TY - JOUR
AU - ŞAHİN, Erkan Melih
AB - INTRODUCTIONThe pathogenesis of diabetic peripheral neuropathy (DPN) has been related to multiple factors, including vascular, metabolic, and immune factors. Oxidative stress also plays an important role in the pathogenesis of DPN.1 Melatonin, the main hormone of the pineal gland, is a very powerful antioxidant molecule. It also has powerful anti‐inflammatory properties. The role of melatonin levels in the pathogenesis of diabetes and its complications has therefore been the subject of many studies. In addition to removing free radicals directly, melatonin also shows protective properties by activating antioxidant enzymes or inhibiting pro‐oxidant enzymes through its receptors. It has been reported that melatonin at pharmacological and possibly physiological levels increases gene expressions or activities of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, glutathione reductase, glucose‐6‐phosphate dehydrogenase, catalase, and Ɣ‐glutamyl cysteine synthetase, thus indirectly suppresses oxidative stress.2,3Emerging evidence show that melatonin reduces diabetes mellitus (DM) and its complications, primarily by improving oxidative damage. Pancreatic β cells are particularly sensitive to oxidative stress as they produce high endogenous levels of ROS (reactive oxygen species) and do not express most of the antioxidant enzymes. Serving as an ROS cleaner, melatonin protects pancreatic tissue and aids in its regeneration.4,5In a study, rats with diabetes 
TI - Melatonin receptor gene polymorphisms as a risk factor in patients with diabetic peripheral neuropathy
JO - Diabetes/Metabolism Research and Reviews
DO - 10.1002/dmrr.3573
DA - 2022-11-01
UR - https://www.deepdyve.com/lp/wiley/melatonin-receptor-gene-polymorphisms-as-a-risk-factor-in-patients-FeFe8WdOVQ
VL - 38
IS - 8
DP - DeepDyve
ER -