Role for insulin signaling in catecholaminergic neurons in control of energy homeostasis
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Dopaminergic midbrain neurons integrate signals on food palatability and food-associated reward into the complex control of energy homeostasis. To define the role of insulin receptor (IR) signaling in this circuitry, we inactivated IR signaling in tyrosine hydroxylase (Th)-expressing cells of mice (IR(ΔTh)). IR inactivation in Th-expressing cells of mice resulted in increased body weight, increased fat mass, and hyperphagia. While insulin acutely stimulated firing frequency in 50% of dopaminergic VTA/SN neurons, this response was abolished in IR(ΔTh) mice. Moreover, these mice exhibited an altered response to cocaine under food-restricted conditions. Taken together, these data provide in vivo evidence for a critical role of insulin signaling in catecholaminergic neurons to control food intake and energy homeostasis.
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In lean healthy individuals, peripheral and central insulin infusion suppresses appetite and feeding.
“in lean healthy individuals, peripheral and even central infusion of insulin suppresses appetite and feeding”
From Role of addiction and stress neurobiology on food intake and obesity (2018) · cites this paper as Konner et al., 2011
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- Authors
- Könner, A. C., Hess, S., Tovar, S., Mesaros, A., Sánchez-Lasheras, C., Evers, N., Verhagen, L. A. W., Brönneke, H. S., Kleinridders, A., Hampel, B., Kloppenburg, P., & Brüning, J. C.
- Affiliations
- University of Cologne (DE)
- Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (DE)
- Corresponding author
- Brüning, Jens C.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2011-06
- Volume
- 13
- Issue
- 6
- Pages
- 720-728
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2051037127
- Cited by
- 194
- References
- 48
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 10 · 2023: 17 · 2022: 11 · 2021: 24 · 2020: 9 · 2019: 12 · 2018: 8 · 2017: 14 · 2016: 12 · 2015: 16 · 2014: 12 · 2013: 17 · 2012: 19
- FWCI
- 7.67
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 777 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- European Commission (FP7-HEALTH-2009-241592)
- Deutsche Forschungsgemeinschaft (BR 1492/7-1, KL 762/2-2, KL 762/4-1)
- Bundesministerium für Bildung und Forschung (FKZ01GIO845)
- Universität zu Köln
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- insulin signaling, insulin receptor, dopaminergic neurons, catecholaminergic neurons, energy homeostasis, dietary intake, hyperphagia, body weight, fat mass, ventral tegmental area, substantia nigra, dietary restriction, tyrosine hydroxylase, food reward
- MeSH terms
- Action Potentials, Animals, Calorimetry, Indirect, Catecholamines, Cocaine, Eating, Energy Metabolism, Homeostasis, Hyperinsulinism, Insulin, Mesencephalon, Mice, Inbred ICR, Motor Activity, Neurons, Receptor, Insulin, Tyrosine 3-Monooxygenase, Signal Transduction, Gene Expression, Receptors, Dopamine D2, Mice, Knockout, Adiposity, Mice
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