Inflammation as a Therapeutic Target for Diabetic Neuropathies

Pop‐Busui, Rodica; Ang, Lynn; Holmes, Crystal M.; Gallagher, Katherine A.; Feldman, Eva L.

doi:10.1007/s11892-016-0727-5

Cited by 189 publications

(142 citation statements)

References 124 publications

(134 reference statements)

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“…Mechanisms postulated to mediate these benefits include: reduction in low-grade inflammation and oxidative stress (43), improvement in endothelial function, increased adiponectin concentrations, decreased blood coagulation, and improved apolipoprotein profiles with lower concentrations of oxidized LDL cholesterol (40–42). However, the metabolic pathways through which the Mediterranean diet influences CVD risk remain largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Structured lifestyle intervention in patients with the metabolic syndrome mitigates oxidative stress but fails to improve measures of cardiovascular autonomic neuropathy

Pennathur

Jaiswal

Vivekanandan-Giri

et al. 2017

Journal of Diabetes and its Complications

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Aims To assess the role of oxidative stress in mediating adverse outcomes in metabolic syndrome (MetS) and resultant cardiovascular autonomic neuropathy (CAN), and to evaluate the effects of lifestyle interventions on measures of oxidative stress and CAN in subjects with MetS. Methods Pilot study in 25 non-diabetic subjects with MetS (age 49±10 years, 76% females) participating in a 24-week lifestyle intervention (supervised aerobic exercise/Mediterranean diet), and 25 age-matched healthy controls. CAN was assessed by cardiovascular reflex tests, heart rate variability (HRV) and PET imaging with sympathetic analog [11C] meta-hydroxyephedrine ([11C]HED). Specific oxidative fingerprints were measured by liquid-chromatography/mass-spectrometry(LC/MS). Results At baseline, MetS subjects had significantly higher oxidative stress markers [3-nitrotyrosine (234±158 vs.54±47 µmol/mol tyrosine), ortho-tyrosine (59±38 vs.18±10 µmol/molphenylalanine, all P<0.0001], and impaired HRV at rest and during deep breathing (P=0.039 and P=0.021 respectively) compared to controls. Twenty-four-week lifestyle intervention significantly reduced all oxidative stress markers(all P < 0.01) but did not change any of the CAN measures. Conclusions Subjects with MetS present with signs of CAN and increased oxidative stress in absence of diabetes. The 24-week lifestyle intervention was effective in ameliorating oxidative stress, but did not improve measures of CAN. Larger clinical trials with longer duration are required to confirm these findings.

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Section: Discussionmentioning

confidence: 99%

Structured lifestyle intervention in patients with the metabolic syndrome mitigates oxidative stress but fails to improve measures of cardiovascular autonomic neuropathy

Pennathur

Jaiswal

Vivekanandan-Giri

et al. 2017

Journal of Diabetes and its Complications

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“…For example, abnormalities in nerve polyol, hexosamine, and protein kinase C pathways are reported, in parallel with changes in advanced glycation endproducts and Poly (ADP-ribose) polymerase. Separately and in concert, these changes produce nervous system oxidative stress and apoptosis of both neurons and supporting glia (6, 7). …”

Section: Effect Of Dm On Peripheral Neuropathymentioning

confidence: 99%

Mediators of diabetic neuropathy: is hyperglycemia the only culprit?

Grisold

Callaghan

Feldman

2017

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

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Purpose of this review Diabetic peripheral neuropathy (DPN) is a disabling, highly prevalent complication of both type 1 and type 2 diabetes mellitus (T1DM, T2DM). Large clinical studies support the concept that, in addition to hyperglycemia, components of the metabolic syndrome (MetS) may underlie the pathogenesis of DPN, especially in T2DM. This review will present the evidence supporting the MetS and its individual components as potential causal factors for the development of neuropathy. Recent findings In addition to poor glycemic control and duration of diabetes, components of MetS such as dyslipidemia, obesity, and hypertension, may have an important impact on the prevalence of DPN. Obesity and prediabetes have the most data to support their role in neuropathy, whereas hypertension and dyslipidemia have more mixed results. Non-metabolic factors, such as genetic susceptibility, age, height, gender, smoking, and alcohol, have also been highlighted as potential risk factors in peripheral neuropathy, although the exact contribution of these factors to DPN remains unknown. Summary DPN is a chronic and disabling disease, and the accurate identification and modification of DPN risk factors is important for clinical management. Recent data support a role for components of the MetS and other risk factors in the development of DPN, offering novel targets beyond hyperglycemia for therapeutic development.

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“…A number of other factors affect the activity of neurons, mitochondrial function, permeability of membranes and endothelial function. These include the activation of polyol aldose reductase pathway [17], activation of poly(ADP ribose) polymerase [18], and modified Na+/K+-ATPase pump function [19].…”

Section: Introductionmentioning

confidence: 99%

Dynamic Properties of Skeletal Muscle Contraction in Rats with Diabetes

Beregova¹,

Nozdrenko²,

SergiiBerehovyi³

et al. 2018

Pathophysiology - Altered Physiological States

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The study was conducted on 20 white nonlinear male rats, which were divided into 2 groups of 10 animals each. Rats in the first group were used as control. Rats in the second group were induced type I diabetes by intraperitoneal (i.p.) administration of streptozotocin (65 mg/kg). Diabetes in rats was confirmed by the presence of hyperglycemia. For the establishment of nociceptive pain sensation, mechanical nociceptive test and tail-flick test were conducted in rats. Further animals were anesthetized by i.p. administration of Nembutal (40 mg/kg). The study of dynamic properties of muscle contraction was performed under conditions of the tibia muscle activation by using the modulated stimulation of efferent n. tibialis. Streptozotocin (STZ) was injected in rats; as a result, the blood glucose level was increased by 4.4 times (p ≤ 0.001). Pain sensitivity in diabetic rats was suppressed, indicating the development of peripheral neuropathy. In rats with diabetes, biomechanical parameters of tibia muscle contraction such as the maximum force of contraction, the speed of maximum force of contraction, the retention time of maximum force of contraction and integrated power of muscle contraction (it is calculated on the total area of the received force curves) were violated. This prevents adequate implementation motor neuron pools muscular system, which will have significant consequences in accurate positional movements.

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Inflammation as a Therapeutic Target for Diabetic Neuropathies

Cited by 189 publications

References 124 publications

Structured lifestyle intervention in patients with the metabolic syndrome mitigates oxidative stress but fails to improve measures of cardiovascular autonomic neuropathy

Structured lifestyle intervention in patients with the metabolic syndrome mitigates oxidative stress but fails to improve measures of cardiovascular autonomic neuropathy

Mediators of diabetic neuropathy: is hyperglycemia the only culprit?

Dynamic Properties of Skeletal Muscle Contraction in Rats with Diabetes

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