Interaction of food deprivation state with food intake recall in humans.

Appetite ◽  
2007 ◽  
Vol 49 (1) ◽  
pp. 316
Author(s):  
J.A. Nasser ◽  
E. Boo ◽  
F.X. Pi-Sunyer ◽  
A. Geliebter
Keyword(s):  
Food Intake ◽  
Food Deprivation ◽  
Deprivation State

Adrenergic Stimulation of the Rat Diencephalon and its Effect on Food Intake and Hoarding Activity

1970 ◽  
Vol 22 (2) ◽  
pp. 125-132 ◽  
Author(s):  
J. E. Blundell ◽  
L. J. Herberg
Keyword(s):  
Electrical Stimulation ◽  
Food Intake ◽  
Food Deprivation ◽  
Lateral Hypothalamus ◽  
Adrenergic Stimulation ◽  
Feeding Mechanism ◽  
Stimulation Of ◽  
Nutritional Depletion

The diencephalic area most sensitive to microinjections of noradrenaline lay outside the area of the lateral hypothalamus in which feeding can be produced by electrical stimulation. Injection of either area, including injections that caused increased feeding, failed to have any effect on hoarding activity. Since hoarding can be elicited both by food deprivation and by electrical stimulation of the lateral hypothalamus, these findings indicate biochemical, anatomical and motivational differences between the central feeding mechanism sensitive to adrenergic stimulation, and that responding to electrical stimulation or nutritional depletion. The former mechanism may be disinhibitory; the latter, excitatory.

Influence of the subfornical organ on meal-associated drinking in rats

2001 ◽  
Vol 280 (3) ◽  
pp. R669-R677 ◽  
Author(s):  
Elizabeth M. Starbuck ◽  
Douglas A. Fitts
Keyword(s):  
Food Intake ◽  
Hypertonic Saline ◽  
Food Deprivation ◽  
Water Deprivation ◽  
Plasma Osmolality ◽  
Subfornical Organ ◽  
Intragastric Administration ◽  
Drinking Patterns ◽  
Ad Libitum ◽  
Ad Libitum Feeding

A lesion of the subfornical organ (SFO) may disrupt drinking after a meal of dry chow as it does drinking after intragastric administration of hypertonic saline. Food and water intakes of SFO-lesioned (SFOX) and sham-lesioned rats were measured during 90-min tests following various lengths of food deprivation. During the tests, all rats began eating before they began drinking. After 20–24 h of food deprivation, latency to begin drinking after eating had started was longer for SFOX than for sham-lesioned rats. Plasma osmolality was elevated by 2–3% in both lesion groups at 12 min, the latency for sham-lesioned rats to drink, but SFOX rats nevertheless continued eating and delayed drinking. Eating after shorter 4-h food deprivations and ad libitum feeding produced more variable drinking latencies and less consistent effects of SFO lesion. During 24 h of water deprivation, SFO lesion had no effect on the suppression of food intake and did not affect food or water intakes during the first 2 h of subsequent rehydration. These findings indicate that the SFO is involved in initiating water intake during eating and in determining drinking patterns and the amount of water ingested during a meal.

Corticotropin-releasing hormone-binding protein in brain and pituitary of food-deprived obese (fa/fa) Zucker rats

1999 ◽  
Vol 277 (6) ◽  
pp. R1749-R1759 ◽  
Author(s):  
Elena Timofeeva ◽  
Yves Deshaies ◽  
Frédéric Picard ◽  
Denis Richard
Keyword(s):  
Food Intake ◽  
Food Deprivation ◽  
Binding Protein ◽  
Mrna Level ◽  
Zucker Rats ◽  
Pituitary Cells ◽  
Dorsal Part ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Ad Libitum

