2018
DOI: 10.1007/s12020-018-1546-z
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Association of glycaemic variability evaluated by continuous glucose monitoring with diabetic peripheral neuropathy in type 2 diabetic patients

Abstract: In addition to conventional risks including diabetic duration, HOMA-IR and HbA1c, increased glycaemic variability assessed by MAGE is a significant independent contributor to DPN in type 2 diabetic patients.

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Cited by 45 publications
(54 citation statements)
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“…Glucose variability has been demonstrated to be an independent risk factor for free radical damage and diabetes complications, yet we did not find that glucose variability was associated with DPN 35 36. There is inconsistency in the relationship between glucose variability and DPN in the literature, and some research indicates that for type 2 DM, glucose variability may be regarded as a marker of beta-cell function rather than direct cause of DPN 37–39…”
Section: Discussioncontrasting
confidence: 69%
“…Glucose variability has been demonstrated to be an independent risk factor for free radical damage and diabetes complications, yet we did not find that glucose variability was associated with DPN 35 36. There is inconsistency in the relationship between glucose variability and DPN in the literature, and some research indicates that for type 2 DM, glucose variability may be regarded as a marker of beta-cell function rather than direct cause of DPN 37–39…”
Section: Discussioncontrasting
confidence: 69%
“…It is believed that impaired early-phase β-cell function is an important pathogenetic mechanism causing postprandial hyperglycaemia excursions [2][3][4]. Given the relationship between glycemic variability and DPN [6,7], we hypothesized that impaired early-phase β-cell function is positively associated with sudomotor dysfunction in T2DM.…”
Section: Discussionmentioning
confidence: 99%
“…The diabetic duration, homeostasis model assessment for insulin resistance, haemoglobin A 1c , and increased glycaemic variability assessed by the mean amplitude of glycaemic excursions are all independent contributors to diabetic peripheral neuropathy in type 2 diabetic (T2D) patients. 3 The pathological mechanisms of diabetic neuropathy are nearly the same as diabetic retinopathy and nephropathy, such as oxidative stress, increased advanced glycation end products and their receptors, activation of the polyol pathway, inducible nitric oxide synthase, and activation of mitogen-activated protein kinases and protein kinase C. Moreover, increased cytokines (eg, nerve growth factor, tumour necrosis factor [TNF] α, and interleukin 6), hypoxia, and ischaemia deficiency are crucial etiologic roles for diabetic neuropathy. 4 Consistent with these findings, dysfunctional metabolic pathways in diabetes result in functional disorder, damage, and cell death, which are inherent to the peripheral nervous system (eg, Schwann cells, dorsal root ganglia neurons, and vasa nervorum).…”
Section: Introductionmentioning
confidence: 99%