ArticleEndocrinology2012
Deficiency of PTP1B in leptin receptor-expressing neurons leads to decreased body weight and adiposity in mice.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 70 citations in OpenAlex.
- Mechanisms, functions and therapeutic targeting of protein tyrosine phosphatases.Nature reviews. Molecular cell biology · 2026Review
- Restoring leptin sensitivity in metabolic and extra-metabolic leptin resistance: Pharmacologic strategies, systemic implications, and future directions.EXCLI journal · 2026Review
- Central leptin pathways in metabolic homeostasis.Clinical science (London, England : 1979) · 2025Review
- Molecular mechanisms and neural mediators of leptin action.Genes & development · 2025Review
- Leptin and Associated Neural Pathways Underlying Obesity-Induced Hypertension.Comprehensive Physiology · 2025Review
- Protein tyrosine phosphatase 1B in metabolic diseases and drug development.Nature reviews. Endocrinology · 2024Review
- MultiscaleJournal of chemical information and modeling · 2024Article
- Breast feeding, obesity, and asthma association: clinical and molecular views.Clinical and molecular allergy : CMA · 2023Review
- Mechanisms of reduced leptin-mediated satiety signaling during obesity.International journal of obesity (2005) · 2022Article
- Leptin as a key regulator of the adipose organ.Reviews in endocrine & metabolic disorders · 2022Review
- Multiple Leptin Signalling Pathways in the Control of Metabolism and Fertility: A Means to Different Ends?International journal of molecular sciences · 2021Review
- In vivo self-assembled small RNAs as a new generation of RNAi therapeutics.Cell research · 2021Article
- Non-redox cycling mechanisms of oxidative stress induced by PM metals.Free radical biology & medicine · 2020Review
- Angiotensin II induces apoptosis of cardiac microvascular endothelial cells via regulating PTP1B/PI3K/Akt pathway.In vitro cellular & developmental biology. Animal · 2019Article
- The Role of Protein Tyrosine Phosphatase (PTP)-1B in Cardiovascular Disease and Its Interplay with Insulin Resistance.Biomolecules · 2019Review
- The melanocortin pathway and control of appetite-progress and therapeutic implications.The Journal of endocrinology · 2019Review
- Small molecules for fat combustion: targeting obesity.Acta pharmaceutica Sinica. B · 2019Review
- Hydroxyoleoside-type seco-iridoids from Symplocos cochinchinensis and their insulin mimetic activity.Scientific reports · 2019Article
- Protein tyrosine phosphatase 1B deficiency in podocytes mitigates hyperglycemia-induced renal injury.Metabolism: clinical and experimental · 2017Article
- The cellular and molecular bases of leptin and ghrelin resistance in obesity.Nature reviews. Endocrinology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Protein tyrosine phosphatase 1B (PTP1B) is a ubiquitously expressed tyrosine phosphatase implicated in the negative regulation of leptin and insulin receptor signaling. PTP1B(-/-) mice possess a lean metabolic phenotype attributed at least partially to improved hypothalamic leptin sensitivity. Interestingly, mice lacking both leptin and PTP1B (ob/ob:PTP1B(-/-)) have reduced body weight compared with mice lacking leptin only, suggesting that PTP1B may have important leptin-independent metabolic effects. We generated mice with PTP1B deficiency specifically in leptin receptor (LepRb)-expressing neurons (LepRb-PTP1B(-/-)) and compared them with LepRb-Cre-only wild-type (WT) controls and global PTP1B(-/-) mice. Consistent with PTP1B's role as a negative regulator of leptin signaling, our results show that LepRb-PTP1B(-/-) mice are leptin hypersensitive and have significantly reduced body weight when maintained on chow or high-fat diet (HFD) compared with WT controls. LepRb-PTP1B(-/-) mice have a significant decrease in adiposity on HFD compared with controls. Notably, the extent of attenuated body weight gain on HFD, as well as the extent of leptin hypersensitivity, is similar between LepRb-PTP1B(-/-) mice and global PTP1B(-/-) mice. Overall, these results demonstrate that PTP1B deficiency in LepRb-expressing neurons results in reduced body weight and adiposity compared with WT controls and likely underlies the improved metabolic phenotype of global and brain-specific PTP1B-deficient models. Subtle phenotypic differences between LepRb-PTP1B(-/-) and global PTP1B(-/-) mice, however, suggest that PTP1B independent of leptin signaling may also contribute to energy balance in mice.
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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.