About this Research Topic
Metabolic syndrome includes factors that increase risk for development of cardiovascular disease e.g. obesity, diabetes and dyslipidemia. The syndrome is diagnosed when several of following factors are present: abdominal obesity, increased fasting glucose level, high blood pressure, hypertriglyceridemia and decreased high-density lipoprotein-C. Despite different pathogeneses and clinical manifestations, metabolic syndromes share a common complication, i.e. a progressive peripheral neuropathy affecting somatic and autonomic nerves that can be acute or chronic, and affects nerve fibres in proximal and/or distal part of the body.
Today, impaired glucose tolerance (IGT) and type 2 diabetes are growing down the ages reaching epidemic proportions in the world. Almost half of the patients with diabetes show symptoms of neuropathy. Loss of thermal and pain sensation shows involvement of small nerve fibres, and damage to large myelinated axons is manifested by loss of touch- and vibration perception. Neuropathic pain, and symptoms related to dysfunction of autonomic nervous system such as cardiac failure occur frequently in the presence of IGT and type 2 diabetes. A high percentage of neuropathy, however, is idiopathic. It has been suggested that some of the patients with idiopathic neuropathy may be in a prediabetes condition (blood glucose levels above normal but below diabetes thresholds) and therefore, evaluation of glucose homeostasis has been recommended for these patients.
Pathogenesis of metabolic peripheral neuropathy is still unknown. The consensus today is that high glucose availability in prediabetes and diabetes conditions is toxic for the cell; hyperglycaemia e.g. leads to production of excessive oxidative stress, and enhances glucose metabolism through polyol pathway leading to production of sorbitol and precursor to advanced glycated end products (AGE). Sorbitol is an alcohol that cannot easily pass the cell membrane and accumulates in the cell causing high osmotic pressure. Protein glycation and formation of AGE disturbs internal cell function such as transport and protein synthesis, and obstructs cell communication with external environment. Other mechanisms that may underly the neuropathy include mitochondrial dysfunction, nerve growth factor deficiency and inability of autophagy machinery to get rid of damaged proteins and organelles in the cell.
Slow nerve conduction velocity, and abnormal temperature and vibration threshold values determined by quantitative sensory testing method (QST) are non-invasive methods used for diagnosis of peripheral neuropathy. Modern imaging technique such as Corneal Confocal Microscopy is another non-invasive technique that can be used for evaluation of corneal and intra-epidermal small nerve fibre abnormalities. Nerve and skin biopsies give valuable information regarding cellular events such as demyelination, loss of nerve fibres or axonal regeneration. Due to their invasive nature and significant complications, however, nerve biopsies are rarely used.
During past decades, scientists have struggled to solve the mystery of metabolic peripheral neuropathy. Today, we have many pieces of the puzzle but some are still missing. Many scientists’ hard work to complete the puzzle gives insight and hope for achievement of the task in near future. This Research Topic will focus on peripheral neuropathy in metabolic syndromes and we welcome reports on clinical and experimental research, reviews, rapid communications and letters related to the topic.
Keywords: Impaired glucose tolerance, Metabolic disorders, Neuropathy, Peripheral nerve, Type 2 diabetes
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