Skip to main content
Log in

Les signaux de la régulation du comportement alimentaire

Signals regulating eating behavior

  • Revue Scientifique / Scientific Review
  • Published:
Obésité

Résumé

Le contrôle de l’homéostasie énergétique fait intervenir un réseau complexe de signaux périphériques et centraux qui renseignent sur l’état nutritionnel d’un organisme. L’intégration de ces signaux au niveau du système nerveux central (SNC) permet de développer une réponse adaptée aux modifications de la disponibilité en nutriments. Le noyau arqué (Arc) de l’hypothalamus contient les neurones à neuropeptide Y et agouti-related protein (NPY/AgRP) et les neurones à pro-opiomélanocortine (POMC) qui sont considérés comme de « premier ordre » dans l’intégration des signaux périphériques de faim et de satiété comme la leptine, l’insuline ou la ghréline. Les nutriments jouent également un rôle de molécules informatives au niveau de l’hypothalamus. D’autres structures centrales comme le tronc cérébral ou le système mésolimbique dopaminergique ainsi qu’une multitude de signaux centraux se conjuguent à cette régulation « hypothalamique » de la prise alimentaire et sont autant de cibles potentielles dans le développement d’une stratégie thérapeutique visant à lutter contre les troubles du comportement alimentaire comme l’anorexie ou, à l’opposé, l’hyperphagie.

Abstract

Control of energy homeostasis involves a complex network of both peripheral and central signals, which continually inform the central nervous system (CNS) about nutritional status, thus allowing an adaptive response with respect to energy demand. Both NPY/AgRP (Neuropeptide Y/Agouti-related protein) and POMC (pro-opiomelanocortin) neurons — known as “1st order” neurons — are located within the hypothalamic arcuate nucleus and are key actors of eating behavior. Changes in the circulating concentration of nutrients and hormones such as leptin, insulin and ghrelin are detected by these neurons. Other areas of CNS such as the brain stem or the dopaminergic mesolimbic system act together with the hypothalamus to finely regulate feeding behavior. Identification of molecular mechanisms involved in nervous control of energy homeostasis including eating behavior, as well as hepatic glucose production or insulin secretion, will enable the development of new therapeutic approaches towards eating disorders such as anorexia, or its opposite, hyperphagia.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Références

  1. Zhang Y (1994) Positional cloning of the mouse obese gene and its human homologue. Nature 372: 425–432

    Article  PubMed  CAS  Google Scholar 

  2. Friedman JM (2000) Obesity in the new millennium. Nature 404: 632–634

    PubMed  CAS  Google Scholar 

  3. Schwartz MW (2000) Central nervous system control of food intake. Nature 404: 661–671

    PubMed  CAS  Google Scholar 

  4. Broberger C, T Hokfelt (2001) Hypothalamic and vagal neuropeptide circuitries regulating food intake. Physiol Behav 74: 669–682

    Article  PubMed  CAS  Google Scholar 

  5. Williams G (2001) The hypothalamus and the control of energy homeostasis: different circuits, different purposes. Physiol Behav 74: 683–701

    Article  PubMed  CAS  Google Scholar 

  6. Lechan RM, Fekete C (2006) The TRH neuron: a hypothalamic integrator of energy metabolism. Prog Brain Res 153: 209–235

    Article  PubMed  CAS  Google Scholar 

  7. Kalra SP (1991) Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food. Proc Natl Acad Sci USA 88: 10931–10935

    Article  PubMed  CAS  Google Scholar 

  8. Viggiano A (2004) Extracellular Gaba in the medial hypothalamus is increased following hypocretin-1 administration. Acta Physiol Scand 182: 89–94

    Article  PubMed  CAS  Google Scholar 

  9. Woods SC, Schwartz MW, Baskin DG, Seeley RJ (2000) Food intake and the regulation of body weight. Annu Rev Psychol 51: 255–277

    Article  PubMed  CAS  Google Scholar 

  10. Berthoud HR, Neuhuber WL (2000) Functional and chemical anatomy of the afferent vagal system. Auton Neurosci 85: 1–17

