Insulin-mediated cortical activity in the slow frequency range is diminished in obese mice and promotes physical inactivity
Open accessAbstract
Aims/hypothesis There is evidence from mouse models and humans that alterations in insulin action in the brain are accompanied by an obese phenotype; however, the impact of insulin with regard to behavioural aspects such as locomotion is unknown.Methods To address insulin action in the brain with regard to cortical activity in distinct frequency bands and the behavioural consequences, the insulin signalling pathway was followed from the receptor to electrical activity and locomotion. Western blot analysis, electrocorticograms with intracerebroventricular (i.c.v.) application of insulin, and measurements of locomotor activity were performed in lean and obese, as well as Toll-like receptor (TLR) 2/4-deficient, mice.Results We show that insulin application i.c.v. into lean mice was accompanied by a profound increase in cortical activity in the slow frequency range, while diet-induced obese mice displayed insulin resistance. In parallel, insulin administered i.c.v. increased locomotor activity in lean mice, whereas a phosphatidylinositol-3 (PI3) kinase inhibitor or obesity abolished insulin-mediated locomotion. A potential candidate that links insulin signalling to locomotion is the Kv1.3 channel that is activated by PI3-kinase. Pharmacological inhibition of Kv1.3 channels that bypassed insulin receptor activation promoted activity. Moreover, mice deficient in TLR2/4-dependent signalling displayed an increase in cortical activity in the slow frequency range that was correlated with improved spontaneous and insulin-mediated locomotor activity.Conclusions/interpretation Our data provide functional evidence for a direct effect of insulin on brain activation patterns in the slow frequency bands and locomotor activity in lean mice, while in obese mice, insulin-mediated locomotion is blunted and further aggravates physical inactivity.
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In animals, intracerebroventricular insulin delivery increases locomotor activity.
“in animals, i.c.v.insulin delivery increases locomotor activity.”
From Intranasal insulin (2021) · cites this paper as [68]
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- Authors
- Hennige, A. M., Sartorius, T., Lutz, S. Z., Tschritter, O., Preissl, H., Hopp, S., Fritsche, A., Rammensee, H.-G., Ruth, P., & Häring, H.-U.
- Affiliations
- University of Tübingen (DE)
- University of Arkansas for Medical Sciences (US)
- Corresponding author
- Häring, H.-U.
- Venue
- Diabetologia
- Published
- 2009-09-15
- Volume
- 52
- Issue
- 11
- Pages
- 2416-2424
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W1982853655
- Cited by
- 41
- References
- 34
- Citations by year
- 2023: 1 · 2022: 4 · 2021: 3 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 5 · 2016: 3 · 2015: 7 · 2014: 3 · 2013: 2 · 2012: 2
- FWCI
- 1.05
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (HE 3653/3-1, KFO 114/2, KFO 114)
- Deutsche Diabetes Gesellschaft
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- diet-induced obesity, insulin resistance, locomotor activity, physical inactivity, Kv1.3 potassium channel, TLR2/4, electrocorticography
- MeSH terms
- Animals, Cerebral Cortex, Cerebral Ventricles, Insulin, Insulin Resistance, Locomotion, Male, Mice, Inbred C57BL, Mice, Obese, Obesity, Phosphorylation, Receptor, Insulin, Telemetry, Signal Transduction, Mice, Knockout, Phosphatidylinositol 3-Kinases, Toll-Like Receptor 2, Mice, Lethargy
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