Mind Over Stomach: A Review of the Cognitive Drivers of Food Satiation

2017 ◽  
Vol 2 (4) ◽  
pp. 419-429 ◽  
Author(s):  
Yann Cornil
Keyword(s):  
Food Satiation

scholarly journals A hindbrain dopaminergic neural circuit prevents weight gain by reinforcing food satiation

2021 ◽  
Vol 7 (22) ◽  
pp. eabf8719
Author(s):  
Yong Han ◽  
Guobin Xia ◽  
Yanlin He ◽  
Yang He ◽  
Monica Farias ◽  
...  
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Neural Circuit ◽  
Neural Circuitry ◽  
Dynamic Regulation ◽  
Satiety Response ◽  
Food Satiation ◽  
Lateral Parabrachial Nucleus ◽  
Genetic Deletion ◽  
Feeding Bout

The neural circuitry mechanism that underlies dopaminergic (DA) control of innate feeding behavior is largely uncharacterized. Here, we identified a subpopulation of DA neurons situated in the caudal ventral tegmental area (cVTA) directly innervating DRD1-expressing neurons within the lateral parabrachial nucleus (LPBN). This neural circuit potently suppresses food intake via enhanced satiation response. Notably, this cohort of DAcVTA neurons is activated immediately before the cessation of each feeding bout. Acute inhibition of these DA neurons before bout termination substantially suppresses satiety and prolongs the consummatory feeding. Activation of postsynaptic DRD1LPBN neurons inhibits feeding, whereas genetic deletion of Drd1 within the LPBN causes robust increase in food intake and subsequent weight gain. Furthermore, the DRD1LPBN signaling manifests the central mechanism in methylphenidate-induced hypophagia. In conclusion, our study illuminates a hindbrain DAergic circuit that controls feeding through dynamic regulation in satiety response and meal structure.

Increased short-term food satiation and sensitivity to cholecystokinin in neurotrophin-4 knock-in mice

2004 ◽  
Vol 287 (5) ◽  
pp. R1044-R1053 ◽  
Author(s):  
Michael M. Chi ◽  
Guoping Fan ◽  
Edward A. Fox
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Knockout Mice ◽  
Meal Frequency ◽  
Short Term ◽  
Daily Food Intake ◽  
Food Satiation ◽  
Daily Food ◽  
Solid Diet

Neurotrophin-4 (NT-4) knockout mice exhibited decreased innervation of the small intestine by vagal intraganglionic laminar endings (IGLEs) and reduced food satiation. Recent findings suggested this innervation was increased in NT-4 knock-in (NT-4KI) mice. Therefore, to further investigate the relationship between intestinal IGLEs and satiation, meal patterns were characterized using solid and liquid diets, and cholecystokinin (CCK) effects on 30-min solid diet intake were examined in NT-4KI and wild-type mice. NT-4KI mice consuming the solid diet exhibited reduced meal size, suggesting increased satiation. However, compensation occurred through increased meal frequency, maintaining daily food intake and body weight gain similar to controls. Mutants fed the liquid diet displayed a decrease in intake rate, again implying increased satiation, but meal duration increased, which led to an increase in meal size. This was compensated for by decreased meal frequency, resulting in similar daily food intake and weight gain as controls. Importantly, these alterations in NT-4KI mice were opposite, or different, from those of NT-4 knockout mice, further supporting the hypothesis that they are specific to vagal afferent signaling. CCK suppressed short-term intake in mutants and controls, but the mutants exhibited larger suppressions at lower doses, implying they were more sensitive to CCK. Moreover, devazepide prevented this suppression, indicating this increased sensitivity was mediated by CCK-1 receptors. These results suggest that the NT-4 gene knock-in, probably involving increased intestinal IGLE innervation, altered short-term feeding, in particular by enhancing satiation and sensitivity to CCK, whereas long-term control of daily intake and body weight was unaffected.

scholarly journals The satiating power of sustainability: the effect of package sustainability on perceived satiation of healthy food

