Research Topic

Mechanisms and Initiators of Painful Neuropathy in Type 1 and Type 2 Diabetes

About this Research Topic

Diabetes is an increasing worldwide epidemic. Prediabetes and diabetes result in dysfunction of the peripheral nervous system, frequently leading to painful diabetic neuropathy. Clinical evidence suggests that blood glucose control reduces the incidence of diabetic neuropathy in patients with type 1 diabetes but not type 2 diabetes. This suggests the existence of distinct mechanisms of pain, even though the clinical presentation may be similar. Most animal studies use the streptozotocin model of type 1 diabetes to investigate the etiology of pain in diabetes, even though type 2 diabetes has a much higher prevalence, and the incidence of diabetic pain may be higher in type 2 versus type 1. This striking mismatch between research using animal models and the diabetic patient landscape needs to be addressed.

Our lack of thorough comparison of the etiology of pain in type 1 and type 2 diabetes has led to numerous failed clinical trials of diabetic neuropathy treatments. Selection of preclinical models of painful diabetic neuropathy, and assessment of pain-like behavior in preclinical research, should better reflect the clinical situation. It is mostly unknown if the mechanisms mediating painful diabetic neuropathy differ between T1D and T2D, but there may be common initiators. For example, the glucose metabolite methylglyoxal accumulates in patients with diabetes, is necessary to drive reflexive pain-like behavior in rodents with type 1 or type 2 diabetes, and causes hyperalgesia and allodynia in healthy human volunteers. Uncovering other common initiators of diabetic pain, the specific mechanisms that mediate painful neuropathy, and how (or if) the initiators and their mechanisms differ in T1D versus T2D is the goal of this research topic.

Original Research of clinical studies or basic science studies using appropriately chosen animal models are welcome. Reviews will also be considered. Studies addressing one of the following topics are strongly encouraged:
- Identification of the initiator(s) of painful diabetic neuropathy
- Comparison of the mechanisms or treatments for pain in type 1 versus type 2 diabetes
All submissions should take great care to avoid discussion of mechanisms that could be common to pain in both types of diabetes unless specific evidence is provided.


Keywords: diabetes, neuropathic pain, diabetic neuropathy, mechanisms


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Diabetes is an increasing worldwide epidemic. Prediabetes and diabetes result in dysfunction of the peripheral nervous system, frequently leading to painful diabetic neuropathy. Clinical evidence suggests that blood glucose control reduces the incidence of diabetic neuropathy in patients with type 1 diabetes but not type 2 diabetes. This suggests the existence of distinct mechanisms of pain, even though the clinical presentation may be similar. Most animal studies use the streptozotocin model of type 1 diabetes to investigate the etiology of pain in diabetes, even though type 2 diabetes has a much higher prevalence, and the incidence of diabetic pain may be higher in type 2 versus type 1. This striking mismatch between research using animal models and the diabetic patient landscape needs to be addressed.

Our lack of thorough comparison of the etiology of pain in type 1 and type 2 diabetes has led to numerous failed clinical trials of diabetic neuropathy treatments. Selection of preclinical models of painful diabetic neuropathy, and assessment of pain-like behavior in preclinical research, should better reflect the clinical situation. It is mostly unknown if the mechanisms mediating painful diabetic neuropathy differ between T1D and T2D, but there may be common initiators. For example, the glucose metabolite methylglyoxal accumulates in patients with diabetes, is necessary to drive reflexive pain-like behavior in rodents with type 1 or type 2 diabetes, and causes hyperalgesia and allodynia in healthy human volunteers. Uncovering other common initiators of diabetic pain, the specific mechanisms that mediate painful neuropathy, and how (or if) the initiators and their mechanisms differ in T1D versus T2D is the goal of this research topic.

Original Research of clinical studies or basic science studies using appropriately chosen animal models are welcome. Reviews will also be considered. Studies addressing one of the following topics are strongly encouraged:
- Identification of the initiator(s) of painful diabetic neuropathy
- Comparison of the mechanisms or treatments for pain in type 1 versus type 2 diabetes
All submissions should take great care to avoid discussion of mechanisms that could be common to pain in both types of diabetes unless specific evidence is provided.


Keywords: diabetes, neuropathic pain, diabetic neuropathy, mechanisms


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

14 June 2021 Abstract
09 October 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

14 June 2021 Abstract
09 October 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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