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10.1523/JNEUROSCI.2119-16.2016 http://scihub22266oqcxt.onion/10.1523/JNEUROSCI.2119-16.2016 C5125227!5125227!27852778     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27852778&cmd=llinks): Failed to open stream: HTTP request failed! 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The Effects of Peripheral and Central High Insulin on Brain Insulin Signaling and Amyloid-? in Young and Old APP/PS1 Mice |pdf=|usr=}}{{27852778}} gab.com Text The Effects of Peripheral and Central High Insulin on Brain Insulin Signaling and Amyloid- in Young and Old APP/PS1 Mice JO: J Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=27852778 #FOAvip Hyperinsulinemia is a risk factor for late-onset Alzheimer's disease (AD). In vitro experiments describe potential connections between insulin, insulin signaling, and amyloid-? (A?), but in vivo experiments are needed to validate these relationships under physiological conditions. First, we performed hyperinsulinemic-euglycemic clamps with concurrent hippocampal microdialysis in young, awake, behaving APPswe/PS1dE9 transgenic mice. Both a postprandial and supraphysiological insulin clamp significantly increased interstitial fluid (ISF) and plasma A? compared with controls. We could detect no increase in brain, ISF, or CSF insulin or brain insulin signaling in response to peripheral hyperinsulinemia, despite detecting increased signaling in the muscle. Next, we delivered insulin directly into the hippocampus of young APP/PS1 mice via reverse microdialysis. Brain tissue insulin and insulin signaling was dose-dependently increased, but ISF A? was unchanged by central insulin administration. Finally, to determine whether peripheral and central high insulin has differential effects in the presence of significant amyloid pathology, we repeated these experiments in older APP/PS1 mice with significant amyloid plaque burden. Postprandial insulin clamps increased ISF and plasma A?, whereas direct delivery of insulin to the hippocampus significantly increased tissue insulin and insulin signaling, with no effect on A? in old mice. These results suggest that the brain is still responsive to insulin in the presence of amyloid pathology but increased insulin signaling does not acutely modulate A? in vivo before or after the onset of amyloid pathology. Peripheral hyperinsulinemia modestly increases ISF and plasma A? in young and old mice, independent of neuronal insulin signaling.SIGNIFICANCE STATEMENT The transportation of insulin from blood to brain is a saturable process relevant to understanding the link between hyperinsulinemia and AD. In vitro experiments have found direct connections between high insulin and extracellular A?, but these mechanisms presume that peripheral high insulin elevates brain insulin significantly. We found that physiological hyperinsulinemia in awake, behaving mice does not increase CNS insulin to an appreciable level yet modestly increases extracellular A?. We also found that the brain of aged APP/PS1 mice was not insulin resistant, contrary to the current state of the literature. These results further elucidate the relationship between insulin, the brain, and AD and its conflicting roles as both a risk factor and potential treatment. Twit Text FOAVip The Effects of Peripheral and Central High Insulin on Brain Insulin Signaling and Amyloid- in Young and Old APP/PS1 Mice ????J Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=27852778 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27852778 #FOAvip English Wikipedia <ref>{{Cite pmid|27852778}}</ref> The Effects of Peripheral and Central High Insulin on Brain Insulin Signaling and Amyloid-? in Young and Old APP/PS1 Mice #MMPMID27852778 Stanley M; Macauley SL; Caesar EE; Koscal LJ; Moritz W; Robinson GO; Roh J; Keyser J; Jiang H; Holtzman DM J Neurosci 2016[Nov]; 36 (46): 11704-15 PMID27852778show ga Hyperinsulinemia is a risk factor for late-onset Alzheimer's disease (AD). In vitro experiments describe potential connections between insulin, insulin signaling, and amyloid-? (A?), but in vivo experiments are needed to validate these relationships under physiological conditions. First, we performed hyperinsulinemic-euglycemic clamps with concurrent hippocampal microdialysis in young, awake, behaving APPswe/PS1dE9 transgenic mice. Both a postprandial and supraphysiological insulin clamp significantly increased interstitial fluid (ISF) and plasma A? compared with controls. We could detect no increase in brain, ISF, or CSF insulin or brain insulin signaling in response to peripheral hyperinsulinemia, despite detecting increased signaling in the muscle. Next, we delivered insulin directly into the hippocampus of young APP/PS1 mice via reverse microdialysis. Brain tissue insulin and insulin signaling was dose-dependently increased, but ISF A? was unchanged by central insulin administration. Finally, to determine whether peripheral and central high insulin has differential effects in the presence of significant amyloid pathology, we repeated these experiments in older APP/PS1 mice with significant amyloid plaque burden. Postprandial insulin clamps increased ISF and plasma A?, whereas direct delivery of insulin to the hippocampus significantly increased tissue insulin and insulin signaling, with no effect on A? in old mice. These results suggest that the brain is still responsive to insulin in the presence of amyloid pathology but increased insulin signaling does not acutely modulate A? in vivo before or after the onset of amyloid pathology. Peripheral hyperinsulinemia modestly increases ISF and plasma A? in young and old mice, independent of neuronal insulin signaling.SIGNIFICANCE STATEMENT The transportation of insulin from blood to brain is a saturable process relevant to understanding the link between hyperinsulinemia and AD. In vitro experiments have found direct connections between high insulin and extracellular A?, but these mechanisms presume that peripheral high insulin elevates brain insulin significantly. We found that physiological hyperinsulinemia in awake, behaving mice does not increase CNS insulin to an appreciable level yet modestly increases extracellular A?. We also found that the brain of aged APP/PS1 mice was not insulin resistant, contrary to the current state of the literature. These results further elucidate the relationship between insulin, the brain, and AD and its conflicting roles as both a risk factor and potential treatment. äThe Effects of Peripheral and Central High Insulin on Brain Insulin Si(epmc).pdf DeepDyve Pubget Overpricing