ArticleMolecular and cellular biology2009
Neuronal protein tyrosine phosphatase 1B deficiency results in inhibition of hypothalamic AMPK and isoform-specific activation of AMPK in peripheral tissues.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 79 citations in OpenAlex.
- Hypothalamic regulation of energy homeostasis: Quo vadis.Reviews in endocrine & metabolic disorders · 2026Review
- Attack of the kinases: JNK signaling in metabolism.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Review
- SF1-specific deletion of the energy sensor AMPKγ2 induces obesity.Molecular metabolism · 2025Article
- Reprogramming energy homeostasis in children with overweight through cognitive training and social interaction. A study protocol to estimate leptin sensitivity.Frontiers in endocrinology · 2025Article
- Rheumatic diseases and metabolism: where centre and periphery meet.Nature reviews. Rheumatology · 2024Review
- Association between PTPN1 polymorphisms and obesity-related phenotypes in European adolescents: influence of physical activity.Pediatric research · 2023Article
- Evidence for a neuromuscular circuit involving hypothalamic interleukin-6 in the control of skeletal muscle metabolism.Science advances · 2022Article
- The role of protein tyrosine phosphatase 1B (PTP1B) in the pathogenesis of type 2 diabetes mellitus and its complications.Journal of physiology and biochemistry · 2022Review
- Targeting Breast Cancer and Their Stem Cell Population through AMPK Activation: Novel Insights.Cells · 2022Review
- Hypothalamic inflammation in metabolic disorders and aging.Cellular and molecular life sciences : CMLS · 2021Review
- Activation of AMPK under Hypoxia: Many Roads Leading to Rome.International journal of molecular sciences · 2020Review
- AMPK in the Ventromedial Nucleus of the Hypothalamus: A Key Regulator for Thermogenesis.Frontiers in endocrinology · 2020Review
- Hypothalamic AMPK as a Mediator of Hormonal Regulation of Energy Balance.International journal of molecular sciences · 2018Review
- Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity.Nature genetics · 2018Article
- Protein tyrosine phosphatase 1B deficiency in podocytes mitigates hyperglycemia-induced renal injury.Metabolism: clinical and experimental · 2017Article
- Deletion of ghrelin prevents aging-associated obesity and muscle dysfunction without affecting longevity.Aging cell · 2017Article
- Protein-Induced Pluripotent Stem Cells Ameliorate Cognitive Dysfunction and Reduce Aβ Deposition in a Mouse Model of Alzheimer's Disease.Stem cells translational medicine · 2017Article
- Hypothalamic AMPK: a canonical regulator of whole-body energy balance.Nature reviews. Endocrinology · 2016Review
- Leptin signalling pathways in hypothalamic neurons.Cellular and molecular life sciences : CMLS · 2016Review
- Histone Deacetylase 1 (HDAC1) Negatively Regulates Thermogenic Program in Brown Adipocytes via Coordinated Regulation of Histone H3 Lysine 27 (H3K27) Deacetylation and Methylation.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 5 countries.
Funding
Abstract
PTP1B(-/-) mice are resistant to diet-induced obesity due to leptin hypersensitivity and consequent increased energy expenditure. We aimed to determine the cellular mechanisms underlying this metabolic state. AMPK is an important mediator of leptin's metabolic effects. We find that alpha1 and alpha2 AMPK activity are elevated and acetyl-coenzyme A carboxylase activity is decreased in the muscle and brown adipose tissue (BAT) of PTP1B(-/-) mice. The effects of PTP1B deficiency on alpha2, but not alpha1, AMPK activity in BAT and muscle are neuronally mediated, as they are present in neuron- but not muscle-specific PTP1B(-/-) mice. In addition, AMPK activity is decreased in the hypothalamic nuclei of neuronal and whole-body PTP1B(-/-) mice, accompanied by alterations in neuropeptide expression that are indicative of enhanced leptin sensitivity. Furthermore, AMPK target genes regulating mitochondrial biogenesis, fatty acid oxidation, and energy expenditure are induced with PTP1B inhibition, resulting in increased mitochondrial content in BAT and conversion to a more oxidative muscle fiber type. Thus, neuronal PTP1B inhibition results in decreased hypothalamic AMPK activity, isoform-specific AMPK activation in peripheral tissues, and downstream gene expression changes that promote leanness and increased energy expenditure. Therefore, the mechanism by which PTP1B regulates adiposity and leptin sensitivity likely involves the coordinated regulation of AMPK in hypothalamus and peripheral tissues.
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Registered trials
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