ArticleDiabetes2011
Deletion of Lkb1 in pro-opiomelanocortin neurons impairs peripheral glucose homeostasis in mice.
Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Insights into targeting LKB1 in tumorigenesis.Genes & diseases · 2025Review
- Systemic Glucose Homeostasis Requires Pancreatic but Not Neuronal ATP-sensitive Potassium Channels.Function (Oxford, England) · 2025Article
- Liver kinase B-1 modulates the activity of dopamine neurons in the ventral tegmental area and regulates social memory formation.Frontiers in molecular neuroscience · 2024Article
- Sex Differences in Glucose Homeostasis.Handbook of experimental pharmacology · 2023Article
- SK3 in POMC neurons plays a sexually dimorphic role in energy and glucose homeostasis.Cell & bioscience · 2022Article
- Sex-specific role of sensory neuron LKB1 on metabolic stress-induced mechanical hypersensitivity and mitochondrial respiration.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Gabra5 plays a sexually dimorphic role in POMC neuron activity and glucose balance.Frontiers in endocrinology · 2022Article
- Central nervous system regulation of organismal energy and glucose homeostasis.Nature metabolism · 2021Review
- Optogenetic stimulation of the liver-projecting melanocortinergic pathway promotes hepatic glucose production.Nature communications · 2020Article
- Interaction of glucose sensing and leptin action in the brain.Molecular metabolism · 2020Review
- Deletion ofeLife · 2020Article
- Central Mechanisms of Glucose Sensing and Counterregulation in Defense of Hypoglycemia.Endocrine reviews · 2019Review
- Remote control of glucose-sensing neurons to analyze glucose metabolism.American journal of physiology. Endocrinology and metabolism · 2018Review
- Emerging Concepts in Brain Glucose Metabolic Functions: From Glucose Sensing to How the Sweet Taste of Glucose Regulates Its Own Metabolism in Astrocytes and Neurons.Neuromolecular medicine · 2018Review
- p53 in AgRP neurons is required for protection against diet-induced obesity via JNK1.Nature communications · 2018Article
- Augmented Insulin and Leptin Resistance of High Fat Diet-Fed APPswe/PS1dE9 Transgenic Mice Exacerbate Obesity and Glycemic Dysregulation.International journal of molecular sciences · 2018Article
- TAp63 contributes to sexual dimorphism in POMC neuron functions and energy homeostasis.Nature communications · 2018Article
- Versatile Roles of LKB1 Kinase Signaling in Neural Development and Homeostasis.Frontiers in molecular neuroscience · 2018Article
- Article
- Knockout of inositol-requiring enzyme 1α in pro-opiomelanocortin neurons decreases fat mass via increasing energy expenditure.Open biology · 2016Article
Corrections and comments
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Authors and funding
23 authors at 3 institutions in 3 countries.
Funding
Abstract
objectiveAMP-activated protein kinase (AMPK) signaling acts as a sensor of nutrients and hormones in the hypothalamus, thereby regulating whole-body energy homeostasis. Deletion of Ampkα2 in pro-opiomelanocortin (POMC) neurons causes obesity and defective neuronal glucose sensing. LKB1, the Peutz-Jeghers syndrome gene product, and Ca(2+)-calmodulin-dependent protein kinase kinase β (CaMKKβ) are key upstream activators of AMPK. This study aimed to determine their role in POMC neurons upon energy and glucose homeostasis regulation. RESEARCH DESIGN AND
methodsMice lacking either Camkkβ or Lkb1 in POMC neurons were generated, and physiological, electrophysiological, and molecular biology studies were performed.
resultsDeletion of Camkkβ in POMC neurons does not alter energy homeostasis or glucose metabolism. In contrast, female mice lacking Lkb1 in POMC neurons (PomcLkb1KO) display glucose intolerance, insulin resistance, impaired suppression of hepatic glucose production, and altered expression of hepatic metabolic genes. The underlying cellular defect in PomcLkb1KO mice involves a reduction in melanocortin tone caused by decreased α-melanocyte-stimulating hormone secretion. However, Lkb1-deficient POMC neurons showed normal glucose sensing, and body weight was unchanged in PomcLkb1KO mice.
conclusionsOur findings demonstrate that LKB1 in hypothalamic POMC neurons plays a key role in the central regulation of peripheral glucose metabolism but not body-weight control. This phenotype contrasts with that seen in mice lacking AMPK in POMC neurons with defects in body-weight regulation but not glucose homeostasis, which suggests that LKB1 plays additional functions distinct from activating AMPK in POMC neurons.
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