ArticleJournal of molecular neuroscience : MN2013
Hypersomnolence and reduced activity in pan-leptin receptor knockout mice.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Leptin's potential mechanisms in ICU-acquired weakness.Lipids in health and disease · 2025Review
- A novel role for phospholamban in the thalamic reticular nucleus.Scientific reports · 2024Article
- Article
- Role of Astrocytes in Leptin Signaling.Journal of molecular neuroscience : MN · 2015Article
- Sleep fragmentation has differential effects on obese and lean mice.Journal of molecular neuroscience : MN · 2015Article
- Sleep restriction impairs blood-brain barrier function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Excessive obesity correlates with hypersomnolence and impaired cognitive function, presumably induced by metabolic factors and cytokines. Production of the adipokine leptin correlates with the amount of adiposity, and leptin has been shown to promote sleep. To determine whether leptin plays a major role in the hypersomnolence of obesity, we measured sleep architecture in pan-leptin receptor knockout (POKO) mice that do not respond to leptin because of the production of a mutant, non-signaling receptor. The obese POKO mice had more non-rapid eye movement (NREM) sleep and less waking time than their littermate controls. This was mainly seen during the light span, although increased bouts of rapid eye movement sleep were also seen in the dark span. The increase of NREM sleep correlated with the extent of obesity. The POKO mice also had decreased locomotor activity and more immobility in the open field test, but there was no increase of forced immobility nor reduction of sucrose intake as would be seen in depression. The increased NREM sleep and reduced locomotor activity in the POKO mice suggest that it was obesity, rather than leptin signaling, that played a predominant role in altering sleep architecture and activity.
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Registered trials
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