Displaying publications 61 - 71 of 71 in total

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  1. Ismail CAN, Suppian R, Ab Aziz CB, Long I
    Neuropeptides, 2020 Feb;79:102003.
    PMID: 31902597 DOI: 10.1016/j.npep.2019.102003
    The complications of diabetic polyneuropathy (DN) determines its level of severity. It may occur with distinctive clinical symptoms (painful DN) or appears undetected (painless DN). This study aimed to investigate microglia activation and signalling molecules brain-derived neurotrophic factor (BDNF) and downstream regulatory element antagonist modulator (DREAM) proteins in spinal cord of streptozotocin-induced diabetic neuropathy rats. Thirty male Sprague-Dawley rats (200-230 g) were randomly assigned into three groups: (1) control, (2) painful DN and (3) painless DN. The rats were induced with diabetes by single intraperitoneal injection of streptozotocin (60 mg/kg) whilst control rats received citrate buffer as a vehicle. Four weeks post-diabetic induction, the rats were induced with chronic inflammatory pain by intraplantar injection of 5% formalin and pain behaviour responses were recorded and assessed. Three days later, the rats were sacrificed and lumbar enlargement region of spinal cord was collected. The tissue was immunoreacted against OX-42 (microglia), BDNF and DREAM proteins, which was also quantified by western blotting. The results demonstrated that painful DN rats exhibited increased pain behaviour score peripherally and centrally with marked increase of spinal activated microglia, BDNF and DREAM proteins expressions compared to control group. In contrast, painless DN group demonstrated a significant reduction of pain behaviour score peripherally and centrally with significant reduction of spinal activated microglia, BDNF and DREAM proteins expressions. In conclusions, the spinal microglia activation, BDNF and DREAM proteins correlate with the pain behaviour responses between the variants of DN.
    Matched MeSH terms: Diabetic Neuropathies/metabolism
  2. Nawfar SA, Yacob NB
    Singapore Med J, 2011 Sep;52(9):669-72.
    PMID: 21947144
    INTRODUCTION: Peripheral diabetic neuropathy, which is a cause of increasing morbidity and mortality following foot ulcers and amputations, is a burden to health and the economy. Various adjunct treatments to improve neuropathy have been introduced into the market; one such treatment is monochromatic infrared energy (MIRE) therapy, which claimed to produce promising results. This study aimed to evaluate the effects of MIRE on diabetic feet with peripheral neuropathy.
    METHODS: A randomised controlled, single-blinded study was conducted at Hospital Universiti Sains Malaysia from February 2008 to October 2008. A total of 30 feet from 24 patients were studied. Neuropathy was screened using the Michigan neuropathy scoring instrument, followed by an assessment of the current perception threshold using a neurometer at frequencies of 2,000 Hz, 250 Hz and 5 Hz. The feet were randomised to receive either daily MIRE or sham treatment for a total of 12 treatments. Each foot was then reassessed using the neurometer at six weeks and three months following treatment.
    RESULTS: The data obtained was analysed using a non-parametric test to compare the pre- and post-treatment groups. No significant difference was found between the neuropathic foot of diabetic patients in both the MIRE and sham groups.
    CONCLUSION: No improvement of neuropathy was observed following MIRE treatment in the neuropathic feet of diabetic patients.
    Matched MeSH terms: Diabetic Neuropathies/radiotherapy*
  3. Ismail CAN, Suppian R, Ab Aziz CB, Long I
    J Mol Neurosci, 2021 Feb;71(2):379-393.
    PMID: 32671697 DOI: 10.1007/s12031-020-01661-1
    The pharmacological inhibition of glial activation is one of the new approaches for combating neuropathic pain in which the role of glia in the modulation of neuropathic pain has attracted significant interest and attention. Neuron-glial crosstalk is achieved with N-methyl-D-aspartate-2B receptor (NMDAR-2B) activation. This study aims to determine the effect of ifenprodil, a potent noncompetitive NMDAR-2B antagonist, on activated microglia, brain-derived neurotrophic factors (BDNF) and downstream regulatory element antagonist modulator (DREAM) protein expression in the spinal cord of streptozotocin-induced painful diabetic neuropathy (PDN) rats following formalin injection. In this experimentation, 48 Sprague-Dawley male rats were randomly selected and divided into four groups: (n = 12): control, PDN, and ifenprodil-treated PDN rats at 0.5 μg or 1.0 μg for 7 days. Type I diabetes mellitus was then induced by injecting streptozotocin (60 mg/kg, i.p.) into the rats which were then over a 2-week period allowed to progress into the early phase of PDN. Ifenprodil was administered in PDN rats while saline was administered intrathecally in the control group. A formalin test was conducted during the fourth week to induce inflammatory nerve injury, in which the rats were sacrificed at 72 h post-formalin injection. The lumbar enlargement region (L4-L5) of the spinal cord was dissected for immunohistochemistry and western blot analyses. The results demonstrated a significant increase in formalin-induced flinching and licking behavior with an increased spinal expression of activated microglia, BDNF and DREAM proteins. It was also shown that the ifenprodil-treated rats following both doses reduced the extent of their flinching and duration of licking in PDN in a dose-dependent manner. As such, ifenprodil successfully demonstrated inhibition against microglia activation and suppressed the expression of BDNF and DREAM proteins in the spinal cord of PDN rats. In conclusion, ifenprodil may alleviate PDN by suppressing spinal microglia activation, BDNF and DREAM proteins.
    Matched MeSH terms: Diabetic Neuropathies/drug therapy*; Diabetic Neuropathies/metabolism
  4. Lim LL, Fu AWC, Lau ESH, Ozaki R, Cheung KKT, Ma RCW, et al.
    Nephrol Dial Transplant, 2019 Aug 01;34(8):1320-1328.
    PMID: 29939305 DOI: 10.1093/ndt/gfy154
    BACKGROUND: Early detection and risk factor control prevent chronic kidney disease (CKD) progression. Evaluation of peripheral autonomic dysfunction may detect incident cardiovascular-renal events in type 2 diabetes (T2D).

