What's the difference between accloy and satiety?

Accloy


Definition:

  • (v. t.) To fill to satiety; to stuff full; to clog; to overload; to burden. See Cloy.

Example Sentences:

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.

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