Modulation of food reward by adiposity signals.
Extensive historical evidence from the drug abuse literature has provided support for the concept that there is functional communication between central nervous system (CNS) circuitries which subserve reward/motivation, and the regulation of energy homeostasis. This concept is substantiated by recent studies that map anatomical pathways, or which demonstrate that hormones and neurotransmitters associated with energy homeostasis regulation can directly modulate reward and motivation behaviors. Studies from our laboratory have focused specifically on the candidate adiposity hormones, insulin and leptin, and show that these hormones can decrease performance in behavioral paradigms that assess the rewarding or motivating properties of food. Additionally we and others have provided evidence that the ventral tegmental area may be one direct target for these effects, and we are currently exploring other potential anatomical targets. Finally, we are beginning to explore the interaction between adiposity signals, chronic maintenance diet of rats, and different types of food rewards to more closely simulate the current food environments of Westernized societies including the U.S. We propose that future studies of food reward should include a more complex environment in the experimental design that takes into account abundance and variety of rewarding foods, psychological stressors, and choices of reward modalities.
Figlewicz
Dianne P
DP
VA Puget Sound Health Care System (151), Seattle WA 98108, USA. latte@u.washington.edu
MacDonald Naleid
Amy
A
Sipols
Alfred J
AJ
D050154:Adiposity / Q000502:physiology*; D000818:Animals; D001069:Appetite Regulation / Q000502:physiology; D001522:Behavior, Animal / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology; D005502:Food; D006706:Homeostasis / Q000502:physiology; D007328:Insulin / Q000502:physiology*; D020738:Leptin / Q000502:physiology*; D009042:Motivation; D051381:Rats; D012201:Reward
D007328:Insulin; D020738:Leptin