Heat-Shock Protein 70–Mediated Heat Preconditioning Attenuates Hepatic Carbohydrate and Oxidative Disturbances in Rats With Type 1 Diabetes
| Autor: | Katerina Gerazova-Efremova, Suzana Dinevska-Kjovkarovska, Biljana Miova |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
medicine.medical_specialty
Endocrinology Diabetes and Metabolism Glutathione reductase 030209 endocrinology & metabolism Carbohydrate metabolism Antioxidants Body Temperature Diabetes Mellitus Experimental 03 medical and health sciences chemistry.chemical_compound Glycogen phosphorylase 0302 clinical medicine Endocrinology Internal medicine Internal Medicine medicine Animals HSP70 Heat-Shock Proteins 030212 general & internal medicine Rats Wistar chemistry.chemical_classification Glycogen business.industry Glutathione peroxidase Hyperthermia Induced General Medicine Glutathione Streptozotocin Rats Hsp70 Oxidative Stress Diabetes Mellitus Type 1 Liver chemistry Carbohydrate Metabolism Female business Oxidation-Reduction Heat-Shock Response medicine.drug |
| Zdroj: | Canadian Journal of Diabetes. 43:345-353 |
| ISSN: | 1499-2671 |
| DOI: | 10.1016/j.jcjd.2019.01.002 |
| Popis: | Objectives Heat preconditioning and heat-shock protein (HSP) synthesis have significant cytoprotective effects against the development of cellular injury caused by the application of a subsequent stressor, which were found to depend on the time period between the stressors. We aimed to determine the most efficient recovery time (6 h or 24 h) following heat-stress exposure and prior application of diabetic streptozotocin (STZ) on the moderation of carbohydrate and oxidative metabolic disturbances caused by diabetes. Methods Experiment animals (Wistar rats) were exposed to acute heat stress at 41±1°C for 45 min, followed by 6-h or 24-h recovery times at room temperature before sacrifice or STZ administration. Results Our findings indicate that acute heat stress with 6-h or 24-h recovery periods results in a significant rise in the hepatic heat-shock protein 70 (HSP70) levels (even more so after 24 h), glycogen breakdown and stable glycemia, followed by reduced glycolytic and gluconeogenic activity (after 24 h) (glucose-6-phosphatase, fructose-1,6-bisphosphatase); stimulates antioxidative activity (glutathione peroxidase, glutathione reductase) (after 6 h); and decreases glutathione and catalase activity (after 24 h). Heat preconditioning (with 6-h and 24-h recovery periods) prior to STZ-induced diabetes increases HSP70 levels and causes lower serum glucose levels, higher glycogen and glucose-6-phosphate levels, lower glucose-6-phosphatase levels and glycogen phosphorylase and hexokinase levels but also elevates glutathione reductase and glutathione peroxidase activity compared to untreated STZ animals. Conclusions Based on our findings, heat preconditioning and HSP70 induction in rats with type 1 diabetes attenuates STZ-induced metabolic alterations in hepatic carbohydrate metabolism and oxidative states. These changes are more evident at 24 h recovery post-acute heat stress, based on the most evident accumulation of HSP70 in this time frame. |
| Databáze: | OpenAIRE |
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