2021 ◽  
Vol 123 (13) ◽  
pp. 162-177
Author(s):  
Carmela Donato ◽  
Ada Maria Barone ◽  
Simona Romani
Keyword(s):  
Design Methodology ◽  
Positive Relationship ◽  
Experimental Studies ◽  
Perceived Quality ◽  
Healthy Food ◽  
Sustainable Food ◽  
Content Type ◽  
Food Satiation ◽  
Food Packages ◽  
Preliminary Study

PurposeThis research investigates the influence of package sustainability on food satiation perception.Design/methodology/approachResearch hypotheses were tested through three experimental studies.FindingsThree experimental studies show that food quality is associated to higher perceived food satiation (preliminary study); that a food packaged in a sustainable package is perceived as more satiating than the same food packaged in a non-sustainable package and that this effect is explained by the higher perceived quality triggered by the presence of a sustainable package (Study 1); and that the positive relationship between higher perceived quality and perceived satiation is verified only for healthy but not for unhealthy foods (Study 2).Originality/valueThe present research advances knowledge on the highly debated issue of sustainable food packages. By proposing that consumers might perceive a healthy food presented in a sustainable package as more satiating, the authors show another extrinsic packaging cue modifying consumers' perception, namely package sustainability.

scholarly journals FOOD SATIATION IN THE PIGEON

1962 ◽  
Vol 5 (2) ◽  
pp. 239-245 ◽  
Author(s):  
T. W. Reese ◽  
Marilyn J. Hogenson
Keyword(s):  
Food Satiation

Organization of synaptic inputs to paracerebral feeding command interneurons of Pleurobranchaea californica. III. Modifications induced by experience

1983 ◽  
Vol 49 (6) ◽  
pp. 1557-1572 ◽  
Author(s):  
W. J. Davis ◽  
R. Gillette ◽  
M. P. Kovac ◽  
R. P. Croll ◽  
E. M. Matera
Keyword(s):  
Tactile Stimulation ◽  
Neural Circuitry ◽  
Cellular Model ◽  
Command Neurons ◽  
Food Avoidance ◽  
Pleurobranchaea Californica ◽  
Inhibitory Postsynaptic Potentials ◽  
Food Satiation ◽  
Behavioral Motivation ◽  
Stimulation Of

Phasic paracerebral feeding command interneurons (PCP's) were studied in whole-animal preparations of Pleurobranchaea drawn from four populations with different behavioral histories: food avoidance conditioned, yoked controls, food satiated, and naive. PCP responses to chemosensory food stimuli (liquefied squid) and mechanosensory touch stimuli (tactile stimulation of anterior and posterior structures) were recorded intracellularly, scored blind, and compared quantitatively across the four populations. PCP's from avoidance-conditioned specimens (10, 18, 19) showed decreased excitatory and increased inhibitory responses to food and touch in comparison with naive (untrained) specimens. Control animals did not show these effects. PCP's from satiated specimens showed decreased excitatory and increased inhibitory responses to food and touch in comparison with PCP's from control, naive, and conditioned specimens. Inhibitory postsynaptic potentials (IPSPs) induced in PCP's of conditioned and satiated specimens by food and touch are indistinguishable in amplitude and waveform from IPSPs produced in the same PCP's by the previously described cyclic inhibitory network (CIN; Ref. 13). In addition, tonic paracerebral neurons (PCT's) that lack input from the CIN, are not inhibited but rather are excited in trained and satiated animals. Therefore the inhibitory responses to food and touch by PCP's of conditioned and satiated specimens appear to be mediated by the CIN. This study demonstrates that associative and nonassociative processes (learning and food satiation, respectively) manifest similarly at the level of command interneurons. The findings furnish a neurophysiological explanation for behavioral motivation in Pleurobranchaea, namely, modulation of the balance of excitation/inhibition in command neurons controlling the corresponding behavior. A cellular model of food avoidance learning and food satiation is formulated to account for these data, based on the identified neural circuitry of the paracerebral command system (15, 17).

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