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And Water Intake (and + water_intake)
Kinds of And Water Intake Selected AbstractsSystemic and local effects of long-term exposure to alkaline drinking water in ratsINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 4 2001Marina E.T. Merne Alkaline conditions in the oral cavity may be caused by a variety of stimuli, including tobacco products, antacids, alkaline drinking water or bicarbonate toothpaste. The effects of alkaline pH on oral mucosa have not been systematically studied. To assess the systemic (organ) and local (oral mucosal) effects of alkalinity, drinking water supplemented with Ca(OH)2 or NaOH, with pH 11.2 or 12 was administered to rats (n = 36) for 52 weeks. Tissues were subjected to histopathological examination; oral mucosal biopsy samples were also subjected to immunohistochemical (IHC) analyses for pankeratin, CK19, CK5, CK4, PCNA, ICAM-1, CD44, CD68, S-100, HSP 60, HSP70, and HSP90. At completion of the study, animals in the study groups had lower body weights (up to 29% less) than controls despite equal food and water intake, suggesting a systemic response to the alkaline treatment. The lowest body weight was found in rats exposed to water with the highest pH value and starting the experiment when young (6 weeks). No histological changes attributable to alkaline exposure occurred in the oral mucosa or other tissues studied. Alkaline exposure did not affect cell proliferation in the oral epithelium, as shown by the equal expression of PCNA in groups. The up-regulation of HSP70 protein expression in the oral mucosa of rats exposed to alkaline water, especially Ca(OH)2 treated rats, may indicate a protective response. Intercellular adhesion molecule-1 (ICAM-1) positivity was lost in 6/12 rats treated with Ca(OH)2 with pH 11.2, and loss of CD44 expression was seen in 3/6 rats in both study groups exposed to alkaline water with pH 12. The results suggest that the oral mucosa in rats is resistant to the effects of highly alkaline drinking water. However, high alkalinity may have some unknown systemic effects leading to growth retardation, the cause of which remains to be determined. [source] Lack of an osmotic constraint on intake rate of the eastern curlew Numenius madagascariensisJOURNAL OF AVIAN BIOLOGY, Issue 4 2006Rachel Blakey Rates of food intake in animals consuming abundant prey can be constrained by the rates of digestion or excretion of ingested substances, such as salt, particularly so in the animals that regularly migrate between freshwater and saltwater environments. We tested this hypothesis in a long-distance migrant shorebird, the eastern curlew Numenius madagascariensis (suborder Charadrii), foraging on intertidal decapods in eastern Australia. We predicted that if food intake rates are constrained osmotically, individuals with access to freshwater and less saline prey (FW group) would have higher rates of food and water intake than individuals with seawater-only access (SW group). Food intake rates did not differ between the FW and SW groups (0.14 g ash-free dry mass min,1), nor did the water influx rates (0.75 g,min,1). Salt intake rates were lower at FW sites (19.3 versus 23.3 mg NaCl min,1) and overall they were similar to those of marine birds. Food intake rate in the eastern curlew appeared limited by digestive rather than by osmoregulatory capacity. [source] Changes in Hypothalamic-Pituitary-Adrenal Function, Body Temperature, Body Weight and Food Intake with Repeated Social Stress Exposure in RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2006S. Bhatnagar Abstract These present studies aimed to compare changes in hypothalamic-pituitary-adrenal (HPA) activity and body temperature in response to acute social defeat, to repeated social stress and to novel restraint after repeated stress, as well as to assess effects on metabolic parameters by measuring body weight gain and food and water intake. We found that social defeat produced a marked increase in both adrenocorticotrophic hormone and corticosterone compared to placement in a novel cage. Similarly, body temperature was also increased during social defeat and during 30 min of recovery from defeat. We then examined the effects of 6 days of repeated social stress and observed minimal HPA responses to repeated social stress compared to control rats. These neuroendocrine responses were contrasted by robust increases in body temperature during stress and during recovery from stress during 6 days of repeated stress. However, in response to novel restraint, repeatedly stressed rats displayed facilitated body temperature responses compared to controls, similar to our previous findings with HPA activity. Food intake was increased during the light period during which defeat took place, but later intake during the dark period was not affected. Repeated stress decreased body weight gain in the dark period but food intake was increased overall during the 6 days of repeated stress in the light period. As a result, repeated stress increased cumulative food intake during the light period in the stressed rats but these relatively small increases in food intake were unable to prevent the diminished total weight gain in repeatedly stressed rats. Overall, the results demonstrate that, although acute social defeat has similar effects on temperature and HPA activity, repeated exposure to social stress has divergent effects on HPA activity compared to body temperature and that dampened weight gain produced by repeated social stress