(1) Release of noradrenaline (NA), adrenaline (A) and dopamine (DA) was measured in vivo per minute before and after food presentation in satiated rats that had a cannula in the mediodorsal hypothalamic area (MDH).
(2) Averaged evoked potentials (EP) to a CS (flash) were recorded sequentially in classical appetitive conditioning, satiated state after appetitive conditioning, highly alert state by noncontingent shocks, and classical aversive conditioning from a rat.
(3) These results demonstrate that systemic administration of baclofen can stimulate ingestive behaviour in satiated rats and suggest a possible role for a GABAB receptor-mediated mechanism in the control of food intake.
(4) Similar experiments in which neurotensin (NT) was perfused in the LH, PVN and VMN revealed virtually the same inverse effects on NE release in the fasted and satiated rat, which again were anatomically specific.
(5) Thus, obese male mice were at least as sensitive to the satiating effect of CCK-8 as lean male mice.
(6) Explanations in terms of satiation theory, learning theory, instructions, and perceptual bias were discussed.
(7) These results indicate that 5-HT exerts its anorectic effect only after some food has been ingested, and support the hypothesis that 5-HT accelerates the development of satiation and satiety.
(8) In order to test this hypothesis in intact, free-moving animals and to determine if the MCCs play a role in satiation of feeding, the behavior of animals that had their MCCs destroyed by intracellular injection of proteases was compared with that of B Cell-Lesion and Dye injection control animals (Experiment 1) or surgical control animals (Experiment 2).
(9) But subsequent research has shown that because fat is more satiating, or filling, eating some higher fat foods can lead to lower calorie intake overall.
(10) The perifornical lateral hypothalamus displayed a different pattern, namely, a significant increase in NPY content in refed as compared to satiated and deprived rats.
(11) The rats' differential responses to alpha-adrenergic and beta-adrenergic drugs injected into different hypothalamic sites indicate the following: (1) the lateral hypothalamic "feeding" center contains beta receptors, the activation of which produces satiation, presumably by inhibition of the lateral "feeding" cells; (2) the ventromedial hypothalamic "satiety" center contains alpha receptors, the activation of which produces eating, presumably by inhibition of the ventromedial "satiety" cells; and (3) the medio-lateral perifornical area of the hypothalamus contains both alpha and beta receptors, which lead to inhibition of the ventromedial or lateral hypothalamic centers respectively.
(12) Spike activity of neurons (areas 3, 4) was studied in cats during conditioned placing reaction before and after food satiation.
(13) Beliefs about the satiating effect of foods varying in contents of proteins, fats, carbohydrates, and fibre were investigated by face-to-face interviews with a random telephone sample of 101 subjects.
(14) Upon sexual satiation with the second male, females either received a novel third male or were reexposed to the original male.
(15) The lack of response of the amygdaloid cortical nucleus to adrenergic stimulation in the satiated rat, under simultaneous stimulation of the lateral hypothalamus with either placebo or an adrenergic blocker, was also demonstrated.
(16) To that end, the present study examined the effects of 90-dB white noise on eating in satiated rats.
(17) 2 This anorexia is also observed in satiated rats, which had ad libitum access to food.
(18) Injected NPY can override a variety of satiating factors, including those arising from normal feed intake, artificial distension of the reticulorumen, and intraruminal infusion of sodium propionate.
(19) Amphetamine also increased all behaviours when rats were tested with their cagemates, when the desire for SI is largely satiated.
(20) This 'satiation' response occurred even though the initial diet was originally highly attractive to foraging workers.
Satiety
Definition:
(n.) The state of being satiated or glutted; fullness of gratification, either of the appetite or of any sensual desire; fullness beyond desire; an excess of gratification which excites wearisomeness or loathing; repletion; satiation.
Example Sentences:
(1) Duodenal infusions of glucose inhibited FI calorically, and generally inhibited GE calorically; but gastric volume at satiety was always equal to control volume.
(2) We considered that if CCK-induced reductions in food intake occur through the mechanism of normal satiety, CCK-induced satiety and normal satiety should respond in the same way to a pharmacological challenge.
(3) The results are consistent with the view that satietin acts by activating a satiety mechanism.
(4) This suggests that brain 5-HT may influence primarily the induction of satiety rather than the suppression of hunger.
(5) It is concluded that at the first central synapse of the taste system of the primate, neural responsiveness is not influenced by the normal transition from hunger to satiety.
(6) The results of these studies, considered as a whole, support the view that McCleary's osmotic postingestional satiety signal acts as an intestinal distention signal rather than by inducing thirst.
(7) Acarbose significantly reduced the satiety effect of corn starch in lean rats (p less than 0.001), and further attenuated satiety in obese rats (p less than 0.02).
(8) Attention to focal stimulation did not mediate differences in sensitivity to satiety cues within the C group.
(9) Eating, in turn, activates inhibitory signals to produce satiety.
(10) Intracarotid administration of isotonic glucose (0.5 ml of 5.4%) in the starving albino rats produced an increase in the multiunit activity (MUA) of ventromedial hypothalamus (satiety centre) and a decrease in the MUA of the lateral hypothalamic area (feeding centre).
(11) Under the conditions of this study, energy density of foods seemed to play a significant role on the occurrence of satiety.
(12) The satiety-inducing effects of centrally and peripherally administered cholecystokinin (CCK) in experimental animals have been well documented.
(13) It is suggested that the ventromedial and lateral hypothalamus are connected by reciprocal circuits, so that activation of the ventromedial center results in stimulation of the lateral beta receptors which inhibit the lateral "feeding" cells, and activation of the lateral center results in stimulation of the ventromedial alpha receptors which inhibit the ventromedial "satiety" cells.
(14) These results suggest that endogenous CCK causes satiety by an agonist action on CCK-B receptors in the brain.
(15) In sensory-specific satiety, the pleasantness of the sight or taste of a food becomes less after it is eaten to satiety, whereas the pleasantness of the sight or taste of other foods which have not been eaten is much less changed; correspondingly, food intake is greater if foods which have not already been eaten to satiety are offered.
(16) These tablets undergo expansion in the stomach and are expected to cause early satiety.
(17) These results indicate that 5-HT exerts its anorectic effect only after some food has been ingested, and support the hypothesis that 5-HT accelerates the development of satiation and satiety.
(18) Thus, CCK concentrations in specific areas of the hypothalamus increased with feeding, supporting the potential role of CCK in the central nervous system as a satiety peptide.
(19) Closing the gastric cannula increased the potency with which ip glucose inhibited eating, suggesting synergy of postabsorptive glucose with other postgastric satiety signals.
(20) The results are discussed in terms of a possible role for peripheral 5-HT in the control of satiety, and implications for the mode of action of serotonergic anorectic agents such as fenfluramine.