ArticleDiabetes2011
Participation of hindbrain AMP-activated protein kinase in glucoprivic feeding.
Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- A network-biology led computational drug repurposing strategy to prioritize therapeutic options for COVID-19.Heliyon · 2022Article
- Attenuation of the Counter-Regulatory Glucose Response in CVLM C1 Neurons: A Possible Explanation for Anorexia of Aging.Biomolecules · 2022Article
- 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
- Hindbrain A2 noradrenergic neuron adenosine 5'-monophosphate-activated protein kinase activation, upstream kinase/phosphorylase protein expression, and receptivity to hormone and fuel reporters of short-term food deprivation are regulated by estradiol.Journal of neuroscience research · 2017Article
- The Effects of Insulin-Induced Hypoglycaemia on Tyrosine Hydroxylase Phosphorylation in Rat Brain and Adrenal Gland.Neurochemical research · 2016Article
- Hypothalamic AMPK: a canonical regulator of whole-body energy balance.Nature reviews. Endocrinology · 2016Review
- Role of estradiol in intrinsic hindbrain AMPK regulation of hypothalamic AMPK, metabolic neuropeptide, and norepinephrine activity and food intake in the female rat.Neuroscience · 2016Article
- Pharmacological and Morphological Evidence of AMPK-Mediated Energy Sensing in the Lower Brain Stem Ependymocytes to Control Reproduction in Female Rodents.Endocrinology · 2015Article
- Catecholaminergic C3 neurons are sympathoexcitatory and involved in glucose homeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Hindbrain lactostasis regulates hypothalamic AMPK activity and metabolic neurotransmitter mRNA and protein responses to hypoglycemia.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Glucose utilization rates regulate intake levels of artificial sweeteners.The Journal of physiology · 2013Article
- 2. Hypoglycemia Detection.Translational endocrinology & metabolism · 2012Article
- Activation of NPY receptors suppresses excitatory synaptic transmission in a taste-feeding network in the lower brain stem.American journal of physiology. Regulatory, integrative and comparative physiology · 2012Article
- The gut-brain dopamine axis: a regulatory system for caloric intake.Physiology & behavior · 2012Review
- Sense and nonsense in metabolic control of reproduction.Frontiers in endocrinology · 2012Article
- Minireview: The value of looking backward: the essential role of the hindbrain in counterregulatory responses to glucose deficit.Endocrinology · 2011Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo examine the role of AMP-activated protein kinase (AMPK) in the control of glucoprivic feeding by hindbrain catecholamine neurons. RESEARCH DESIGN AND
methodsMicropunched hindbrain samples were collected from control and 2-deoxy-d-glucose (2DG)-injected rats for Western blot analysis of phosphorylated (activated) AMPK (pAMPK). Samples also were collected from 2DG-injected rats pretreated with anti-dopamine-β-hydroxylase conjugated to saporin to lesion hindbrain catecholamine neurons. In a second experiment, rats were given a fourth-ventricle injection of compound C (CC) or 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR), an inhibitor and activator of AMPK, to identify a role for AMPK in hindbrain neurons required for elicitation of 2DG-induced feeding.
resultsSystemic 2DG stimulated food intake in controls but not in catecholamine-lesioned rats. In controls, but not catecholamine-lesioned rats, 2DG also increased phosphorylated Thr172 at AMPKα subunits (pAMPKα) in hindbrain micropunches containing catecholaminergic cell groups A1 through the middle region of C1 (A1-C1m). Increased pAMPKα was not observed in the adjacent noncatecholaminergic ventromedial medulla or in the A2-C2 catecholamine cell groups in the dorsal hindbrain. Fourth-ventricle injection of CC attenuated 2DG-induced feeding during the first 2 h of the test, and AICAR alone increased food intake only during the first 60 min of the 4-h test.
conclusionsResults indicate that AMPK in catecholaminergic A1-C1m neurons is activated by glucoprivation. Therefore, AMPK may contribute to the glucose-sensing mechanism by which these neurons detect and signal a glucose deficit in the service of systemic glucoregulation.
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Registered trials
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