Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0020175 (
hunger
)
5,670
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
It has been suggested that obese individuals over-eat in order to compensate for deficits in the dopaminergic reward system. The current study used acute tyrosine/phenylalanine depletion (ATPD) to investigate the effect of reduced dopamine function on appetite and the reward value of food in healthy volunteers. The compensatory-eating hypothesis would predict an increase in the reward value and consumption of food following depletion by this method. In a double-blind, counterbalanced, crossover study, 17 male participants (mean age=29.2 (SEM=2.7) years; mean body mass index=24.4 (SEM=0.6) kg/m(2)) were administered with a tyrosine/phenylalanine-free mixture (TYR/PHE-free; depletion condition) and a balanced amino acid mixture (
BAL
; control). Plasma amino acid levels were measured at baseline and peak depletion (300 min). Appetite, willingness to pay for food, liking, desired portion size and ad libitum food intake were also assessed. The TYR/PHE-free mixture was associated with significant decreases in tyrosine, phenylalanine, and the ratio of tyrosine+phenylalanine to the other large neutral amino acids (all p<.001). There were no effects on our measures of willingness to pay for food or liking. However, in the TYR/PHE-free condition, participants reported significantly lower levels of
hunger
following a fixed-test meal relative to the
BAL
condition. In conclusion, we found no evidence for compensatory eating following ATPD. Our results also provide support for the role of dopamine in motivational components of eating.
...
PMID:Dopamine and food reward: effects of acute tyrosine/phenylalanine depletion on appetite. 2223 Feb 53
The impact of sitting and energy imbalance on appetite and appetite-regulating hormones (acylated ghrelin and leptin) was assessed in response to 1 day of sitting, with and without changes in energy intake. Fourteen men and women completed each of three 24-h conditions: high energy expenditure (standing) with energy balance (STAND), low energy expenditure (sitting) with energy surplus (SIT), and sitting with energy balance (SIT-BAL). Ghrelin, leptin, and appetite were measured in the fasted state and following a standardized meal. In the fasted state, there were no differences among conditions. Following the meal, ghrelin was lower in SIT than in STAND, with no change in appetite. When intake was reduced (SIT-BAL), the decrease in ghrelin when sitting was attenuated,
hunger
increased, and fullness decreased. SIT led to lower ghrelin concentrations in the men, whereas in the women, leptin increased. SIT-
BAL
led to an increase in ghrelin in the men but attenuated the leptin response, reduced ghrelin, increased
hunger
, and decreased fullness in the women. Because a dramatic reduction in energy expenditure was not accompanied by reduced appetite, prolonged sitting may promote excess energy intake, leading to weight gain in both men and women.
...
PMID:Appetite regulation in response to sitting and energy imbalance. 2246 36