treatment of DN. Method: The study examined journal articles and standard textbooks, as it relates to diabetes mellitus and its complications. Search for articles on DN was carried out in the literature. These were identified and reviewed for selection using chemical abstracts service, pubmed, google scholar, crossreference, web of science, pubmed central free article, and scopus. The key words used for search were: diabetic neuropathy; diabetic peripheral neuropathy; peripheral neuropathy; microvascular complications of diabetes mellitus; and neuromuscular complications of diabetes mellitus. Result &amp; Discussion: Two hundred and fifty (250) articles and other works were identified, while ninety-seven (97) articles and non-journal materials were extracted and reviewed, taking into account the criteria for selection. Studies done in the last 4.5 decades were included, while works written on other languages, outside English were excluded. Findings indicate that DN is a complex disorder that affects the peripheral and/or cranial nerves, which is caused by unattended or poorly attended, long-term increase in blood glucose concentrations. It relatively manifests early, affecting a significant proportion of the micro-blood vessels in the middle-aged and elderly diabetic patients. DN causes numbness, loss of sensation, and sometimes pain in the feet, legs, arms or hands. Hyperglycaemia causes the activation and inhibition of several molecular pathways that are crucial for homeostasis in neuronal and neuroglial cells. Conclusion: DN is the commonest complication of diabetes mellitus. It has no known definitive therapy. Treatment is essentially symptomatic with huge economic and psychological burden, hence the rationale for a cost effective and targeted therapies. Achieving euglycaemia using anti-diabetic regimens (i.e., insulin and oral hypoglycaemic agents), foot care, changes in feeding habits and lifestyle modification are critical to holistically address the problem.

Extraction and evaluation for anti-diabetic effects of some Indian plant extracts

Diabetes is a metabolic disease associated with changes in the structure and function of several biological systems. The main cause of tissue injury is persistent hyperglycaemia. The past 20 years have seen increased expansion of the harmful effects of persistent hyperglycaemia, even if peripheral neuropathy and small and large vascular disease can also be used to explain diabetes-related organ failure. Liophyllum decastes, Butea monosperma, and Opuntia dillenil fruit extracts were shown to pass phytochemical testing. The study findings of Butea Monosperma, Opuntia dillenil, and Liophyllum decastes distilled (150 mg/kg) and (300 mg/kg) on STZ-tempted DM rats were paired with Glibenclamide. The glucometer method, serum and urine analysis, as well as factors including body weight, food consumption, glucose levels, and biochemical analysis, were used to determine the blood sugar rankings. Liophyllum decastes fungus fruit, Opuntia dillenil Planned fruit, and distilled Butea monosperma leaves all have anti-diabetic properties for diabetics.