Early disruption of nerve mitochondrial and myelin lipid homeostasis in obesity-induced diabetes.

ABSTRACT: Diabetic neuropathy is a major complication of diabetes. Current treatment options alleviate pain but do not stop the progression of the disease. At present, there are no approved disease-modifying therapies. Thus, developing more effective therapies remains a major unmet medical need. Seeking to better understand the molecular mechanisms driving peripheral neuropathy, as well as other neurological complications associated with diabetes, we performed spatiotemporal lipidomics, biochemical, ultrastructural, and physiological studies on PNS and CNS tissue from multiple diabetic preclinical models. We unraveled potentially novel molecular fingerprints underlying nerve damage in obesity-induced diabetes, including an early loss of nerve mitochondrial (cardiolipin) and myelin signature (galacto

SUBMITTER: Palavicini JP 

PROVIDER: S-EPMC7710310 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature