ArticleCell metabolism2015
Diet-induced obese mice retain endogenous leptin action.
Article in Cell metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Is leptin resistance the cause or the consequence of diet-induced obesity?International journal of obesity (2005) · 2018Pooled it
- Leptin-sensitive hypothalamic Lepr+/Glp1r+ neurons limit hyperphagia and weight gain in diet-induced obesity.The EMBO journal · 2026Article
- Cardiometabolic regulation by adipocyte-derived leptin and the brain melanocortin system.Clinical science (London, England : 1979) · 2026Review
- Tanycytes: bloodhounds of the metabolic brain.Trends in endocrinology and metabolism: TEM · 2026Review
- Increased leptin signaling drives the response of hypothalamic LepRb neurons to diet-induced obesity.Molecular metabolism · 2026Article
- TonEBP as a key regulator of hypothalamic leptin signaling and resistance.Cellular and molecular life sciences : CMLS · 2026Article
- Obesity dysregulates feeding-evoked response dynamics in hypothalamic satiety neurons.Scientific reports · 2025Article
- An alternative neural basis underlying leptin resistance.Cell reports · 2025Article
- Heat-InactivatedInternational journal of molecular sciences · 2025Article
- Roles of thyroid and leptin hormones and their crosstalk in male reproductive functions: an updated review.Endocrine · 2025Review
- Hypothalamic neural circuits regulating energy expenditure.Vitamins and hormones · 2025Review
- History and future of leptin: Discovery, regulation and signaling.Metabolism: clinical and experimental · 2024Review
- Interplay between the brain and adipose tissue: a metabolic conversation.EMBO reports · 2024Review
- Article
- Leptin Reduction as a Required Component for Weight Loss.Diabetes · 2024Article
- The Mechanism of Leptin Resistance in Obesity and Therapeutic Perspective.Advances in experimental medicine and biology · 2024Review
- The melanocortin action is biased toward protection from weight loss in mice.Nature communications · 2023Article
- Ultra-Processed Food Impairs Bone Quality, Increases Marrow Adiposity and Alters Gut Microbiome in Mice.Foods (Basel, Switzerland) · 2021Article
- Obesity-associated hyperleptinemia alters the gliovascular interface of the hypothalamus to promote hypertension.Cell metabolism · 2021Article
- LRP1 regulates food intake and energy balance in GABAergic neurons independently of leptin action.American journal of physiology. Endocrinology and metabolism · 2021Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Obesity is characterized by hyperleptinemia and decreased response to exogenous leptin. This has been widely attributed to the development of leptin resistance, a state of impaired leptin signaling proposed to contribute to the development and persistence of obesity. To directly determine endogenous leptin activity in obesity, we treated lean and obese mice with a leptin receptor antagonist. The antagonist increased feeding and body weight (BW) in lean mice, but not in obese models of leptin, leptin receptor, or melanocortin-4 receptor deficiency. In contrast, the antagonist increased feeding and BW comparably in lean and diet-induced obese (DIO) mice, an increase associated with decreased hypothalamic expression of Socs3, a primary target of leptin. These findings demonstrate that hyperleptinemic DIO mice retain leptin suppression of feeding comparable to lean mice and counter the view that resistance to endogenous leptin contributes to the persistence of DIO in mice.
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.