Mediators of diabetic neuropathy: is hyperglycemia the only culprit?

Grisold, Anna; Callaghan, Brian C.; Feldman, Eva L.

doi:10.1097/med.0000000000000320

Cited by 86 publications

(32 citation statements)

References 65 publications

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“…A significant relationship has been found between hypertension and the incidence of neuropathy in patients with type 1 diabetes (T1DM) 3 , 7 , 8 but not in those with type 2 diabetes (T2DM) 9 , 10 , 11 , 12 , 13 , 14 , 15 . The current evidence also supports an association between hypertension and neuropathy in T1DM but not in T2DM 16 .…”

Section: Introductionsupporting

confidence: 81%

Superimposition of hypertension on diabetic peripheral neuropathy affects small unmyelinated sensory nerves in the skin and myelinated tibial and sural nerves in rats with alloxan-induced type 1 diabetes

Ozaki

Matsuura

2020

J Toxicol Pathol

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Section: Introductionsupporting

confidence: 81%

Superimposition of hypertension on diabetic peripheral neuropathy affects small unmyelinated sensory nerves in the skin and myelinated tibial and sural nerves in rats with alloxan-induced type 1 diabetes

Ozaki

Matsuura

2020

J Toxicol Pathol

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“…In good GC subgroup, BMI significantly decreased after GC, and hence, good response to lifestyle intervention may improve the neuropathy outcomes ( 6 ). Among the components of metabolic syndrome affecting DPN ( 36 ), dyslipidemia had a marginal impact on neuropathy outcome measures. Smoking and alcohol consumption, which may influence on DPN ( 36 ), had no impact on DPN.…”

Section: Discussionmentioning

confidence: 99%

“…Among the components of metabolic syndrome affecting DPN ( 36 ), dyslipidemia had a marginal impact on neuropathy outcome measures. Smoking and alcohol consumption, which may influence on DPN ( 36 ), had no impact on DPN.…”

Section: Discussionmentioning

confidence: 99%

Impact of Normoglycemia in Reducing Microvascular Complications in Patients with Type 2 Diabetes: A Follow-Up Study

Ishibashi

Tavakoli

2018

Front. Endocrinol.

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AimsHyperglycemia is associated with an increased risk of microvascular complications in patients with type 2 diabetes. The aim of the present study was to investigate whether the reduction of the levels of HbA1c by tight glycemic control (GC) decreases the rate of microvascular complications and improves the neurological measures in patients with type 2 diabetes.MethodsDetailed clinical and neurological examinations including corneal confocal microscopy (CCM) were performed in 141 Japanese patients with type 2 diabetes and 60 age-matched control subjects at baseline and follow-up with GC for 4 years. Patients were stratified according to the mean HbA1c level during follow-up into good (HbA1c < 53.0 mmol/mol, mean; 47.5 mmol/mol), fair (53.0 mmol/mol ≤HbA1c < 58.5 mmol/mol, mean; 55.6 mmol/mol), and poor (HbA1c ≥ 58.5 mmol/mol, mean; 68.9 mmol/mol) GC groups with similar HbA1c levels at baseline (84.5–88.2 mmol/mol).ResultsAt baseline, CCM revealed significant nerve fiber damage in all patients compared to that in controls. The interval changes in most corneal nerve fiber (CNF) parameters and neurophysiological functions were significantly related with the mean HbA1c levels during follow-up. Interestingly, the baseline HbA1c level did not impact on neurological functions at follow-up. Interval changes in neuropathy outcomes were associated with mean clinical factors during follow-up and hypoglycemic strategies. Good GC improved all nerve functions, including CNF branch density and bead, but not the length and main fiber density. Fair GC deteriorated some nerve functions. Poor GC compromised all neuropathy outcomes. Irrespective of GC levels, retinopathy increased after follow-up period, while nephropathy decreased.ConclusionThis study showed that tight GC was beneficial just for nephropathy among microvascular complications. Despite strict GC, the retinopathy progressed in patients with type 2 diabetes. Glucose control did not improve neurophysiological and corneal nerve measurements unless near-normoglycemia was reached.

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“…Moreover, neuropathy is also present in individuals with prediabetes (i.e., not yet having developed hyperglycemia) [ 137 ], indicating factors other than hyperglycemia are involved. Large clinical studies support the concept that components of the metabolic syndrome, (notably obesity and prediabetes) which include elevated levels of the amyloidogenic protein hIAPP, may underlie the pathogenesis of DPN, especially in T2DM [ 138 ].…”

Section: Peripheral Amyloid Neuropathiesmentioning

confidence: 99%

Amyloid Proteins and Peripheral Neuropathy

Asiri

Engelsman

Eijkelkamp

et al. 2020

Cells

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Painful peripheral neuropathy affects millions of people worldwide. Peripheral neuropathy develops in patients with various diseases, including rare familial or acquired amyloid polyneuropathies, as well as some common diseases, including type 2 diabetes mellitus and several chronic inflammatory diseases. Intriguingly, these diseases share a histopathological feature—deposits of amyloid-forming proteins in tissues. Amyloid-forming proteins may cause tissue dysregulation and damage, including damage to nerves, and may be a common cause of neuropathy in these, and potentially other, diseases. Here, we will discuss how amyloid proteins contribute to peripheral neuropathy by reviewing the current understanding of pathogenic mechanisms in known inherited and acquired (usually rare) amyloid neuropathies. In addition, we will discuss the potential role of amyloid proteins in peripheral neuropathy in some common diseases, which are not (yet) considered as amyloid neuropathies. We conclude that there are many similarities in the molecular and cell biological defects caused by aggregation of the various amyloid proteins in these different diseases and propose a common pathogenic pathway for “peripheral amyloid neuropathies”.

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Mediators of diabetic neuropathy: is hyperglycemia the only culprit?

Cited by 86 publications

References 65 publications

Superimposition of hypertension on diabetic peripheral neuropathy affects small unmyelinated sensory nerves in the skin and myelinated tibial and sural nerves in rats with alloxan-induced type 1 diabetes

Superimposition of hypertension on diabetic peripheral neuropathy affects small unmyelinated sensory nerves in the skin and myelinated tibial and sural nerves in rats with alloxan-induced type 1 diabetes

Impact of Normoglycemia in Reducing Microvascular Complications in Patients with Type 2 Diabetes: A Follow-Up Study

Amyloid Proteins and Peripheral Neuropathy

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