Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic polyneuropathy (DPN) is the most common complication of diabetes and may frequently be the presenting symptom in type 2 diabetes mellitus (T2DM). Metabolic syndrome and T2DM are associated with multiple metabolic toxicities. These substrate toxicities support the formation of reactive oxygen species (ROS), which are so damaging to cells, tissues and organs and play an important role in the development of multiple diabetic complications. The importance of redox stress (ROS) and their effect on the neuronal unit are discussed. There are at least 5 major pathways involved in the development of DPN: metabolic, vascular, immunologic-autoimmune, neurohormonal growth factor deficiency, and extracellular matrix neuronal unit remodeling. Each of these five pathways are reviewed and related to neural redox stress and the role of ROS. The identification of the toxic substrates (A-FLIGHT acronym), earlier diagnosis of T2DM at the stage of impaired glucose tolerance or impaired fasting glucose, and aggressive global risk reduction with the use of a simple RAAS acronym will assist the clinician in slowing the natural progressive history, and possibly preventing the complications associated with DPN. The pain, foot ulceration, limb loss, organ dysfunction, and the associated morbidity and financial burden all contribute to the need for a better understanding of DPN and the role of redox stress and global risk reduction.
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PMID:Neural redox stress and remodeling in metabolic syndrome, type 2 diabetes mellitus, and diabetic neuropathy. 1556 93

Diabetic polyneuropathy is a common and disturbing complication of diabetes mellitus, presenting patients and caregivers with a substantial disease burden. Emerging mechanisms which are underlying diabetes may provide novel pathways to understand diabetic polyneuropathy (DPN). Specifically, non-coding RNA molecules consisting of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are implicated in the biological processes underlying DPN, and may link it to clinical spheres such as other metabolic and neural pathologies. Here, we elaborate on several candidate non-coding RNAs which may be associated with DPN via regulatory roles governing phenomena related to inflammatory, pain-provoking, and metabolic syndrome pathways. Specific examples include miRNAs such as miR-106a, -146a, -9, -29b, -466a, and -98; likewise, lncRNAs MIAT, PVT1, H19, MEG3, and MALAT1 are implicated, often co-affecting the involved pathways. Incorporating newly discovered regulators into what we know about specific clinical applications may highlight novel avenues for diagnosis, prevention, and intervention with DPN.
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PMID:Non-coding RNA regulators of diabetic polyneuropathy. 3245 50