ArticleDiabetologia2012
Mouse hypothalamic GT1-7 cells demonstrate AMPK-dependent intrinsic glucose-sensing behaviour.
Article in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 60 citations in OpenAlex.
- Dysfunctional TRIM31 of POMC Neurons Provokes Hypothalamic Injury and Peripheral Metabolic Disorder under Long-Term Fine Particulate Matter Exposure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Roles of Oxidative Phosphorylation and Fatty Acid Oxidation in Neuroinflammation Induced by Lipopolysaccharide in Hypothalamic Neuronal Cells.International journal of inflammation · 2026Article
- Remembrance of things past: The consequences of recurrent hypoglycaemia in diabetes.Diabetic medicine : a journal of the British Diabetic Association · 2022Review
- Small extracellular vesicle-mediated targeting of hypothalamic AMPKα1 corrects obesity through BAT activation.Nature metabolism · 2021Article
- Consequences of recurrent hypoglycaemia on brain function in diabetes.Diabetologia · 2021Review
- Insulin actions on hypothalamic glucose-sensing neurones.Journal of neuroendocrinology · 2021Review
- Brain Permeable AMP-Activated Protein Kinase Activator R481 Raises Glycaemia by Autonomic Nervous System Activation and Amplifies the Counterregulatory Response to Hypoglycaemia in Rats.Frontiers in endocrinology · 2021Article
- Ventromedial hypothalamus glucose-inhibited neurones: A role in glucose and energy homeostasis?Journal of neuroendocrinology · 2020Review
- Potential role of hypothalamic microRNAs in regulation of FOS and FTO expression in response to hypoglycemia.The journal of physiological sciences : JPS · 2019Article
- Identification of Candidate Genes for the Plateau Adaptation of a Tibetan Amphipod,Frontiers in genetics · 2019Article
- High glucose stimulates cell proliferation and Collagen IV production in rat mesangial cells through inhibiting AMPK-KInternational urology and nephrology · 2017Article
- High glucose increases action potential firing of catecholamine neurons in the nucleus of the solitary tract by increasing spontaneous glutamate inputs.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Oleate induces KNeuroscience · 2017Article
- Recent Advances in the Cellular and Molecular Mechanisms of Hypothalamic Neuronal Glucose Detection.Frontiers in physiology · 2017Article
- Glucose-Sensing in the Reward System.Frontiers in neuroscience · 2017Review
- Mediobasal hypothalamic overexpression of DEPTOR protects against high-fat diet-induced obesity.Molecular metabolism · 2016Article
- Article
- Brain glucose sensing, glucokinase and neural control of metabolism and islet function.Diabetes, obesity & metabolism · 2014Review
- AMP kinase regulates K-ATP currents evoked by NMDA receptor stimulation in rat subthalamic nucleus neurons.Neuroscience · 2014Article
- Hypothalamic glucose sensing: making ends meet.Frontiers in systems neuroscience · 2014Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
aims/hypothesisHypothalamic glucose-excited (GE) neurons contribute to whole-body glucose homeostasis and participate in the detection of hypoglycaemia. This system appears defective in type 1 diabetes, in which hypoglycaemia commonly occurs. Unfortunately, it is at present unclear which molecular components required for glucose sensing are produced in individual neurons and how these are functionally linked. We used the GT1-7 mouse hypothalamic cell line to address these issues.
methodsElectrophysiological recordings, coupled with measurements of gene expression and protein levels and activity, were made from unmodified GT1-7 cells and cells in which AMP-activated protein kinase (AMPK) catalytic subunit gene expression and activity were reduced.
resultsHypothalamic GT1-7 neurons express the genes encoding glucokinase and ATP-sensitive K(+) channel (K(ATP)) subunits K ( ir ) 6.2 and Sur1 and exhibit GE-type glucose-sensing behaviour. Lowered extracellular glucose concentration hyperpolarised the cells in a concentration-dependent manner, an outcome that was reversed by tolbutamide. Inhibition of glucose uptake or metabolism hyperpolarised cells, showing that energy metabolism is required to maintain their resting membrane potential. Short hairpin (sh)RNA directed to Ampkα2 (also known as Prkaa2) reduced GT1-7 cell AMPKα2, but not AMPKα1, activity and lowered the threshold for hypoglycaemia-induced hyperpolarisation. shAmpkα1 (also known as Prkaa1) had no effect on glucose-sensing or AMPKα2 activity. Decreased uncoupling protein 2 (Ucp2) mRNA was detected in AMPKα2-reduced cells, suggesting that AMPKα2 regulates UCP2 levels. CONCLUSIONS/
interpretationWe have demonstrated that GT1-7 cells closely mimic GE neuron glucose-sensing behaviour, and reducing AMPKα2 blunts their responsiveness to hypoglycaemic challenge, possibly by altering UCP2 activity. These results show that suppression of AMPKα2 activity inhibits normal glucose-sensing behaviour and may contribute to defective detection of hypoglycaemia.
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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.