ArticleCell metabolism2014
Insulin excites anorexigenic proopiomelanocortin neurons via activation of canonical transient receptor potential channels.
Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
137 citing papers in PubMed, 218 citations in OpenAlex.
- Optical control of the hypothalamic arcuate nucleus kisspeptin neuronal network with a photoswitchable peptide that drives luteinizing hormone release in female mice.Journal of neuroendocrinology · 2026Article
- Reduced melanocortin tone modulates feeding during pregnancy in mice.Nature communications · 2026Article
- Scalable hypothalamic neuron differentiation from human pluripotent stem cells suitable for modeling metabolic disorders.Stem cell reports · 2026Article
- 17α-Estradiol: A mildly feminizing estrogen with sex-specific metabolic and lifespan benefits.Ageing research reviews · 2026Review
- Hypothalamic insulin resistance in type 2 diabetes is localized to the posterior hypothalamus.JCI insight · 2026Article
- Hypothalamus-liver talks: whispers in the language of metabolism.Reviews in endocrine & metabolic disorders · 2026Review
- From brain bioenergetics to hypothalamic glucoregulation: A shared-systems hypothesis for intrinsic dysglycemia in schizophrenia.Reviews in endocrine & metabolic disorders · 2026Review
- Cav3.1 is a neuronal leucine sensor that mediates satiety and weight loss in response to dietary protein.Cell metabolism · 2026Article
- TOX3 in hypothalamic POMC-lineage cells regulates energy balance via the PTEN-AKT signaling axis.Nature communications · 2026Article
- Article
- Insulin and IGF signaling in the brain: multilevel regulation of synaptic and network homeostasis.Frontiers in endocrinology · 2026Review
- Neuroendocrine crosstalk between sex and metabolic hormones: mechanisms and implications across the female reproductive spectrum.Discover endocrinology and metabolism · 2026Review
- Sex-Specific Thermoregulatory Effects of Estrogen Signaling in Reprimo Lineage Cells.Endocrinology · 2025Article
- Sex-specific thermoregulatory effects of estrogen signaling inbioRxiv : the preprint server for biology · 2025Article
- Article
- G proteins of the GScience advances · 2025Article
- Glutamatergic Input From Arcuate Nucleus Kiss1 Neurons to Preoptic Kiss1 Neurons Is Required for LH Surge in Female Mice.Endocrinology · 2025Article
- Regulation of BAT thermogenesis via TRPA1-expressing hypothalamic POMC neurons.Animal cells and systems · 2025Article
- Brain-Body Communication in Glucose Metabolism.Advances in experimental medicine and biology · 2025Review
- Article
77 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Proopiomelanocortin (POMC) neurons within the hypothalamic arcuate nucleus are vital anorexigenic neurons. Although both the leptin and insulin receptors are coupled to the activation of phosphatidylinositide 3 kinase (PI3K) in POMC neurons, they are thought to have disparate actions on POMC excitability. Using whole-cell recording and selective pharmacological tools, we have found that, similar to leptin, purified insulin depolarized POMC and adjacent kisspeptin neurons via activation of TRPC5 channels, which are highly expressed in these neurons. In contrast, insulin hyperpolarized and inhibited NPY/AgRP neurons via activation of KATP channels. Moreover, Zn(2+), which is found in insulin formulations at nanomolar concentrations, inhibited POMC neurons via activation of KATP channels. Finally, as predicted, insulin given intracerebroventrically robustly inhibited food intake and activated c-fos expression in arcuate POMC neurons. Our results show that purified insulin excites POMC neurons in the arcuate nucleus, which we propose is a major mechanism by which insulin regulates energy homeostasis.
Indexed as
Identifiers
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.