The present study was conducted to verify whether experimental conditions such as obesity and food deprivation, which promote food intake and reduce thermogenesis, could modify the expression of the corticotropin-releasing hormone (CRH)-binding protein (BP) in the rat brain. In situ hybridization, histochemistry, and immunohistochemistry were used to assess the expression of CRH-BP in lean ( Fa/?) and obese ( fa/fa) Zucker rats that were fed ad libitum, food deprived for 24 h, or food deprived for 24 h and refed for 6 h. In both lean and obese rats, food deprivation led to a reduction in body weight that was accompanied by a reversible increase in plasma corticosterone levels. Food deprivation and, to a lesser degree, obesity induced the expression of CRH-BP mRNA in the dorsal part of the medial preoptic area (MPOA). This induction of the CRH-BP gene led to by food deprivation was confirmed by the appearance in the dorsal part of the MPOA of neurons immunoreactive to CRH-BP. Food deprivation (in particular) and obesity also increased the levels of CRH-BP mRNA in the basolateral amygdala (BLA). The enhanced CRH-BP expression in the MPOA and BLA in response to food deprivation was reversed by refeeding. In lean Fa/? rats, the CRH-BP mRNA level in the pituitary cells was significantly decreased after food deprivation and restored after refeeding. When food was provided ad libitum, the number of cells expressing CRH-BP in the anterior pituitary was significantly higher in lean rats than in obese animals. Food deprivation for 24 h decreased dramatically the number of pituitary cells expressing CRH-BP in lean rats. Altogether, the present results demonstrate that food deprivation and, to a lesser extent, obesity can selectively affect the expression of CRH-BP. Given both the inactivating effect of CRH-BP on the CRH system and the potential roles played by the MPOA and BLA in the thermogenic and anorectic effects of CRH, it can be argued that the induction of the CRH-BP gene in obesity and after food deprivation occurs as a mechanism to reduce energy expenditure and to stimulate food intake.

Cholecystokinin-decreased food intake in rhesus monkeys

1976 ◽  
Vol 230 (1) ◽  
pp. 15-18 ◽  
Author(s):  
J Gibbs ◽  
JD Falasco ◽  
PR McHugh
Keyword(s):  
Biological Activity ◽  
Food Intake ◽  
Food Deprivation ◽  
Test Meal ◽  
Rhesus Monkeys ◽  
Significant Inhibition ◽  
Solid Food ◽  
Threshold Dose

Five rhesus monkeys were infused intravenously with partially purified cholecystokinin (CCK) Just prior to a test meal of solid food after overnight food deprivation; CCK produced large, rapid, dose related suppressions of feeding. The lowest dose tested (5 Ivy U/kg body wt) produced a significant inhibition of food intake (26% suppression, P less than 0.05). Equivalent infusions of partially purified CCK or the synthetic COOH-terminal octapeptide of CCK (a pure fragment with all the biological activity of the full molecule) produced equivalent suppressions. In a second experiment, gastric preloads of a potent releaser of endogenous CCK, L-phenylalanine (L-Phe), and a weak releaser, D-phenylalanine (D-Phe) were compared for their relative abilities to suppress food intake at a test meal in nine rhesus monkeys after overnight deprivation. L-Phenylalanine produced large, rapid, dose-related suppressions of feeding, but D-Phe did not. The threshold dose of L-Phe was 0.5 g/kg (32% suppression, P less than 0.01). Neither CCK nor L-Phe caused signs of illness in these experiments. The results demonstrate that intravenous exogenous CCK suppresses feeding in rhesus monkeys and suggest that endogenous CCK has the same effect; they are consistent with the hypothesis that CCK is a satiety signal.

A role for neuropeptide-Y, dynorphin, and noradrenaline in the central control of food intake after food deprivation.

Endocrinology ◽  
1993 ◽  
Vol 133 (1) ◽  
pp. 29-32 ◽  
Author(s):  
P D Lambert ◽  
J P Wilding ◽  
A A al-Dokhayel ◽  
C Bohuon ◽  
E Comoy ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Food Deprivation ◽  
Central Control

The Rat's Adjustment to Repeated Exposure to 72-Hour Food Deprivation

1965 ◽  
Vol 17 (2) ◽  
pp. 467-472
Author(s):  
John H. Wright
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Food Deprivation ◽  
Recovery Time ◽  
Wheel Running ◽  
Previous History ◽  
Albino Rats ◽  
Second Phase ◽  
History Of ◽  
Time Required

