ArticleDiabetes2013
Blunted refeeding response and increased locomotor activity in mice lacking FoxO1 in synapsin-Cre-expressing neurons.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- G Protein-Coupled Receptor 17 (Gpr17) Enhances Leptin and Insulin Sensitivity in Lean and Obese Mouse Models.Obesity (Silver Spring, Md.) · 2026Review
- Tirzepatide Synergizes with Leptin on Weight Loss and Restoring Metabolic Homeostasis in Diet-induced Obesity Model.bioRxiv : the preprint server for biology · 2025Article
- Hot Spots for the Use of Intranasal Insulin: Cerebral Ischemia, Brain Injury, Diabetes Mellitus, Endocrine Disorders and Postoperative Delirium.International journal of molecular sciences · 2023Review
- Role of FoxO transcription factors in aging and age-related metabolic and neurodegenerative diseases.Cell & bioscience · 2021Review
- Tissue-Specific Effects of Leptin on Glucose and Lipid Metabolism.Endocrine reviews · 2021Review
- Neuron-specific Kv1.1 deficiency is sufficient to cause epilepsy, premature death, and cardiorespiratory dysregulation.Neurobiology of disease · 2020Article
- Acid-Sensing Ion Channels: Novel Mediators of Cerebral Vascular Responses.Circulation research · 2019Article
- Neuronal Dnmt1 Deficiency Attenuates Diet-Induced Obesity in Mice.Endocrinology · 2018Article
- FOXO in Neural Cells and Diseases of the Nervous System.Current topics in developmental biology · 2018Review
- Embryonic ablation of neuronal VGF increases energy expenditure and reduces body weight.Neuropeptides · 2017Article
- Obese Neuronal PPARγ Knockout Mice Are Leptin Sensitive but Show Impaired Glucose Tolerance and Fertility.Endocrinology · 2017Article
- Sweet old memories: a review of the experimental models of the association between diabetes, senility and dementia.Metabolic brain disease · 2016Review
- FoxO1 in dopaminergic neurons regulates energy homeostasis and targets tyrosine hydroxylase.Nature communications · 2016Article
- Molecular and biochemical trajectories from diabetes to Alzheimer's disease: A critical appraisal.World journal of diabetes · 2015Review
- Minireview: Central Sirt1 regulates energy balance via the melanocortin system and alternate pathways.Molecular endocrinology (Baltimore, Md.) · 2014Review
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Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Successful development of antiobesity agents requires detailed knowledge of neural pathways controlling body weight, eating behavior, and peripheral metabolism. Genetic ablation of FoxO1 in selected hypothalamic neurons decreases food intake, increases energy expenditure, and improves glucose homeostasis, highlighting the role of this gene in insulin and leptin signaling. However, little is known about potential effects of FoxO1 in other neurons. To address this question, we executed a broad-based neuronal ablation of FoxO1 using Synapsin promoter-driven Cre to delete floxed Foxo1 alleles. Lineage-tracing experiments showed that NPY/AgRP and POMC neurons were minimally affected by the knockout. Nonetheless, Syn-Cre-Foxo1 knockouts demonstrated a catabolic energy homeostatic phenotype with a blunted refeeding response, increased sensitivity to leptin and amino acid signaling, and increased locomotor activity, likely attributable to increased melanocortinergic tone. We confirmed these data in mice lacking the three Foxo genes. The effects on locomotor activity could be reversed by direct delivery of constitutively active FoxO1 to the mediobasal hypothalamus, but not to the suprachiasmatic nucleus. The data reveal that the integrative function of FoxO1 extends beyond the arcuate nucleus, suggesting that central nervous system inhibition of FoxO1 function can be leveraged to promote hormone sensitivity and prevent a positive energy balance.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.