title: Arachidonic acid and lipoxin A4 as possible endogenous anti-diabetic molecules.
abstract: In both type 1 and type 2 diabetes mellitus, increased production of pro-inflammatory cytokines and reactive oxygen species (ROS) occurs that induce apoptosis of β cells and cause peripheral insulin resistance respectively though the degree of their increased production is higher in type 1 and less in type 2 diabetes mellitus. Despite this, the exact mechanism(s) that lead to increased production of pro-inflammatory cytokines: interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) and ROS is not known. Studies showed that plasma concentrations of arachidonic acid (AA) and lipoxin A4 (LXA4) are low in alloxan-induced type 1 diabetes mellitus in experimental animals and patients with type 2 diabetes mellitus. Prior administration of AA, eicosapentaenoic and docosahexaenoic acids (EPA and DHA, respectively) and transgenic animals that produce increased amounts of EPA and DHA acids were protected from chemical-induced diabetes mellitus that was associated with enhanced formation of LXA4 and resolvins, while protectin D1 ameliorated peripheral insulin resistance. AA, LXA4, resolvins and protectins inhibit IL-6 and TNF-α production and suppress ROS generation. Thus, AA and lipoxins, resolvins and protectins may function as endogenous anti-diabetic molecules implying that their administration could be useful in the prevention and management of both types of diabetes mellitus.
authors.affiliation: UND Life Sciences, 13800 Fairhill Road 321, Shaker Heights, OH 44120, USA. Undurti@hotmail.com
authors.forename: Undurti N
authors.initials: UN
authors.lastname: Das
mesh_terms: D000818:Animals; D016718:Arachidonic Acid / Q000502:physiology*; D019208:Brain-Derived Neurotrophic Factor / Q000502:physiology; D003920:Diabetes Mellitus / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005231:Fatty Acids, Unsaturated / Q000502:physiology; D006801:Humans; D007031:Hypothalamus / Q000276:immunology / Q000473:pathology; D007249:Inflammation / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D050356:Lipid Metabolism; D044045:Lipoxins / Q000502:physiology*; D009765:Obesity / Q000276:immunology / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D005231:Fatty Acids, Unsaturated; D018836:Inflammation Mediators; D044045:Lipoxins; D043562:Receptors, G-Protein-Coupled; C040527:lipoxin A4; D016718:Arachidonic Acid