    METHODS: SUDOSCAN, a non-invasive tool, provides an age-adjusted electrochemical skin conductance (ESC) composite score incorporating hands/feet ESC measurements, with a score ≤53 indicating sudomotor dysfunction. A consecutive cohort of 2833 Chinese adults underwent structured diabetes assessment in 2012-13; 2028 participants without preexisting cardiovascular disease (CVD) and CKD were monitored for incident cardiovascular-renal events until 2015.

    RESULTS: In this prospective cohort {mean age 57.0 [standard deviation (SD) 10.0] years; median T2D duration 7.0 [interquartile range (IQR) 3.0-13.0] years; 56.1% men; 72.5% never-smokers; baseline ESC composite score 60.7 (SD 14.5)}, 163 (8.0%) and 25 (1.2%) participants developed incident CKD and CVD, respectively, after 2.3 years of follow-up. The adjusted hazard ratios (aHRs) per 1-unit decrease in the ESC composite score for incident CKD, CVD and all-cause death were 1.02 [95% confidence interval (CI) 1.01-1.04], 1.04 (1.00-1.07) and 1.04 (1.00-1.08), respectively. Compared with participants with an ESC composite score >53, those with a score ≤53 had an aHR of 1.56 (95% CI 1.09-2.23) for CKD and 3.11 (95% CI 1.27-7.62) for CVD, independent of common risk markers. When added to clinical variables (sex and duration of diabetes), the ESC composite score improved discrimination of all outcomes with appropriate reclassification of CKD risk.

    CONCLUSIONS: A low ESC composite score independently predicts incident cardiovascular-renal events and death in T2D, which may improve the screening strategy for early intervention.

    Matched MeSH terms: Diabetic Neuropathies/complications; Diabetic Neuropathies/diagnosis*
  5. Ismail CAN, Suppian R, Abd Aziz CB, Haris K, Long I
    Diabetes Metab J, 2019 Apr;43(2):222-235.
    PMID: 30604591 DOI: 10.4093/dmj.2018.0020
    BACKGROUND: This study investigated the role of NR2B in a modulated pain process in the painful diabetic neuropathy (PDN) rat using various pain stimuli.

