Non-glucose risk factors in the pathogenesis of diabetic peripheral neuropathy.
Kyung Ae LeeTae Sun ParkHeung Yong JinPublished in: Endocrine (2020)
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.
Keyphrases
- type diabetes
- risk factors
- cardiovascular disease
- glycemic control
- metabolic syndrome
- insulin resistance
- end stage renal disease
- diabetic rats
- blood glucose
- chronic kidney disease
- oxidative stress
- newly diagnosed
- emergency department
- ejection fraction
- radiation therapy
- squamous cell carcinoma
- prognostic factors
- risk assessment
- physical activity
- peritoneal dialysis
- uric acid
- locally advanced
- human health
- adverse drug
- high fat diet induced