Non-glucose risk factors in the pathogenesis of diabetic peripheral neuropathy
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REVIEW
Non-glucose risk factors in the pathogenesis of diabetic peripheral neuropathy Kyung Ae Lee1 Tae Sun Park1 Heung Yong Jin ●
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Received: 6 February 2020 / Accepted: 23 August 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract In this review, we consider the diverse risk factors in diabetes patients beyond hyperglycemia that are being recognized as contributors to diabetic peripheral neuropathy (DPN). Interest in such alternative mechanisms has been encouraged by the recognition that neuropathy occurs in subjects with metabolic syndrome and pre-diabetes and by the reporting of several large clinical studies that failed to show reduced prevalence of neuropathy after intensive glucose control in patients with type 2 diabetes. Animal models of obesity, dyslipidemia, hypertension, and other disorders common to both pre-diabetes and diabetes have been used to highlight a number of plausible pathogenic mechanisms that may either damage the nerve independent of hyperglycemia or augment the toxic potential of hyperglycemia. While pathogenic mechanisms stemming from hyperglycemia are likely to be significant contributors to DPN, future therapeutic strategies will require a more nuanced approach that considers a range of concurrent insults derived from the complex pathophysiology of diabetes beyond direct hyperglycemia. Keywords Diabetes Diabetic peripheral neuropathy Dyslipidemia Hypertension Pathogenesis ●
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Introduction Peripheral neuropathy can arise from diverse conditions such as diabetes, endocrinopathies, infections, toxins, and various drugs [1], all of which can share similar clinical features such as sensory loss and pain. Diabetes has become a common condition, mainly due to the dramatic increase in the prevalence of type 2 diabetes; it afflicts 5–15% of people in many populations, depending on local genetic and environmental factors. It is therefore not unreasonable that diabetes patients may suffer from concurrent conditions that produce neuropathy independent of diabetes. It is established good clinical practice to initially
Supplementary information The online version of this article (https:// doi.org/10.1007/s12020-020-02473-4) contains supplementary material, which is available to authorized users. * Heung Yong Jin [email protected] 1
Division of Endocrinology and Metabolism, Department of Internal Medicine, Research Institute of Clinical Medicine of Jeonbuk National University-Jeonbuk National University Hospital, Jeonbuk National University, Medical School, Jeonju, South Korea
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exclude alternatives such as history of alcoholism, HIV infection, and chemotherapy before attributing neuropathy in a diabetes patient to the diabetic condition per se. Currently, standard of care guidelines in many countries recommend institution and maintenance of tight glycemic control to prevent the progression of the complications of chronic diabetes, including neuropathy [2, 3]. Indeed, professional and regulatory bodies in most regions wo
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