    METHODS: Thirty-two Sprague-Dawley male rats were randomly allocated into four groups (n=8): control, diabetes mellitus (DM) rats and diabetic rats treated with ifenprodil at a lower dose (0.5 μg/day) (I 0.5) or higher dose (1.0 μg/day) (I 1.0). DM was induced by a single injection of streptozotocin at 60 mg/kg on day 0 of experimentation. Diabetic status was assessed on day 3 of the experimentation. The responses on both tactile and thermal stimuli were assessed on day 0 (baseline), day 14 (pre-intervention), and day 22 (post-intervention). Ifenprodil was given intrathecally for 7 days from day 15 until day 21. On day 23, 5% formalin was injected into the rats' hind paw and the nociceptive responses were recorded for 1 hour. The rats were sacrificed 72 hours post-formalin injection and an analysis of the spinal NR2B expression was performed.

    RESULTS: DM rats showed a significant reduction in pain threshold in response to the tactile and thermal stimuli and higher nociceptive response during the formalin test accompanied by the higher expression of phosphorylated spinal NR2B in both sides of the spinal cord. Ifenprodil treatment for both doses showed anti-allodynic and anti-nociceptive effects with lower expression of phosphorylated and total spinal NR2B.

    CONCLUSION: We suggest that the pain process in the streptozotocin-induced diabetic rat that has been modulated is associated with the higher phosphorylation of the spinal NR2B expression in the development of PDN, which is similar to other models of neuropathic rats.

    Matched MeSH terms: Diabetic Neuropathies/drug therapy; Diabetic Neuropathies/metabolism*
  6. Najafi R, Hosseini A, Ghaznavi H, Mehrzadi S, Sharifi AM
    Brain Res Bull, 2017 May;131:117-122.
    PMID: 28373151 DOI: 10.1016/j.brainresbull.2017.03.013
    OBJECTIVE: Neuropathies are a nerve disorders that caused by diabetes. Neuropathy affects over 50% of diabetic patients. High blood glucose and their toxic byproducts are the main causes for nerve dysfunction. In the present study, we examined the neroprotective effects of cerium oxide (CeO2) nanoparticles in diabetic rats.

    METHOD: Rats divided into four groups: control group, diabetic group, the diabetic group treated with CeO2nanoparticle at a dose of 65mg/kg and diabetic group received CeO2nanoparticle at a dose of 85mg/kg. Diabetes was induced by single intraperitoneal injection of 65mg/kg streptozotocin (STZ). 8 weeks after the induction of diabetes, body weight and pain sensitivity in all groups were measured. The blood sample was collected for biochemical analysis. The dorsal root ganglion (DRG) neurons were isolated for histopathological stain and morphometric parameters studies.

    RESULTS: Reduction of body weight, total thiol molecules (TTM), total antioxidant power (TAP) and ADP/ATP ratio in diabetic rat was reversed by CeO2nanoparticles administration. We showed that lipid peroxidation (LPO) and nociception latency were significantly increased in STZ-treated rats and decreased after CeO2nanoparticles administration. DRG neurons showed obvious vacuole and various changes in diameter, area and the count of A and B cells in STZ-diabetic rat. CeO2nanoparticles improved the histopathology and morphological abnormalities of DRG neurons.

    CONCLUSION: Our study concluded the CeO2nanoparticles have a protective effect against the development of DN.

    Matched MeSH terms: Diabetic Neuropathies/drug therapy*
  7. Rana B, Bukhsh A, Khan TM, Sarwar A, Omer MO, Jamshed SQ
    J Pharm Bioallied Sci, 2017 Apr-Jun;9(2):121-125.
    PMID: 28717335 DOI: 10.4103/jpbs.JPBS_29_17
    AIM: The present study was aimed to highlight the current prescribing pattern of oral hypoglycemia in type 2 diabetes mellitus and to evaluate the therapeutic effectiveness of these therapeutic categories in achieving target glycemic control.

    METHODS: This is a prospective, cross-sectional, observational study of 6 months' duration conducted in a tertiary care hospital of Lahore, Pakistan.

