Changes in glucose transporter expression and nitric oxide production are associated with liver injury in diabetes

• DOI: 10.1002/cbf.3123
• Publication Date: 2015-09-08T02:54:49Z
• Authors: Jeļizaveta Sokolo...; Sergejs Isajevs; Evita Rostoka; Tatjana Sjakste; Ilva Trapiņa; Kristīne Ošiņa; Natalia Paramonova; Nikolajs Sjakste
• Keywords: Pathogenesis

In diabetes mellitus (DM), both hyperglycaemia and hyperlipidaemia can initiate accumulation of fat in the liver, which might be further mediated by inducible nitric oxide synthase. We have studied changes GLUT1, (NO · ) concentration liver damage two rat DM models. STZ model was induced strepozotocin 50 mg/kg. HS high‐fat diet 30 mg/kg streptozotocin. GLUT1 expression means real‐time RT‐PCR immunohistochemistry. Production NO monitored erythrocyte sedimentation rate spectroscopy Fe‐DETC‐NO complex. Liver assessed using histological activity index (HAI). increased rats, but it did not change rats (control 36.8 ± 10.3; 142.1 31.1; 35.4 9.8 ng/g). HAI higher group, 8.6 0.17 versus 4.7 0.31, p < 0.05. protein elevated only 16 3 cells/mm 2 Control 5 , = 0.007. Hyperglycaemia sooner causes severe models DM, compared with hyperlipidaemia, is associated production. transporter involved toxic effects glucose liver. obtained novel data about association metabolism pathogenesis injury DM. Increased observed together overproduction pronounced severely hyperglycaemic rats. On contrary, moderately hyperlipidaemic developed moderate steatosis no increase . overexpression implicated Glycotoxicity oxidative stress hyperproduction. become therapeutic targets steatosis. Copyright © 2015 John Wiley & Sons, Ltd.