Premium
Mechanisms by which erythritol prevents glucose‐induced endothelial cell damage
Author(s) -
Hartog Gertjan,
Berger Alvin,
Cock Peter,
Boesten Daniëlle,
Bast Aalt
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.95.8
Diabetes is characterized by hyperglycemia and development of vascular pathology. Endothelial cell (EC) dysfunction (ECD) is a starting point for pathogenesis of vascular complications in diabetes. Hyperglycemia‐induced oxygen radical formation plays a role in EC damage. We previously showed the sugar alcohol erythritol (ERT) to be a hydroxyl radical scavenger preventing ECD onset in diabetic rats. To better understand how ERT mediates this protective effect, ERT and mannitol (structurally related) were studied in EC (HUVECs) exposed to diabetic stressors (Tables 1–2). Exposure to diabetic stressors decreased viability of EC and increased oxidative damage; and altered activities of enzymes responsible for EC functions. Several of these changes were attenuated by pre‐incubation with ERT or mannitol. Protective effects of ERT during hyperglycemia were confirmed and mechanistically expanded upon, with transcriptomics. Research financially supported by Cargill Inc.