18 male albino rats were exposed to repeated cycles of 72-hr. food deprivation and 120 hr. of recovery. Over successive recovery periods Ss exhibited increases in food intake, decreases in wheel running, and decreases in the amount of recovery time required to regain and surpass pre-deprivation body-weight levels. Increases in activity occurred during 72-hr. deprivation and were found to show an increase over successive deprivations. In a second phase of the experiment the response to 72-hr. deprivation with increases in wheel running was found to be greater for rats permitted to run during recovery than for rats not permitted to run during recovery. These findings suggested that the response to 72-hr. deprivation with increases in activity is determined in part by a previous history of opportunity for reinforcement of the wheel-running response by ingestion.

Effect of temporary food or water deprivation on milk secretion and milk composition in the goat

1987 ◽  
Vol 54 (2) ◽  
pp. 153-163 ◽  
Author(s):  
Kristina Dahlborn
Keyword(s):  
Fatty Acids ◽  
Food Intake ◽  
Food Deprivation ◽  
Water Deprivation ◽  
Short Chain ◽  
Free Access ◽  
Long Chain Fatty Acids ◽  
Milk Secretion ◽  
Long Chain ◽  
Chain Fatty Acids

SummaryWhen four goats were subjected to total water deprivation for 48 h once in early lactation and once in mid lactation and their voluntary food intake and effects on milk secretion were observed, milk volume decreased and lactose and fat concentration increased during both periods. However, when the goats were then fed the mean of their own food intake at the two previous water deprivation experiments, and were left free access to water, it was found that decreased food consumption had only a minor influence on milk secretion. When six goats were subjected to 48 h of food deprivation and six to 48 h of water deprivation, milk secretion decreased, but the reduction was delayed and of smaller magnitude during water deprivation. During food deprivation lactose concentration decreased and the milk protein and fat increased; the fatty acid composition changed from a greater proportion of short-chain to more long-chain fatty acids. During water deprivation milk fat and lactose concentrations increased, and only after 44 h did a change from short-chain to a larger proportion of long-chain fatty acids become evident. These experiments indicate that not only food intake, but also water intake are concerned with milk production.

Chronic food restriction and acute food deprivation decrease mRNA levels of opioid peptides in arcuate nucleus

1996 ◽  
Vol 270 (5) ◽  
pp. R1019-R1024 ◽  
Author(s):  
E. M. Kim ◽  
C. C. Welch ◽  
M. K. Grace ◽  
C. J. Billington ◽  
A. S. Levine
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Food Deprivation ◽  
Food Restriction ◽  
Arcuate Nucleus ◽  
Mrna Levels ◽  
Endogenous Opioid ◽  
Pomc Mrna ◽  
Opioid Administration ◽  
Ad Libitum Intake

Although opioid administration induces food intake, the relationship between endogenous opioid synthesis and food consumption is unclear. Two studies examined the effects of food restriction and deprivation on opioid mRNA levels in the arcuate nucleus (ARC) of the rat. Body weight significantly decreased following food restriction and deprivation (P < 0.0001). In experiment 1, food restriction of 10,20,30, and 40% (g) of ad libitum intake for 14 days decreased proDynorphin (proDyn), proEnkephalin (proEnk), and proOpiomelanocortin (POMC) mRNA levels in a linear fashion relative to changes in body weight (r = 0.398, P = 0.0011; r = 0.455, P = 0.0028; r = 0.292, P = 0.0642, respectively). In experiment 2, 48 h deprivation significantly decreased mRNA levels of proDyn and POMC by 23.7% (P < 0.05) and 45.6% (P < 0.01), respectively, whereas 24 h food deprivation decreased POMC mRNA by 43.% (P < 0.01). proEnk mRNA was not affected by 24- or 48-h food deprivation. Restricting food intake suppressed mRNA levels of proDyn, proEnk, and POMC by 29.7, 22.3, and 44.4%, respectively, in 20% restricted rats and by 35.5, 26.8, and 45.6%, respectively, in 40%restricted rats (P < 0.01). It appears that ARC mRNA levels of proDyn, proEnk, and POMC are directly related to the amount of food consumed and/or changes in body weight in food-restricted and food-deprived rats.

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