    RESULTS: The current research recruited 145 patients presented in diabetes management center of a tertiary care hospital in Lahore, Pakistan. Mean age of the participants was 50.2 (± 8.5) years. Out of the 145 patients, 63% were females and 37% were males. Most patients were diagnosed to have diabetes within the past 5 years. Diabetes-induced neuropathy was the most common complication (71.7%) among the patients. A large proportion of these patients (70.3%) were also suffering from other comorbidities among which the most common one is hypertension. The average number of prescribed medications was 1.31. Metformin was prescribed to a majority of patients (64%) as monotherapy while 28.96% received combination therapy. Mean glycated hemoglobin (HBA1c) before and after 3 months of treatment was 8.5 (± 2.3) and 8.04 (± 2.1), respectively. Inferential statistics show a strong association between HBA1c and life style modifications and adherence to medication therapy (P = 0.05). However, the correlation between HBA1c and Morisky score and duration of disease was inverse and weak (P = 0.6, 0.4). The t-test values show a small difference between HBA1c values before and after 3 months (t = 0.440 and 0.466, respectively).

    CONCLUSION: Optimization of medication regimen and continuous patient education regarding life style modification and adherence to medication therapy are necessitated to bring HBA1c values near to target.
    Matched MeSH terms: Diabetic Neuropathies
  8. Ismail CAN, Aziz CBA, Suppian R, Long I
    J Diabetes Metab Disord, 2018 Dec;17(2):129-136.
    PMID: 30918846 DOI: 10.1007/s40200-018-0350-x
    Purpose: Diabetic neuropathy is a prolonged symptom of diabetes mellitus that affect a number of diabetes mellitus patients. So far, the variants of diabetic neuropathy, either painful (PDN) or non-painful (or painless, non-PDN) response have distinctive clinical entities. This study aims to determine the effects of oxidative stress parameters and pro-inflammatory factors at spinal cord level of streptozotocin-induced diabetic neuropathy rat model.

    Methods: Thirty Sprague-Dawley rats were randomly assigned to control (non-diabetic), PDN and non-PDN groups (n = 10). The rats were induced with diabetes by streptozotocin injection (60 mg/kg). Tactile allodynia and thermal hyperalgesia were assessed on day 0, 14 (week 2) and 21 (week 3) in the rats. The rats were sacrificed and the spinal cord tissue was collected for the measurement of oxidative stress (malondialdehyde (MDA), superoxide dismutase (SOD) and catalase) and pro-inflammatory markers (interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α)).

    Results: PDN rats demonstrated a marked tactile allodynia with no thermal hyperalgesia whilst non-PDN rats exhibited a prominent hypo-responsiveness towards non-noxious stimuli and hypoalgesia towards thermal input. The MDA level and pro-inflammatory TNF-α was significantly increased in PDN rats whilst catalase was reduced in these rats. Meanwhile, non-PDN rats demonstrated reduced SOD enzyme activity and TNF-α level and increased MDA and catalase activity.

    Conclusion: The changes in oxidative stress parameters and pro-inflammatory factors may contribute to the changes in behavioural responses in both PDN and non-PDN rats.

