Regulation of the anorectic drug recognition site during glucoprivic feeding
Brain Research Bulletin, ISSN: 0361-9230, Vol: 28, Issue: 2, Page: 201-207
1992
- 7Citations
- 9Captures
Metric Options: Counts1 Year3 YearSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Article Description
The acute effects of 2-deoxy-D-glucose (2-DG)-induced glucoprivic feeding on the anorectic drug recognition site and Na + K + -ATPase in the brain were examined in adult rats and in lean and genetically obese mice. The marked hyperglycemia and the induction of feeding caused by the administration of 2-DG to satiated rats and lean mice were associated with significant increases in Na + K + -ATPase activity, and in [ 3 H]ouabain binding and [ 3 H]mazindol binding to the anorectic drug recognition site in hypothalamic membranes. Basal and 2-DG-stimulated levels of blood glucose were significantly correlated to the levels of hypothalamic [ 3 H]ouabain ( r = +.91, p <0.01) and [ 3 H]mazindol ( r = +.87, p <0.01) binding. A significant correlation ( r =.74, p <0.05) was also observed between [ 3 H]mazindol binding and [ 3 H]ouabain binding supporting the hypothesis that these hypothalamic binding sites are functionally coupled in their response to circulating glucose. Following the intracerebroventricular (ICV) administration of the diabetogenic drug alloxan, 2-DG did not stimulate feeding or increase [ 3 H]mazindol and [ 3 H]ouabain binding sites in the hypothalamic paraventricular area. Since 2-DG still caused hyperglycemia in alloxan-treated rats, alloxan-induced inactivation of glucoreceptor mechanisms led to an uncoupling of the anorectic drug recognition site from a hypothalamic glucostat. In genetically obese mice (ob/ob), 2-DG also could not induce feeding or increase hypothalamic [ 3 H]ouabain or [ 3 H]mazindol binding, despite a significant hyperglycemic response. In contrast, 2-DG did increase feeding and the binding of [ 3 H]ouabain and [ 3 H]mazindol to the hypothalamus of lean littermates. The dissociation of the anorectic drug recognition site from blood glucose responses to 2-DG suggests that the glucoprivic feeding response in obese mice is impaired. In conclusion, the [ 3 H]mazindol recognition site and the neuronal Na + K + -ATPase labelled by [ 3 H]ouabain binding constitutes a glucoreceptive system which in response to changes in circulating glucose levels modulates feeding. Since the coupling of this anorectic ding recognition site to brain glucostats is defective in genetically obese mice, this system may have an important role in pathological hyperphagia and the development of obesity.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/0361923092901806; http://dx.doi.org/10.1016/0361-9230(92)90180-6; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0026569737&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/1317740; https://linkinghub.elsevier.com/retrieve/pii/0361923092901806; http://dx.doi.org/10.1016/0361-9230%2892%2990180-6; https://dx.doi.org/10.1016/0361-9230%2892%2990180-6
Elsevier BV
Provide Feedback
Have ideas for a new metric? Would you like to see something else here?Let us know