Daily profile of glut1 and glut4 expression in tissues inside and outside the blood-brain barrier in control and streptozotocin-treated rats
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
24329691
DOI
10.33549/physiolres.932596
PII: 932596
Knihovny.cz E-resources
- MeSH
- Circadian Clocks * MeSH
- Circadian Rhythm * MeSH
- Diabetes Mellitus, Experimental chemically induced metabolism MeSH
- Glucose metabolism MeSH
- Blood-Brain Barrier metabolism MeSH
- Rats MeSH
- Rats, Wistar MeSH
- Glucose Transporter Type 1 metabolism MeSH
- Glucose Transporter Type 4 metabolism MeSH
- Streptozocin MeSH
- Tissue Distribution drug effects MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Glucose MeSH
- Glucose Transporter Type 1 MeSH
- Glucose Transporter Type 4 MeSH
- Slc2a1 protein, rat MeSH Browser
- Slc2a4 protein, rat MeSH Browser
- Streptozocin MeSH
Glucose is molecule usually studied in relation to metabolism. Except for this traditional view, it is known that under certain conditions glucose can serve as a signal molecule for the circadian system. The circadian system is entrained by relevant synchronizing cues that can be tissue-dependent. Central oscillator is synchronized mainly by light-dark cycle, while peripheral oscillators can be entrained by food intake. Glucose transport in the organism is controlled by insulin dependent and independent mechanism. Therefore, we employed streptozotocin-induced diabetes to elucidate the influence of metabolic changes on glucose transporter (glut1, glut4) 24-h expression profile in peripheral oscillators in tissues, inside (frontal cortex, cerebellum) and outside (heart) the blood-brain barrier. Diabetes was induced by streptozotocin injection. Seventeen days later, sampling was performed during a 24-h cycle. Gene expression was measured using real-time PCR. We observed down-regulation of glut1 and glut4 expression in the heart of diabetic rats. The expression of glut1 and glut4 in brain areas was not down-regulated, however, we observed trend to phase advance in glut1 expression in the cerebellum. These results may indicate higher glucose levels in diabetic brain, which might influence regulation of clock gene expression in different manner in brain compared to periphery.
References provided by Crossref.org