ArticleAmerican journal of physiology. Endocrinology and metabolism2011
Deficiency of PTP1B in POMC neurons leads to alterations in energy balance and homeostatic response to cold exposure.
Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Thermal challenge and food intake: Mutual regulatory mechanisms.Neural regeneration research · 2026Article
- Beyond satiety: unraveling the complex roles of POMC neurons in behavior and metabolism.Reviews in endocrine & metabolic disorders · 2026Review
- Deletion of PTP1B in cardiomyocytes alters cardiac metabolic signaling to protect against cardiomyopathy induced by a high-fat diet.Science signaling · 2025Article
- The Mechanism of Leptin Resistance in Obesity and Therapeutic Perspective.Advances in experimental medicine and biology · 2024Review
- Myeloid PTP1B deficiency protects against atherosclerosis by improving cholesterol homeostasis through an AMPK-dependent mechanism.Journal of translational medicine · 2023Article
- Association between PTPN1 polymorphisms and obesity-related phenotypes in European adolescents: influence of physical activity.Pediatric research · 2023Article
- Therapeutic Role of Protein Tyrosine Phosphatase 1B in Parkinson's Disease via Antineuroinflammation and NeuroprotectionParkinson's disease · 2020Article
- Review
- Effects of thyroid hormones and cold acclimation on the energy metabolism of the striped hamster (Cricetulus barabensis).Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2019Article
- Regulation of intestinal growth in response to variations in energy supply and demand.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2018Review
- Lipoprotein Lipase Expression in Hypothalamus Is Involved in the Central Regulation of Thermogenesis and the Response to Cold Exposure.Frontiers in endocrinology · 2018Article
- Reestablishment of Energy Balance in a Male Mouse Model With POMC Neuron Deletion of BMPR1A.Endocrinology · 2017Article
- Between fire and ice: refractory hypothermia and warmth-induced pain in inherited erythromelalgia.BMJ case reports · 2017Article
- Hypothalamic inflammation in obesity and metabolic disease.The Journal of clinical investigation · 2017Review
- Early leptin intervention reverses perturbed energy balance regulating hypothalamic neuropeptides in the pre- and postnatal calorie-restricted female rat offspring.Journal of neuroscience research · 2015Article
- Angiotensin type 1a receptors in the forebrain subfornical organ facilitate leptin-induced weight loss through brown adipose tissue thermogenesis.Molecular metabolism · 2015Article
- Improved metabolic phenotype of hypothalamic PTP1B-deficiency is dependent upon the leptin receptor.Molecular metabolism · 2014Article
- Relationship status update for PTP1B and LepR: It׳s complicated.Molecular metabolism · 2014Article
- Metabolic regulation by protein tyrosine phosphatases.Journal of biomedical research · 2014Article
- New pharmacological perspectives for the leptin receptor in the treatment of obesity.Frontiers in endocrinology · 2014Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
The adipose tissue-derived hormone leptin regulates energy balance through catabolic effects on central circuits, including proopiomelanocortin (POMC) neurons. Leptin activation of POMC neurons increases thermogenesis and locomotor activity. Protein tyrosine phosphatase 1B (PTP1B) is an important negative regulator of leptin signaling. POMC neuron-specific deletion of PTP1B in mice results in reduced high-fat diet-induced body weight and adiposity gain due to increased energy expenditure and greater leptin sensitivity. Mice lacking the leptin gene (ob/ob mice) are hypothermic and cold intolerant, whereas leptin delivery to ob/ob mice induces thermogenesis via increased sympathetic activity to brown adipose tissue (BAT). Here, we examined whether POMC PTP1B mediates the thermoregulatory response of CNS leptin signaling by evaluating food intake, body weight, core temperature (T(C)), and spontaneous physical activity (SPA) in response to either exogenous leptin or 4-day cold exposure (4°C) in male POMC-Ptp1b-deficient mice compared with wild-type controls. POMC-Ptp1b(-/-) mice were hypersensitive to leptin-induced food intake and body weight suppression compared with wild types, yet they displayed similar leptin-induced increases in T(C). Interestingly, POMC-Ptp1b(-/-) mice had increased BAT weight and elevated plasma triiodothyronine (T(3)) levels in response to a 4-day cold challenge, as well as reduced SPA 24 h after cold exposure, relative to controls. These data show that PTP1B in POMC neurons plays a role in short-term cold-induced reduction of SPA and may influence cold-induced thermogenesis via enhanced activation of the thyroid axis.
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