ArticleThe Journal of clinical investigation2017
A leptin-regulated circuit controls glucose mobilization during noxious stimuli.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 36 citations in OpenAlex.
- Control of physiologic glucose homeostasis via hypothalamic modulation of gluconeogenic substrate availability.Molecular metabolism · 2025Article
- Molecular mechanisms and neural mediators of leptin action.Genes & development · 2025Review
- Central and peripheral neural circuits regulating glucose homeostasis.npj biomedical innovations · 2025Review
- Article
- History and future of leptin: Discovery, regulation and signaling.Metabolism: clinical and experimental · 2024Review
- Ventromedial hypothalamic nucleus subset stimulates tissue thermogenesis via preoptic area outputs.Molecular metabolism · 2024Article
- In light of breathing: environmental light is an important modulator of breathing with clinical implications.Frontiers in neuroscience · 2023Article
- Leptin signaling and leptin resistance.Medical review (2021) · 2022Review
- NTS Prlh overcomes orexigenic stimuli and ameliorates dietary and genetic forms of obesity.Nature communications · 2021Article
- The Role of Mediobasal Hypothalamic PACAP in the Control of Body Weight and Metabolism.Endocrinology · 2021Article
- Tissue-Specific Effects of Leptin on Glucose and Lipid Metabolism.Endocrine reviews · 2021Review
- Ventromedial hypothalamic nucleus neuronal subset regulates blood glucose independently of insulin.The Journal of clinical investigation · 2020Article
- Calcitonin Receptor Neurons in the Mouse Nucleus Tractus Solitarius Control Energy Balance via the Non-aversive Suppression of Feeding.Cell metabolism · 2020Article
- Article
- Distinct Neuronal Projections From the Hypothalamic Ventromedial Nucleus Mediate Glycemic and Behavioral Effects.Diabetes · 2018Article
- Remote control of glucose-sensing neurons to analyze glucose metabolism.American journal of physiology. Endocrinology and metabolism · 2018Review
- The Parabrachial Nucleus: CGRP Neurons Function as a General Alarm.Trends in neurosciences · 2018Review
- In Uncontrolled Diabetes, Hyperglucagonemia and Ketosis Result From Deficient Leptin Action in the Parabrachial Nucleus.Endocrinology · 2018Article
- Leptin and the maintenance of elevated body weight.Nature reviews. Neuroscience · 2018Review
- Differential contribution of POMC and AgRP neurons to the regulation of regional autonomic nerve activity by leptin.Molecular metabolism · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 3 countries.
Funding
Abstract
Adipocytes secrete the hormone leptin to signal the sufficiency of energy stores. Reductions in circulating leptin concentrations reflect a negative energy balance, which augments sympathetic nervous system (SNS) activation in response to metabolically demanding emergencies. This process ensures adequate glucose mobilization despite low energy stores. We report that leptin receptor-expressing neurons (LepRb neurons) in the periaqueductal gray (PAG), the largest population of LepRb neurons in the brain stem, mediate this process. Application of noxious stimuli, which often signal the need to mobilize glucose to support an appropriate response, activated PAG LepRb neurons, which project to and activate parabrachial nucleus (PBN) neurons that control SNS activation and glucose mobilization. Furthermore, activating PAG LepRb neurons increased SNS activity and blood glucose concentrations, while ablating LepRb in PAG neurons augmented glucose mobilization in response to noxious stimuli. Thus, decreased leptin action on PAG LepRb neurons augments the autonomic response to noxious stimuli, ensuring sufficient glucose mobilization during periods of acute demand in the face of diminished energy stores.
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.