Diabetic Polyneuropathy in Type 2 Diabetes Mellitus: Inflammation, Oxidative Stress, and Mitochondrial Function.

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Term Occurence Count Dictionary
diabetic retinopathy 2 endocrinologydiseases
hyperglycemia 14 endocrinologydiseases
hypoglycemia 1 endocrinologydiseases
obesity 4 endocrinologydiseases
vitamin B12 deficiency 5 endocrinologydiseases
diabetes mellitus 3 endocrinologydiseases
diabetic neuropathy 2 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Select Disease Character Offset Disease Term Instance
diabetes mellitus 53323 NCS93.157.7 ≥2 nerves w/abnormal NCS8191.2 ≥3 nerves w/abnormal NCS51.797.8 DM, diabetes mellitus ; IDDM, insulin-dependent diabetes mellitus; NIDDM, non-insulin-dependent diabetes mellitus; IGT, impaired
diabetes mellitus 53366 NCS8191.2 ≥3 nerves w/abnormal NCS51.797.8 DM, diabetes mellitus; IDDM, insulin-dependent diabetes mellitus ; NIDDM, non-insulin-dependent diabetes mellitus; IGT, impaired glucose tolerance; MNSI, Michigan Neuropathy
diabetes mellitus 53414 NCS51.797.8 DM, diabetes mellitus; IDDM, insulin-dependent diabetes mellitus; NIDDM, non-insulin-dependent diabetes mellitus ; IGT, impaired glucose tolerance; MNSI, Michigan Neuropathy Screening.Instrument; NCS, Nerve Conduction
diabetic neuropathy 26365 mechanism to explain how impaired regulation of peak glucose levels leads to ROS-induced injury in diabetic neuropathy [[90]]. Antioxidant Status. Antioxidants participate in mechanisms to reduce the deleterious effects
diabetic neuropathy 37364 [[126]]. Recently, Hasanvand et al. demonstrated that the activation of AMP kinase signaling pathway in diabetic neuropathy might be associated with the anti-inflammatory response, and Metformin reduced the levels of inflammatory
diabetic retinopathy 11887 diet-only (54.7, 50.6, and 42.1%, respectively; p = 0.0001) [[47]].DPN is strongly associated with diabetic retinopathy (OR 1.10, p < 0.01), not considered as a risk factor, but part of the same physiopathological cause
diabetic retinopathy 41497 peroxisome proliferator activated-receptor alpha (PPARα) agonist recently approved for the management of diabetic retinopathy (DR). A subgroup of 1012 patients with DR aged 50–75 years who had type 2 diabetes in the Fenofibrate
hyperglycemia 1149 factor kappa B, activator protein 1, and mitogen-activated protein kinases. Oxidative stress induced by hyperglycemia is mediated by several identified pathways: polyol, hexosamine, protein kinase C, advanced glycosylation
hyperglycemia 2591 insulin resistance, with or without insulin deficiency that induces organ dysfunction [[2]]. Persistent hyperglycemia in DM generates reactive oxygen species (ROS) and nitrosative species (RNS); both are considered an
hyperglycemia 14716 segmental demyelination are the main pathological characteristics of neuropathic damage induced by hyperglycemia . It has been established that the first pathologic changes in DPN are axonal degeneration with subsequent
hyperglycemia 14926 subsequent regeneration, but insufficient to reestablish the structural abnormalities due to chronic hyperglycemia . Onion bulbs are shown in nerve biopsies, characteristic of hypertrophic neuropathy, representing the
hyperglycemia 16495 (IL-) 6, cyclooxygenase 2 (COX-2), and inducible nitric oxide synthase (iNOS). The MAPK is promoted by hyperglycemia through apoptosis signaling kinase 1 or directly by ROS and causes activation of cytosolic NF-κB [[61]].
