Cerebrocortical Beta Activity in Overweight Humans Responds to Insulin Detemir
Author(s) / Creator(s)
Tschritter, Otto
Hennige, Anita M.
Preissl, Hubert
Porubska, Katarina
Schäfer, Silke A.
Lutzenberger, Werner
Machicao, Fausto
Birbaumer, Niels
Fritsche, Andreas
Häring, Hans-Ulrich
Abstract / Description
Background
Insulin stimulates cerebrocortical beta and theta activity in lean humans. This effect is reduced in obese individuals indicating cerebrocortical insulin resistance. In the present study we tested whether insulin detemir is a suitable tool to restore the cerebral insulin response in overweight humans. This approach is based on studies in mice where we could recently demonstrate increased brain tissue concentrations of insulin and increased insulin signaling in the hypothalamus and cerebral cortex following peripheral injection of insulin detemir.
Methodology/Principal Findings
We studied activity of the cerebral cortex using magnetoencephalography in 12 lean and 34 overweight non-diabetic humans during a 2-step hyperinsulinemic euglycemic clamp (each step 90 min) with human insulin (HI) and saline infusion (S). In 10 overweight subjects we additionally performed the euglycemic clamp with insulin detemir (D). While human insulin administration did not change cerebrocortical activity relative to saline (p = 0.90) in overweight subjects, beta activity increased during D administration (basal 59±3 fT, 1st step 62±3 fT, 2nd step 66±5, p = 0.001, D vs. HI). As under this condition glucose infusion rates were lower with D than with HI (p = 0.003), it can be excluded that the cerebral effect is the consequence of a systemic effect. The total effect of insulin detemir on beta activity was not different from the human insulin effect in lean subjects (p = 0.78).
Conclusions/Significance
Despite cerebrocortical resistance to human insulin, insulin detemir increased beta activity in overweight human subjects similarly as human insulin in lean subjects. These data suggest that the decreased cerebral beta activity response in overweight subjects can be restored by insulin detemir.
Keyword(s)
Übergewicht Langsames Hirnpotenzial Insulinresistenz Übergewicht Langsames Hirnpotenzial Insulinresistenz insulin resistance cerebrocortical beta activity insulin detemir experiment overweight humans MEGPersistent Identifier
Date of first publication
2007
Publication status
unknown
Review status
unknown
Citation
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Tschritter_PLOS.pdfAdobe PDF - 191.1KBMD5: babe118cf41b2247a57197f1691d5459
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There are no other versions of this object.
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Author(s) / Creator(s)Tschritter, Otto
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Author(s) / Creator(s)Hennige, Anita M.
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Author(s) / Creator(s)Preissl, Hubert
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Author(s) / Creator(s)Porubska, Katarina
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Author(s) / Creator(s)Schäfer, Silke A.
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Author(s) / Creator(s)Lutzenberger, Werner
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Author(s) / Creator(s)Machicao, Fausto
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Author(s) / Creator(s)Birbaumer, Niels
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Author(s) / Creator(s)Fritsche, Andreas
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Author(s) / Creator(s)Häring, Hans-Ulrich
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PsychArchives acquisition timestamp2022-11-22T06:49:52Z
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Made available on2008-08-08
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Made available on2015-12-01T10:32:16Z
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Made available on2022-11-22T06:49:52Z
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Date of first publication2007
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Abstract / DescriptionBackground Insulin stimulates cerebrocortical beta and theta activity in lean humans. This effect is reduced in obese individuals indicating cerebrocortical insulin resistance. In the present study we tested whether insulin detemir is a suitable tool to restore the cerebral insulin response in overweight humans. This approach is based on studies in mice where we could recently demonstrate increased brain tissue concentrations of insulin and increased insulin signaling in the hypothalamus and cerebral cortex following peripheral injection of insulin detemir. Methodology/Principal Findings We studied activity of the cerebral cortex using magnetoencephalography in 12 lean and 34 overweight non-diabetic humans during a 2-step hyperinsulinemic euglycemic clamp (each step 90 min) with human insulin (HI) and saline infusion (S). In 10 overweight subjects we additionally performed the euglycemic clamp with insulin detemir (D). While human insulin administration did not change cerebrocortical activity relative to saline (p = 0.90) in overweight subjects, beta activity increased during D administration (basal 59±3 fT, 1st step 62±3 fT, 2nd step 66±5, p = 0.001, D vs. HI). As under this condition glucose infusion rates were lower with D than with HI (p = 0.003), it can be excluded that the cerebral effect is the consequence of a systemic effect. The total effect of insulin detemir on beta activity was not different from the human insulin effect in lean subjects (p = 0.78). Conclusions/Significance Despite cerebrocortical resistance to human insulin, insulin detemir increased beta activity in overweight human subjects similarly as human insulin in lean subjects. These data suggest that the decreased cerebral beta activity response in overweight subjects can be restored by insulin detemir.en
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Publication statusunknown
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Review statusunknown
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ISSN1932-6203
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Persistent Identifierhttps://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bsz:291-psydok-21523
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Persistent Identifierhttps://hdl.handle.net/20.500.11780/1151
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Persistent Identifierhttps://doi.org/10.23668/psycharchives.11309
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Language of contenteng
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Is part ofPLoS ONE 2(11): e1196. doi:10.1371/journal.pone.0001196
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Keyword(s)Übergewichtde
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Keyword(s)Langsames Hirnpotenzialde
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Keyword(s)Insulinresistenzde
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Keyword(s)Übergewichtde
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Keyword(s)Langsames Hirnpotenzialde
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Keyword(s)Insulinresistenzde
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Keyword(s)insulin resistanceen
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Keyword(s)cerebrocortical beta activityen
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Keyword(s)insulin detemiren
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Keyword(s)experimenten
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Keyword(s)overweight humansen
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Keyword(s)MEGen
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Dewey Decimal Classification number(s)150
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TitleCerebrocortical Beta Activity in Overweight Humans Responds to Insulin Detemiren
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DRO typearticle
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Visible tag(s)PsyDok