No abstract available.
Animals ; Cyclophosphamide* ; Food Deprivation* ; Mice*

No abstract available.
Animals ; Cyclophosphamide* ; Food Deprivation* ; Mice*

Food deprivation can affect performance on difficult cognitive task, such as the delayed nonmatch-to-place T-maze task (DNMT). The importance of food deprivation on maintaining high motivation for DNMT task has been emphasized, but not many studies have investigated the optimal conditions for depriving rodents to maximize performance. Establishing appropriate conditions for food deprivation is necessary to maintain DNMT task motivation. We applied different conditions of food deprivation (1-h food restriction vs. 1.5-g food restriction; single caging vs. group caging) and measured body weight and the number of correct choices that 8-week-old C57BL/6J mice made during the DNMT task. The 1.5-g food restriction group maintained 76.0+/-0.6% of their initial body weight, but the final body weight of the 1-h food restriction condition group was reduced to 62.2+/-0.8% of their initial body weight. These results propose that 1.5-g food restriction condition is effective condition for maintaining both body weight and motivation to complete the DNMT task.
Animals ; Body Weight ; Food Deprivation ; Mice ; Motivation ; Rodentia

The effects of ration level and feeding frequency on digestibility in juvenile soft-shelled turtle, Pelodiscus sinensis, were investigated. Four ration levels 1.5%, 2.5%, 4.0% and satiation (6.0% BW/d) were used. Apparent digestibility (AD) of dry matter (DMAD), protein (PAD) and protein real digestibility (PRD) were significantly affected by ration level, but not by feeding frequency when the ration level was similar. However, the feeding frequency affected the AD, DMAD, PAD and PRD significantly when the turtles were fed to satiation. The relationship between fecal protein content (Y) and protein intake (X) can be expressed as a quadric equation: Y=-0.1742+0.1476X-0.0003X(2) (r(2)=0.876, n=27, F=93.92, P<0.01).
Animal Feed ; analysis ; classification ; Animals ; Digestion ; physiology ; Feeding Behavior ; physiology ; Food Analysis ; Food Deprivation ; physiology ; Periodicity ; Turtles ; physiology

BACKGROUND: There are reports that food deprivation causes emphysematous changes in the lungs of rats and humans. However, the meaning of this phenomenon in patients with chronic obstructive pulmonary disease has not been evaluated. The aim of this study was to determine the correlations between the caloric intake and parameters of the lung function in patients with chronic obstructive pulmonary disease. METHODS: Patients with chronic obstructive pulmonary disease who had visited the respiratory clinic from March, 2006 for one year were enrolled in this study. The patients underwent pulmonary function tests, and a dietitian evaluated their nutritional intake using a food record method. RESULTS: There was no correlation between the total caloric intake and forced vital capacity (FVC, %predicted) or forced expiratory volume in one second (FEV1, %predicted). The total caloric intake showed a positive correlation with the diffusing capacity of carbon monoxide (DLCO %predicted, DLCO/VA %predicted), and a negative correlation with the total lung capacity (TLC, %predicted). Of the calories taken, only calories from protein intake correlated with the diffusing capacity of carbon monoxide (DLCO %predicted, DLCO/VA %predicted). CONCLUSION: The total caloric intake of patients with chronic obstructive pulmonary disease showed a positive correlation with the diffusing capacity of the lung, and a negative correlation with the total lung capacity. Further study on the linkage between the caloric intake and severity of emphysema is needed.
Animals ; Carbon Monoxide ; Emphysema ; Energy Intake ; Food Deprivation ; Forced Expiratory Volume ; Humans ; Lung ; Pulmonary Disease, Chronic Obstructive ; Rats ; Respiratory Function Tests ; Total Lung Capacity ; Vital Capacity