    Matched MeSH terms: Diabetic Neuropathies
  9. Ng YT, Phang SCW, Tan GCJ, Ng EY, Botross Henien NP, M Palanisamy UD, et al.
    Nutrients, 2020 May 23;12(5).
    PMID: 32456230 DOI: 10.3390/nu12051522
    Chronic hyperglycemia increases oxidative stress, activates inflammatory pathways and reduces nerve growth factor (NGF) among diabetic patients, which contribute to development of diabetic peripheral neuropathy (DPN). Tocotrienol-Rich Vitamin E (Tocovid) possesses potent antioxidant and anti-inflammatory properties which are postulated to target these pathogeneses in order to ameliorate DPN. This study aims to evaluate the effects of Tocovid on nerve conduction parameters and serum biomarkers among diabetic patients. This multicenter, prospective, randomized, double-blind, placebo-controlled clinical trial was conducted on 80 eligible participants. The intervention group (n = 39) was randomly allocated to receive 200 mg of Tocovid twice a day, and the control group (n = 41) received placebo twice a day. At the end of eight weeks, the nerve conduction parameters, as assessed by nerve conduction study, as well as serum biomarkers (NGF, malondialdehyde, vascular cell adhesion molecule 1, tumor necrosis factor receptor 1 and thromboxane B2) were compared between the two groups. Compared to placebo, Tocovid significantly improves the nerve conduction velocities of all nerves (+1.25 m/s, interquartile range [IQR] 3.35, p < 0.001, median nerve; +1.60 m/s, IQR 1.80, p < 0.001, sural nerve; +0.75 m/s, IQR 2.25, p < 0.001, tibial nerve). Meanwhile, the levels of serum NGF were significantly higher in the Tocovid group as compared to placebo at eight weeks post-intervention. Participants receiving Tocovid illustrated highly significant improvement in terms of nerve conduction velocities for all nerves tested after eight weeks of supplementation. In addition, Tocovid supplementation elevated the levels of serum NGF, in which its increase is postulated to reflect enhanced neuronal functions. This novel finding suggests that Tocovid could be a disease-modifying agent targeting serum NGF to improve nerve conduction velocities.
    Matched MeSH terms: Diabetic Neuropathies
  10. Tajuddin K, Justine M, Mohd Mustafah N, Latif L, Manaf H
    Malays J Med Sci, 2021 Apr;28(2):63-71.
    PMID: 33958961 DOI: 10.21315/mjms2021.28.2.6
    Background: Stroke survivors depend on the unaffected leg during walking and standing. The presence of diabetic peripheral neuropathy (DPN) affecting both legs may further affect the postural balance and gait instability and increase the risk for falls in such patients. Thus, this study was conducted to investigate the effect of dual taskings on the gait and turning performance of stroke survivors with DPN.

    Methods: Forty stroke survivors were recruited (20 with DPN and 20 without DPN) in this cross-sectional study design. Instrumented timed up and go (iTUG) tests were conducted in three different tasking conditions (single task, dual motor and dual cognitive). APDM® Mobility Lab system was used to capture the gait parameters during the iTUG tests. A two-way mixed analysis of variance was used to determine the main effects of gait performance on three taskings during the iTUG test.

    Results: Spatiotemporal gait parameters and turning performance (turning time and turning step times) were more affected by the tasking conditions in stroke survivors with DPN compared to those without DPN (P < 0.05).

    Conclusion: Stroke survivors with DPN had difficulty walking while turning and performing a secondary task simultaneously.

    Matched MeSH terms: Diabetic Neuropathies
  11. Pabreja K, Dua K, Sharma S, Padi SS, Kulkarni SK
    Eur J Pharmacol, 2011 Jul 1;661(1-3):15-21.
    PMID: 21536024 DOI: 10.1016/j.ejphar.2011.04.014
    Painful neuropathy, a common complication of diabetes mellitus is characterized by allodynia and hyperalgesia. Recent studies emphasized on the role of non-neuronal cells, particularly microglia in the development of neuronal hypersensitivity. The purpose of the present study is to evaluate the effect of minocyline, a selective inhibitor of microglial activation to define the role of neuroimmune activation in experimental diabetic neuropathy. Cold allodynia and thermal and chemical hyperalgesia were assessed and the markers of inflammation and oxidative and nitrosative stress were estimated in streptozotocin-induced diabetic rats. Chronic administration of minocycline (40 and 80 mg/kg, i.p.) for 2 weeks started 2 weeks after diabetes induction attenuated the development of diabetic neuropathy as compared to diabetic control animals. In addition, minocyline treatment reduced the levels of interleukin-1β and tumor necrosis factor-α, lipid peroxidation, nitrite and also improved antioxidant defense in spinal cords of diabetic rats as compared to diabetic control animals. In contrast, minocycline (80 mg/kg, per se) had no effect on any of these behavioral and biochemical parameters assessed in age-matched control animals. The results of the present study strongly suggest that activated microglia are involved in the development of experimental diabetic neuropathy and minocycline exerted its effect probably by inhibition of neuroimmune activation of microglia. In addition, the beneficial effects of minocycline are partly mediated by its anti-inflammatory effect by reducing the levels of proinflammatory cytokines and in part by modulating oxidative and nitrosative stress in the spinal cord that might be involved in attenuating the development of behavioral hypersensitivity in diabetic rats.
    Matched MeSH terms: Diabetic Neuropathies/complications*
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