The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Characteristics and mechanisms of hypothalamic neuronal fatty acid sensing
Open accessAbstract
We assessed the mechanisms by which specialized hypothalamic ventromedial nucleus (VMN) neurons utilize both glucose and long-chain fatty acids as signaling molecules to alter their activity as a potential means of regulating energy homeostasis. Fura-2 calcium (Ca 2+) and membrane potential dye imaging, together with pharmacological agents, were used to assess the mechanisms by which oleic acid (OA) alters the activity of dissociated VMN neurons from 3- to 4-wk-old rats. OA excited up to 43% and inhibited up to 29% of all VMN neurons independently of glucose concentrations. In those neurons excited by both 2.5 mM glucose and OA, OA had a concentration-dependent effective excitatory concentration (EC 50) of 13.1 nM. Neurons inhibited by both 2.5 mM glucose and OA had an effective inhibitory concentration (IC 50) of 93 nM. At 0.5 mM glucose, OA had markedly different effects on these same neurons. Inhibition of carnitine palmitoyltransferase, reactive oxygen species formation, long-chain acetyl-CoA synthetase and ATP-sensitive K+channel activity or activation of uncoupling protein 2 (UCP2) accounted for only ∼20% of OA's excitatory effects and ∼40% of its inhibitory effects. Inhibition of CD36, a fatty acid transporter that can alter cell function independently of intracellular fatty acid metabolism, reduced the effects of OA by up to 45%. Thus OA affects VMN neuronal activity through multiple pathways. In glucosensing neurons, its effects are glucose dependent. This glucose-OA interaction provides a potential mechanism whereby such “metabolic sensing” neurons can respond to differences in the metabolic states associated with fasting and feeding.
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“However, basal levels of FAO enzymes and FA transport proteins (such as FATP-1, FATP-4, and FAT/CD36) are expressed in hypothalamic neurons ([93](#B93), [95](#B95)).”
From Mitochondrial fatty acid oxidation in obesity (2013) · cites this paper as [95]
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“and the capacity of hypothalamic neurons to sense glucose and FFA simultaneously and to integrate other nutritional and hormonal inputs ([95](#B95), [99](#B99))”
From Mitochondrial fatty acid oxidation in obesity (2013) · cites this paper as [95]
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UCP2 mediates ghrelin’s action on NPY/AgRP neurons by lowering free radicals
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Central Administration of Oleic Acid Inhibits Glucose Production and Food Intake
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Schönfeld, P., & Reiser, G. (2013) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2013.128 · Cited by 457
Hypothalamic nutrient sensing in the control of energy homeostasis
Blouet, C., & Schwartz, G. J. (2009) · Behavioural Brain Research · doi:10.1016/j.bbr.2009.12.024 · Cited by 343
Lipid Processing in the Brain: A Key Regulator of Systemic Metabolism
Bruce, K. D., Zsombok, A., & Eckel, R. H. (2017) · Frontiers in Endocrinology · doi:10.3389/fendo.2017.00060 · Cited by 279
“Similarly, inhibition of FAS activity by central administration of the pharmacological FAS inhibitor C75 has been shown to reduce food intake (73) and to elevate malonyl-CoA levels (74).”
BackgroundInfluentialTaste of Fat: A Sixth Taste Modality?
Besnard, P., Passilly‐Degrace, P., & Khan, N. A. (2016) · Physiological Reviews · doi:10.1152/physrev.00002.2015 · Cited by 269
“By its expression in the gustatory papillae (105), as well as the small intestine (160) and hypothalamus (106), CD36 might also be the cornerstone of a “functional continuum” along the oro-intestinal-brain axis, responsible for a real-time adaptation of food selection and the subsequent metabolic fate of dietary lipid…”
BackgroundMitochondrial fatty acid oxidation in obesity
Serra, D., Mera, P., Malandrino, M. I., Mir, J. F., & Herrero, L. (2013) · Antioxidants & Redox Signaling · doi:10.1089/ars.2012.4875 · Cited by 246
“Nonetheless, the direct correlation observed between fasting and FFA levels (156) and the capacity of hypothalamic neurons to sense glucose and FFA simultaneously and to integrate other nutritional and hormonal inputs (95, 99) seem to throw light on how important FAO really is in hypothalamic nuclei.”
Metadata
- Authors
- Le Foll, C., Irani, B. G., Magnan, C., Dunn-Meynell, A. A., & Levin, B. E.
- ORCID
- Levin, Barry E.
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2009-09
- Volume
- 297
- Issue
- 3
- Pages
- R655-R664
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- PMC
- PMC2739790
- OpenAlex
- W2067285665
- Cited by
- 159
- References
- 57
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 7 · 2023: 7 · 2022: 4 · 2021: 7 · 2020: 6 · 2019: 6 · 2018: 3 · 2017: 15 · 2016: 13 · 2015: 15 · 2014: 18 · 2013: 17 · 2012: 9
- FWCI
- 4.79
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 53181, R01DK053181)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- ventromedial hypothalamus, oleic acid, fatty acid sensing, glucose detection, energy homeostasis, neuronal excitation and inhibition, CD36, fatty acid transporters, carnitine palmitoyltransferase, reactive oxygen species, ATP-sensitive potassium channels, UCP2, fasting and feeding
- MeSH terms
- Uncoupling Protein 2, Animals, Carnitine O-Palmitoyltransferase, Coenzyme A Ligases, Energy Metabolism, Enzyme Inhibitors, Glucose, Homeostasis, Ion Channels, Male, Membrane Potentials, Microscopy, Fluorescence, Neural Inhibition, Neurons, Time Factors, Ventromedial Hypothalamic Nucleus, Free Radical Scavengers, Rats, Sprague-Dawley, Reactive Oxygen Species, CD36 Antigens, Oleic Acid, Calcium Signaling, Mitochondrial Proteins, Potassium Channel Blockers, Rats, KATP Channels
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