| dc.creator | Cisternas, Pedro | |
| dc.creator | Inestrosa-Cantin, Nibaldo Manuel | |
| dc.date | 2022-05-20T20:45:48Z | |
| dc.date | 2022-06-18T20:44:03Z | |
| dc.date | 2022-05-20T20:45:48Z | |
| dc.date | 2022-06-18T20:44:03Z | |
| dc.date | March10 | |
| dc.date | 2018 | |
| dc.date | 2018 | |
| dc.date | March7 | |
| dc.date.accessioned | 2023-08-22T01:36:32Z | |
| dc.date.available | 2023-08-22T01:36:32Z | |
| dc.identifier | 1160724 | |
| dc.identifier | https://hdl.handle.net/10533/254044 | |
| dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/8306689 | |
| dc.description | The brain is an organ with a high rate of glucose consumption and in several disorders, it has
been described a decrease in the brain capacity to utilize glucose including in Alzheimer´s
disease (AD) and obesity. Despite the importance of this process little is know about the
regulation in this process in both pathologies. In the lasts year has been described that obesity
increase the risk of AD in several models. The proposal mechanism for explain these results
evolve the action of adipokines, released by the fat tissue. Adipokines regulates different
biological processes in target organs, including control of appetite, fat distribution, insulin
sensitivity and energy expenditure. In the brain, the most studied adipokines are adiponectin,
leptin and resistin, all of these has been related with dementia and their role is mainly related
with glucose metabolism through the regulation of insulin metabolism. Otherwise, has been
described that adiponectin and resistin could impact the hippocampus and considering that both
impact in an opposite manner the insulin signaling (an important risk factor for AD), in the
present work we studied the effect of these adipokines over the glucose metabolism.
We used cortical neurons and glucose radiolabeled analogous to study several parameters of
energy metabolism, including uptake of glucose (Km and Vmax values), glycolytic rate, pentose
phosphate pathway (PPP) and production of ADP/ATP. We observed that the adiponectin
induces an increase in the uptake of glucose and in the PPP activity. Meanwhile resistin induce
and strong inhibition in the glycolytic rate. Also, using hippocampal slices of a transgenic mouse
of AD (APPswe/PSEN1DE9) we observed that the treatment with adiponectin improve de
energy metabolism, the contrary effect was observed after the treatment with resistin. Our result
suggest that the levels of adipokines could be important in the regulation of glucose metabolism
in the context of AD and obesity.
Supported by CONICYT- PFB 12/2007 to N.C.I., FONDECYT (no. 1120156) to N.C.I., and
FONDECYT (no. 11160651) to P.C. We also thank our special grants “The role of K+ on
Hypertension and Cognition” from the Sociedad Química y Minera de Chile (SQM). | |
| dc.description | FONDECYT | |
| dc.description | FONDECYT | |
| dc.language | eng | |
| dc.relation | instname: ANID | |
| dc.relation | reponame: Repositorio Digital RI2.0 | |
| dc.relation | International Conference on Brain Energy Metabolism | |
| dc.relation | 13° | |
| dc.rights | http://creativecommons.org/licenses/by/3.0/cl/ | |
| dc.title | Regulation of glucose metabolism in neurons by adiponectin and resistin, a possible
molecular link between brain dysfunction and obesity | |
| dc.type | info:eu-repo/semantics/lecture | |
| dc.type | info:eu-repo/semantics/publishedVersion | |
| dc.coverage | Valdivia | |