    Article  PubMed  CAS  Google Scholar 

  11. Glatzle J (2001) Postprandial neuronal activation in the nucleus of the solitary tract is partly mediated by CCK-A receptors. Am J Physiol Regul Integr Comp Physiol 281: R222–R229

    PubMed  CAS  Google Scholar 

  12. Luckman SM, Lawrence CB (2003) Anorectic brainstem peptides: more pieces to the puzzle. Trends Endocrinol Metab 14: 60–65

    Article  PubMed  CAS  Google Scholar 

  13. Murphy KG, Bloom SR (2004) Gut hormones in the control of appetite. Exp Physiol 89: 507–516

    Article  PubMed  CAS  Google Scholar 

  14. Batterham RL (2003) Inhibition of food intake in obese subjects by peptide YY3-36. N Engl J Med 349: 941–948

    Article  PubMed  CAS  Google Scholar 

  15. Batterham RL (2002) Gut hormone PYY(3–36) physiologically inhibits food intake. Nature 418: 650–654

    Article  PubMed  CAS  Google Scholar 

  16. Kojima M (1999) Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 402: 656–660

    Article  PubMed  CAS  Google Scholar 

  17. Tschop M, Smiley DL, Heiman ML (2000) Ghrelin induces adiposity in rodents. Nature 407: 908–913

    Article  PubMed  CAS  Google Scholar 

  18. Cummings DE (2001) A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans. Diabetes 50: 1714–1719

    Article  PubMed  CAS  Google Scholar 

  19. Chen AS (2000) Inactivation of the mouse melanocortin-3 receptor results in increased fat mass and reduced lean body mass. Nat Genet 26: 97–102

    Article  PubMed  CAS  Google Scholar 

  20. Luquet S, Phillips CT, Palmiter RD (2007) NPY/AgRP neurons are not essential for feeding responses to glucoprivation. Peptides 28: 214–225

    Article  PubMed  CAS  Google Scholar 

  21. Yang J (2008) Identification of the acyltransferase that octanoylates ghrelin, an appetite-stimulating peptide hormone. Cell 132: 387–396

    Article  PubMed  CAS  Google Scholar 

  22. Bruning JC (2000) Role of brain insulin receptor in control of body weight and reproduction. Science 289: 2122–2125

    Article  PubMed  CAS  Google Scholar 

  23. Obici S (2002) Central administration of oleic acid inhibits glucose production and food intake. Diabetes 51: 271–275

    Article  PubMed  CAS  Google Scholar 

  24. Cowley MA (2001) Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus. Nature 411: 480–484

    Article  PubMed  CAS  Google Scholar 

  25. Dhillon H (2006) Leptin directly activates SF1 neurons in the VMH, and this action by leptin is required for normal body-weight homeostasis. Neuron 49: 191–203

    Article  PubMed  CAS  Google Scholar 

  26. Fulton S, Woodside B, Shizgal P (2000) Modulation of brain reward circuitry by leptin. Science 287: 125–128

    Article  PubMed  CAS  Google Scholar 

  27. Batterham RL (2007) PYY modulation of cortical and hypothalamic brain areas predicts feeding behaviour in humans. Nature 450: 106–109

    Article  PubMed  CAS  Google Scholar 

  28. Fulton S (2006) Leptin regulation of the mesoaccumbens dopamine pathway. Neuron 51: 811–822

    Article  PubMed  CAS  Google Scholar 

  29. Gietzen DW (2004) Phosphorylation of eIF2alpha is involved in the signalling of indispensable amino acid deficiency in the anterior piriform cortex of the brain in rats. J Nutr 134: 717–723

    PubMed  CAS  Google Scholar 

  30. Thibault L, Booth DA (1999) Macronutrient-specific dietary selection in rodents and its neural bases. Neurosci Biobehav Rev 23: 457–528

    Article  PubMed  CAS  Google Scholar 

  31. Westerterp-Plantenga MS (2003) The significance of protein in food intake and body weight regulation. Curr Opin Clin Nutr Metab Care 6: 635–638

    Article  PubMed  CAS  Google Scholar 

  32. Mithieux G (2005) Portal sensing of intestinal gluconeogenesis is a mechanistic link in the diminution of food intake induced by diet protein. Cell Metab 2: 321–329

