ArticleMolecular metabolism2014
Leptin receptor neurons in the dorsomedial hypothalamus are key regulators of energy expenditure and body weight, but not food intake.
Article in Molecular metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.
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
113 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.
- Is leptin resistance the cause or the consequence of diet-induced obesity?International journal of obesity (2005) · 2018Pooled it
- Leptin administration in physiological or pharmacological doses does not alter circulating irisin levels in humans.International journal of obesity (2005) · 2016Trial
- Brain-Wide Connectivity and Topographic Organization of Leptin Receptor Neurons in the Dorsomedial Hypothalamus.CNS neuroscience & therapeutics · 2026Article
- The hypothalamus as a therapeutic target: Towards novel approaches for managing antipsychotic-induced weight gain.Reviews in endocrine & metabolic disorders · 2026Review
- A direct SCN-to-DMH output pathway organizes circadian behavioral timing.bioRxiv : the preprint server for biology · 2026Article
- Obesogenic effects of warm temperature involve feeding adaptation by preoptic area leptin receptor neurons.Communications biology · 2026Article
- Thermoregulatory Dysfunction in Parkinson's Disease: Mechanisms, Implications, and Therapeutic Perspectives.Cells · 2025Review
- Central leptin pathways in metabolic homeostasis.Clinical science (London, England : 1979) · 2025Review
- Molecular mechanisms and neural mediators of leptin action.Genes & development · 2025Review
- Melanocortin-responsive Kiss1 neurons of the arcuate nucleus drive energy expenditure through glutamatergic signaling to the dorsomedial hypothalamus.bioRxiv : the preprint server for biology · 2025Article
- Leptin receptor neurons in the dorsomedial hypothalamus require distinct neuronal subsets for thermogenesis and weight loss.Metabolism: clinical and experimental · 2025Article
- Thermally induced neuronal plasticity in the hypothalamus mediates heat tolerance.Nature neuroscience · 2025Article
- Hypothalamic neural circuits regulating energy expenditure.Vitamins and hormones · 2025Review
- History and future of leptin: Discovery, regulation and signaling.Metabolism: clinical and experimental · 2024Review
- Article
- The Role of BDNF and TrkB in the Central Control of Energy and Glucose Balance: An Update.Biomolecules · 2024Review
- Central Mechanisms of Thermoregulation and Fever in Mammals.Advances in experimental medicine and biology · 2024Review
- Leptin signaling in the dorsomedial hypothalamus couples breathing and metabolism in obesity.Cell reports · 2023Article
- Brown adipocyte and browning thermogenesis: metabolic crosstalk beyond mitochondrial limits and physiological impacts.Adipocyte · 2023Review
- Suppression of food intake by Glp1r/Lepr-coexpressing neurons prevents obesity in mouse models.The Journal of clinical investigation · 2023Article
53 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
9 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveLeptin responsive neurons play an important role in energy homeostasis, controlling specific autonomic, behavioral, and neuroendocrine functions. We have previously identified a population of leptin receptor (LepRb) expressing neurons within the dorsomedial hypothalamus/dorsal hypothalamic area (DMH/DHA) which are related to neuronal circuits that control brown adipose tissue (BAT) thermogenesis. Intra-DMH leptin injections also activate sympathetic outflow to BAT, but whether such effects are mediated directly via DMH/DHA LepRb neurons and whether this is physiologically relevant for whole body energy expenditure and body weight regulation has yet to be determined.
methodsWe used pharmacosynthetic receptors (DREADDs) to selectively activate DMH/DHA LepRb neurons. We further deleted LepRb with virally driven cre-recombinase from DMH/DHA neurons and determined the physiological importance of DMH/DHA LepRb neurons in whole body energy homeostasis.
resultsNeuronal activation of DMH/DHA LepRb neurons with DREADDs promoted BAT thermogenesis and locomotor activity, which robustly induced energy expenditure (p < 0.001) and decreases body weight (p < 0.001). Similarly, intra-DMH/DHA leptin injections normalized hypothermia and attenuated body weight gain in leptin-deficient ob/ob mice. Conversely, ablation of LepRb from DMH/DHA neurons remarkably drives weight gain (p < 0.001) by reducing energy expenditure (p < 0.001) and locomotor activity (p < 0.001). The observed changes in body weight were largely independent of food intake.
conclusionTaken together, our data highlight that DMH/DHA LepRb neurons are sufficient and necessary to regulate energy expenditure and body weight.
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.