PURPOSE: Starvation causes impairment in the urinary concentration ability. However, the molecular basis for the impaired urinary concentration and polyuria remains undefined. We examined the effects of food deprivation on the water handling by the kidney and it's regulatory mechanism. METHODS: Sprague-Dawley rats were used. They were placed in metabolic cages and deprived of food but had free access to water for 24 hours. Control rats had free access to both water and food. Protein expression of aquaporin-2 (AQP2) and Na+-K+-2Cl- cotransporter (NKCC2) was determined in the kidney by Western blot analysis. Protein expression of type VI adenylyl cyclase and prostaglandin E2 synthase (PGES) was determined. Urinary PGE2 excretion was also determined by radioimmunoassay. RESULTS: Food deprivation (FD) resulted in impaired urinary concentration associated with decreased tubular water reabsorption and increased urine output. The expression of AQP2 proteins was significantly decreased in the inner stripe of the outer medulla (ISOM). The expression of NKCC2 was not affected in ISOM. The adenylyl cyclase VI expression was increased in ISOM in FD rats. The protein expression of PGES was decreased in the cortex/OSOM and ISOM. The 24 hr urinary excretion of PGE2 was significantly decreased in FD rats compared with controls. CONCLUSION: These findings indicate that FD-induced urinary concentration defect may related to a reduced abundance of AQP2 in the kidney. It is also suggested that the primary impairment in the pathway to the activation of AQP2 in food deprivation is independent of vasopressin/cAMP or prostaglandin activity.
Adenylyl Cyclases ; Animals ; Aquaporin 2 ; Aquaporins* ; Attention ; Blotting, Western ; Dinoprostone ; Food Deprivation ; Kidney* ; Polyuria* ; Prostaglandins E ; Radioimmunoassay ; Rats* ; Rats, Sprague-Dawley ; Sodium* ; Starvation ; Water*

The current study was designed to examine the effects of intracerebroventricular injections of SHU9119 [a nonselective melanocortin receptor (McR) antagonist] and MCL0020 (a selective McR antagonist) on the serotonin-induced eating and drinking responses of broiler cockerels deprived of food for 24 h (FD24). For Experiment 1, the chickens were intracerebroventricularly injected with 2.5, 5, and 10 microg serotonin. In Experiment 2, the chickens received 2 nmol SHU9119 before being injected with 10 microg serotonin. For Experiment 3, the chickens were given 10 microg serotonin after receiving 2 nmol MCL0020, and the level of food and water intake was determined 3 h post-injection. Results of this study showed that serotonin decreased food intake but increased water intake among the FD24 broiler cockerels and that these effects occurred in a dose-dependent manner. The inhibitory effect of serotonin on food intake was significantly attenuated by pretreatment with SHU9119 and MCL0020. However, the stimulatory effect of serotonin on water intake was not altered by this pretreatment. These results suggest that serotonin hypophagia and hyperdipsia were mediated by different mechanisms in the central nervous system, and that serotonin required downstream activation of McRs to promote hypophagia but not hyperdipsia in the FD24 chickens.
Animals ; Chickens ; Dose-Response Relationship, Drug ; Drinking Behavior/*drug effects ; Feeding Behavior/*drug effects ; Food Deprivation ; Injections, Intraventricular/veterinary ; Male ; Melanocyte-Stimulating Hormones/*pharmacology ; Oligopeptides/*pharmacology ; Receptor, Melanocortin, Type 3/*antagonists & inhibitors ; Receptor, Melanocortin, Type 4/*antagonists & inhibitors ; Serotonin/pharmacology

BACKGROUND: Adrenalectomy does impair the expression of hypothalamic NPY gene in the rat and replacement of glucocorticoid by intracerebroventricular(ICV) route resulted in a normalization of refeeding hyperphagia and weight gain in adrenalectomized(ADX), food-deprived rats. The purpose of this study was to assess the direct effect of CNS glucocorticoid on hypothalamic NPY gene expression which occurs following food deprivation in ADX rats. METHODS: Adult male Wistar rats were fitted with ICV cannulae and restricted the food intake for 14 days. Adrenalectomy and sham operation were done on the 10th day and single ICV corticosterone acetate(100ug/2uL) was given in one ADX group(ADX+CORT, n=9) and vehicle (2uL) was given in another ADX group(ADX+VEH, n=9) and sham rats(SHAM+VEH, n=7). After experiment, we measured NPY mRNA on arcuate nucleus by in situ hybridization. RESULTS: The rate of weight loss of ADX rats closely parallded that of sham-operated rats. Plasma glucose and insulin levels were not significantly different in three groups. Hybridization density on the ARC in ADX+VEH rats(0.42+/-0.02uCi/g: p<0.05) was significantly reduced compared to that in sham controls(0.68+/-0. 11uCi/g). ICV corticosterone injection increased the hybridization density in ADX+CORT rats(0.53+/-0.04uCi/g) compared to vehicle alone, although this did not reach that of controls. NPY gene expression was 40% in ADX+VEH rats and 62% in ADX+CORT rats compared to control rats. CONCLUSIONS: These results are consistent with the hypothesis that CNS glucocorticoid deficiency appears to be responsible for the impairment of refeeding hyperphagia in ADX rats and the effect of CNS glucocorticoid deficiency is a manifestation of impaired activation of hypothalamic NPY gene expression in the ARC.
Adrenalectomy ; Adult ; Animals ; Arcuate Nucleus ; Blood Glucose ; Catheters ; Corticosterone* ; Eating ; Food Deprivation ; Gene Expression ; Humans ; Hyperphagia ; In Situ Hybridization ; Insulin ; Male ; Rats* ; Rats, Wistar ; RNA, Messenger* ; Weight Gain ; Weight Loss