hyperglycemia 21516 radicals through the production of nicotinamide adenine dinucleotide phosphate (NADPH), induced by hyperglycemia [[75]]. In hexosamine pathway, fructose-6-phosphate is diverted from glycolysis to produce glucosamine-6-phosphate,
hyperglycemia 22005 induce an increased expression of transforming growth factor beta (TGF-β) [[77]–[79]]. Intracellular hyperglycemia also induces the formation of diacylglycerol (DAG) from the glycolytic intermediate dihydroxyacetone
hyperglycemia 28027 DysfunctionMitochondria are intrinsically associated with ROS production; its normal function is altered by hyperglycemia [[101]]. More than 90% of ROS are generated in the mitochondria [[102]]. The damage to this organelle
hyperglycemia 28991 to oxidative stress damage due to a high energetic demand and elevated lipids content [[105]]. When hyperglycemia is controlled, the mitochondria experience a reduction of O2•− inhibition, along with improvement
hyperglycemia 29173 inhibition, along with improvement of mitochondrial function and DNA [[106]].It has been proved that hyperglycemia induces a dose-dependent effect on cleavage of caspases through ATP depletion. Hyperglycemia generates
hyperglycemia 36599 mitochondria, which traduce in cell protection from apoptosis induced by mitochondria-related toxicity of hyperglycemia [[124]]. Furthermore, another investigation of Metformin effects on mitochondria revealed that elevated
hyperglycemia 44795 proanthocyanidins of the grape seed. They can also maintain the normal morphology of nerve tissue by reducing hyperglycemia and calcium overload in sciatic nerves [[150]]. Grape seed proanthocyanidins reduced low-density lipoproteins
hyperglycemia 50931 ConclusionsThere is still a lot of research to be done to fully understand the complex pathways in which hyperglycemia alters nerve function and even more regarding therapeutic approaches to reduce inflammatory, oxidative
hyperglycemia 52131 percentiles 25, 50, and 75 of epidemiology studies.Figure 2Mechanisms of nerve dysfunction induced by hyperglycemia . The description of how inflammation, oxidative stress, and mitochondrial dysfunction contributes to
hypoglycemia 35911 type 2 DM. It has many advantages when compared to other OAs, such as lack of weight gain, low risk of hypoglycemia , and favorable effects on the lipid profile [[122]]. Beneficial effects of Metformin have also been
obesity 1840 factors include age, male gender, duration of diabetes, uncontrolled glycaemia, height, overweight and obesity , and insulin treatment. Several diagnostic methods have been developed, and composite scores combined
obesity 9110 (sural r = 0.6518, peroneal r = 0.4583, tibiae r = 0.7217, and median r = 0.5440) [[49]]. Overweight and obesity are considered as risk factors for the presence of DPN with OR 1.036 (95% CI 1.005–1.068, p = 0.022)
obesity 9477 diabetes outpatient clinics in Japan, where 298 patients were included, reported that overweight and obesity are risk factors for pain and numbness in patients with DPN [[52]]. In type 2 DM patients with BMI ≥
obesity 17499 is related to higher fasting plasma glucose and triglycerides, lower HDL cholesterol, and visceral obesity and also to higher levels of inflammatory cytokines (IL-6 and IL-1) and C reactive protein (CRP) in
vitamin B12 deficiency 37647 conduction velocities of the sciatic nerves [[127]].Recent studies have addressed the importance of vitamin B12 deficiency among long-term users of Metformin as OA therapy. The prevalence varies depending on the cut-off point
vitamin B12 deficiency 38211 2 DM patients and the association with DPN was evaluated. Forty-three (35.54%) patients had DPN and vitamin B12 deficiency was defined as levels <150 pmol/L. The prevalence of vitamin B12 deficiency was 28.1%; however, there
vitamin B12 deficiency 38289 patients had DPN and vitamin B12 deficiency was defined as levels <150 pmol/L. The prevalence of vitamin B12 deficiency was 28.1%; however, there was no association between vitamin B12 deficiency and DPN, and Metformin dose
vitamin B12 deficiency 38365 <150 pmol/L. The prevalence of vitamin B12 deficiency was 28.1%; however, there was no association between vitamin B12 deficiency and DPN, and Metformin dose did not confer an increase risk on DPN presence [[129]]. Similar results
vitamin B12 deficiency 38582 results were reported by other authors, with controversial results, but without strong evidence that vitamin B12 deficiency influences the presence or severity of peripheral neuropathy [[130]–[132]]. We recommend supplementation

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