ArticleJCI insight2017
PI3Kα inactivation in leptin receptor cells increases leptin sensitivity but disrupts growth and reproduction.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 40 citations in OpenAlex.
- IGF-1 and insulin receptors in LepRb neurons jointly regulate body growth, bone mass, reproduction, and metabolism.Molecular metabolism · 2026Article
- Hypothalamic BCL6 signaling modulates energy homeostasis and metabolism by inhibiting STAT3 transcription.Journal of advanced research · 2026Article
- Neuroendocrine plasticity and crosstalk in pubertal development.Journal of neuroendocrinology · 2026Review
- Lack of glutamate neurotransmission in melanin-concentrating hormone neurons alters mouse reproduction and metabolism in a sex-specific manner.Biology of sex differences · 2025Article
- PI3K in the VMH Attenuates Diet-Induced Obesity and Participates in the Effects of E2 on Energy Expenditure in Mice.Journal of the Endocrine Society · 2025Article
- A Leptin Receptor Mutation Which Impairs Fertility in Ewes Causes Delayed Puberty in Male and Female Mice.Endocrinology · 2025Article
- Transcriptome and DNA methylation analysis of the goat pineal gland during puberty.Scientific reports · 2025Article
- Article
- The ventral premammillary nucleus at the interface of environmental cues and social behaviors.Frontiers in neuroscience · 2025Review
- History and future of leptin: Discovery, regulation and signaling.Metabolism: clinical and experimental · 2024Review
- Signatures of metabolic diseases on spermatogenesis and testicular metabolism.Nature reviews. Urology · 2024Review
- Article
- IGF-1 Acts through Kiss1-expressing Cells to Influence Metabolism and Reproduction.bioRxiv : the preprint server for biology · 2024Article
- Genetic and epigenetic differentiation in response to genomic selection for avian lay date.Evolutionary applications · 2024Article
- Metabolic control of puberty: 60 years in the footsteps of Kennedy and Mitra's seminal work.Nature reviews. Endocrinology · 2024Review
- Multiple Leptin Signalling Pathways in the Control of Metabolism and Fertility: A Means to Different Ends?International journal of molecular sciences · 2021Review
- Protocol to extract actively translated mRNAs from mouse hypothalamus by translating ribosome affinity purification.STAR protocols · 2021Article
- ERα Signaling in GHRH/Kiss1 Dual-Phenotype Neurons Plays Sex-Specific Roles in Growth and Puberty.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Article
- Lack of AR in LepRb Cells Disrupts Ambulatory Activity and Neuroendocrine Axes in a Sex-Specific Manner in Mice.Endocrinology · 2020Article
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 4 institutions in 2 countries.
Funding
Abstract
The role of PI3K in leptin physiology has been difficult to determine due to its actions downstream of several metabolic cues, including insulin. Here, we used a series of mouse models to dissociate the roles of specific PI3K catalytic subunits and of insulin receptor (InsR) downstream of leptin signaling. We show that disruption of p110α and p110β subunits in leptin receptor cells (LRΔα+β) produces a lean phenotype associated with increased energy expenditure, locomotor activity, and thermogenesis. LRΔα+β mice have deficient growth and delayed puberty. Single subunit deletion (i.e., p110α in LRΔα) resulted in similarly increased energy expenditure, deficient growth, and pubertal development, but LRΔα mice have normal locomotor activity and thermogenesis. Blunted PI3K in leptin receptor (LR) cells enhanced leptin sensitivity in metabolic regulation due to increased basal hypothalamic pAKT, leptin-induced pSTAT3, and decreased PTEN levels. However, these mice are unresponsive to leptin's effects on growth and puberty. We further assessed if these phenotypes were associated with disruption of insulin signaling. LRΔInsR mice have no metabolic or growth deficit and show only mild delay in pubertal completion. Our findings demonstrate that PI3K in LR cells plays an essential role in energy expenditure, growth, and reproduction. These actions are independent from insulin signaling.
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What Socratic 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 Socratic graph.