BACKGROUND: Short-term interruption of feeding is ordinary in modern life but negatively impacts appetite control and body weight. Estradiol (E) imposes long-term inhibitory tonus on food consumption; however, E influence on energy repletion secondary to food deprivation (FD) is unclear. This study investigated the hypothesis that E signal strength regulates hyperphagic responses to FD of varying duration. METHODS: Ovariectomized female rats were implanted with E-containing silastic capsules (30 [E-30] or 300 µg [E-300]/mL) to replicate plasma concentrations at cycle nadir versus peak levels. RESULTS: Data show that food intake was increased equally in E-30 and E-300 rats after 12 hours of food deprivation (FD-12); yet, FD of 18 hours (FD-18) amplified refeeding by E-300 versus E-30. Caudal fourth ventricular administration of the 5′-monophosphate-activated protein kinase (AMPK) inhibitor compound C (Cc) did not modify FD-induced hyperphagia in E-30 (regardless of FD interval) or E-300 animals exposed to FD-12, but diminished refeeding after FD-18 in E-300 rats. Cc-reversible hyperglycemia occurred in refed FD-18 groups. Serum insulin was resistant to FD-12 plus refeeding, but was elevated by AMPK-dependent mechanisms in refed E-300 FD-18 rats; equivalent Cc-insensitive decrements in circulating leptin occurred in all FD groups. CONCLUSION: Current results show that estrous cycle peak, but not baseline, E levels engage hindbrain AMPK signaling to intensify hyperphagia in response to prolongation of FD. Observations of hindbrain AMPK-dependent hyperglycemia, alongside elevated insulin secretion, in refed rats exposed to FD-18 implicate this sensor in insulin resistance mechanisms of glucose partitioning in response to this metabolic imbalance.
AMP-Activated Protein Kinases ; Animals ; Appetite ; Body Weight ; Capsules ; Eating* ; Estradiol* ; Estrous Cycle* ; Female ; Food Deprivation ; Glucose ; Humans ; Hyperglycemia ; Hyperphagia ; Insulin ; Insulin Resistance ; Leptin ; Plasma ; Protein Kinases ; Rats ; Rhombencephalon

This study was conducted to define the molecular mechanism of fasting-induced down-regulation of neuronal nitric oxide synthase (nNOS) expression in the hypothalamic paraventricular nucleus (PVN). Rats were adrenalectomized (ADX), and then either underwent food deprivation or received varying doses of dexamethasone for 48 h. The brain tissues were processed for NADPH-diaphorase (NADPH-d) staining, a histochemical marker of nNOS enzyme activity. Both the ADX and the sham operated rats showed a significant weight loss after 48 h of food deprivation. Food deprivation decreased the number of NADPH-d containing cells in the PVN of sham rats, however, not in the ADX rats. Dexamethasone dose- dependently decreased NADPH-d cells in the PVN of ADX rats. The effect of ADX or dexamethasone was limited to the parvocellular subdivision of PVN. These results suggest that the adrenal glucocorticoids may down-regulate nNOS expression in the PVN during food deprivation.
*Adrenalectomy ; Animals ; Biological Markers ; Dexamethasone/blood/pharmacology ; Down-Regulation/physiology ; Fasting/*physiology ; Food Deprivation/physiology ; Glucocorticoids/blood/pharmacology ; Male ; NADPH Dehydrogenase/*metabolism ; Nitric-Oxide Synthase/*metabolism ; Paraventricular Hypothalamic Nucleus/*enzymology ; Rats ; Rats, Sprague-Dawley ; Support, Non-U.S. Gov't