    Article  PubMed  CAS  Google Scholar 

  33. Raybould HE (2002) Visceral perception: sensory transduction in visceral afferents and nutrients. Gut 51(Suppl 1): i11–i14

    Article  PubMed  Google Scholar 

  34. Gilbert M (2003) Leptin receptor-deficient obese Zucker rats reduce their food intake in response to a systemic supply of calories from glucose. Diabetes 52: 277–282

    Article  PubMed  CAS  Google Scholar 

  35. Drazen DL, Woods SC (2003) Peripheral signals in the control of satiety and hunger. Curr Opin Clin Nutr Metab Care 6: 621–629

    Article  PubMed  CAS  Google Scholar 

  36. Fioramonti X (2007) Characterization of glucosensing neuron subpopulations in the arcuate nucleus: integration in neuropeptide Y and pro-opiomelanocortin networks? Diabetes 56: 1219–1227

    Article  PubMed  CAS  Google Scholar 

  37. Levin BE (2004) Neuronal glucosensing: what do we know after 50 years? Diabetes 53: 2521–2528

    Article  PubMed  CAS  Google Scholar 

  38. Matveyenko AV, Donovan CM (2006) Metabolic sensors mediate hypoglycemic detection at the portal vein. Diabetes 55: 1276–1282

    Article  PubMed  CAS  Google Scholar 

  39. Laugerette F (2005) CD36 involvement in orosensory detection of dietary lipids, spontaneous fat preference and digestive secretions. J Clin Invest 115: 3177–3184

    Article  PubMed  CAS  Google Scholar 

  40. Cummings DE, Overduin J (2007) Gastrointestinal regualtion of food intake. J Clin Invest 117: 13–23

    Article  PubMed  CAS  Google Scholar 

  41. Wang R (2006) Effects of oleic acid on distinct populations of neurons in the hypothalamic arcuate nucleus are dependent on extracellular glucose levels. J Neurophysiol 95: 1491–1498

    Article  PubMed  CAS  Google Scholar 

  42. Kelley AE (2005) Corticostriatal-hypothalamic circuitry and food motivation: integration of energy, action and reward. Physiol Behav 86: 773–795

    Article  PubMed  CAS  Google Scholar 

  43. Farooqi IS (2007) Leptin regulates striatal regions and human eating behavior. Science 317: 1355

    Article  PubMed  CAS  Google Scholar 

  44. Bouret SG, Draper SJ, Simerly RB (2004) Trophic action of leptin on hypothalamic neurons that regulate feeding. Science 304: 108–110

    Article  PubMed  CAS  Google Scholar 

  45. Pinto S (2004) Rapid rewiring of arcuate nucleus feeding circuits by leptin. Science 304: 110–115

    Article  PubMed  CAS  Google Scholar 

  46. Qian S (2002) Neither agouti-related protein nor neuropeptide Y is critically required for the regulation of energy homeostasis in mice. Mol Cell Biol 22: 5027–5035

    Article  PubMed  CAS  Google Scholar 

  47. Gropp E (2005) Agouti-related peptide-expressing neurons are mandatory for feeding. Nat Neurosci 8: 1289–1291

    Article  PubMed  CAS  Google Scholar 

  48. Luquet S (2005) NPY/AgRP neurons are essential for feeding in adult mice but can be ablated in neonates. Science 310: 683–685

    Article  PubMed  CAS  Google Scholar 

  49. Xu AW (2005) Effects of hypothalamic neurodegeneration on energy balance. PLoS Biol 3: e415

    Article  PubMed  Google Scholar 

  50. Di Marzo V, Matias I (2005) Endocannabinoid control of food intake and energy balance. Nat Neurosci 8: 585–589

    Article  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to S. Luquet.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Luquet, S., Marsollier, N., Cruciani-Guglielmacci, C. et al. Les signaux de la régulation du comportement alimentaire. Obes 3, 167–176 (2008). https://doi.org/10.1007/s11690-008-0133-5

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11690-008-0133-5

Mots clés

Keywords

Navigation