cannot be fully explained by changes in food intake. [source] Time Course of Elevated Ethanol Intake in Adolescent Relative to Adult Rats Under Continuous, Voluntary-Access ConditionsALCOHOLISM, Issue 7 2007Courtney S. Vetter Background: Adolescence is a period of elevated alcohol consumption in humans as well as in animal models. Previous studies in our laboratory have shown that adolescent Sprague,Dawley rats consume approximately 2 times more ethanol on a gram per kilogram basis than adult animals in a 2-bottle choice free-access situation. The purpose of the present study was to examine the time course and pattern of elevated ethanol intake during adolescence and the adolescent-to-adult transition, contrast this intake with ontogenetic patterns of food and water intake, and determine whether adolescent access to ethanol elevates voluntary consumption of ethanol in adulthood. Methods: Adolescent [postnatal day (P)27,28] and adult (P69,70) male Sprague,Dawley rats were singly housed with continuous access to both water and 1 of 3 experimental solutions in ball-bearing,containing sipper tubes: unsweetened ethanol (10% v/v), sweetened ethanol (10% v/v+0.1% w/v saccharin), and saccharin alone (0.1% w/v). Results: Ethanol consumption plateaued at approximately 7.5 g/kg/d during the first 2 weeks of measurement (i.e., P28,39) in early adolescence, before declining sharply at approximately P40 to levels that were only modestly elevated compared with adult-typical consumption patterns that were reached by approximately P70. In contrast, intake of food and total calories showed a more gradual decline into adulthood with no distinguishable plateaus in early adolescence. When adolescent-initiated and adult-initiated animals were tested at the same chronological age in adulthood, animals drank similar amounts regardless of the age at which they were first given voluntary access to ethanol. Conclusions: Taken together, these data suggest that the elevated ethanol intake characteristic of early-to-mid adolescence is not simply a function of adolescent-typical hyperphagia or hyperdipsia, but instead may reflect age-related differences in neural substrates contributing to the rewarding or aversive effects of ethanol, as well as possible modulatory influences of ontogenetic differences in sensitivity to novelty or in ethanol pharmacokinetics. Voluntary home cage consumption of ethanol during adolescence, however, was not found to subsequently elevate ethanol drinking in adulthood. [source] Dietary NaCl Does Not Affect Blood Pressure in Healthy CatsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2004Nicole Luckschander The purpose of this study was to assess the effects of dietary salt intake on systolic blood pressure, water intake, urine output, and urine concentration in cats. Ten healthy young adult cats (mean age 2.5 years) were randomly divided into 2 groups and fed either a control diet (0.46% Na and 1.33% Cl on a dry matter [DM] basis) or a diet with a moderately increased salt content (1.02% Na and 2.02% Cl on a DM basis) for 2 weeks. After a 1-week wash-out period, each group was switched to the opposite diet for 2 weeks. During each 2-week study period, food and water intake, urine volume, urine specific gravity, and urine osmolality were measured daily. Systolic blood pressure (calculated as the mean of 5 readings measured with a Doppler flow detector) was assessed twice daily. No significant effect of diet composition was found on systolic blood pressure, and blood pressure measurements remained within reference limits throughout the study in all 10 cats. However, animals fed the higher salt diet had significantly increased water intake and urine osmolality, and significantly decreased urine specific gravity in comparison to animals fed the control diet. Examination of results of this preliminary study suggests that feeding a diet with moderately increased salt content increases water intake and causes diuresis without increasing systolic blood pressure in healthy adult young cats. [source] Subchronic toxicity of chloral hydrate on rats: a drinking water studyJOURNAL OF APPLIED TOXICOLOGY, Issue 4 2002R. Poon Abstract The subchronic toxicity of chloral hydrate, a disinfection byproduct, was studied in rats following 13 weeks of drinking water exposure. Male (262 ± 10 g) and female (190 ± 8 g) Sprague-Dawley rats, ten animals per group, were administered chloral hydrate via drinking water at 0.2, 2, 20 and 200 ppm. Control animals received distilled water only. Gross and microscopic examinations, serum chemistry, hematology, biochemical analysis, neurogenic amine analysis and serum trichloroacetic acid (TCA) analysis were performed at the end of the treatment period. Bronchoalveolar fluids were collected at necropsy and urine specimens were collected at weeks 2, 6 and 12 for biochemical analysis. No treatment-related changes in food and water intakes or body weight gains were observed. There were no significant changes in the weights of major organs. Except for a mild degree of vacuolation within the myelin sheath of the optic nerves in the highest dose males, there were no notable histological changes in the tissues examined. Statistically significant treatment-related effects were biochemical in nature, with the most pronounced being increased liver catalase activity in male rats starting at 2 ppm. Liver aldehyde dehydrogenase (ALDH) was significantly depressed, whereas liver aniline hydroxylase activity was significantly elevated in both males and females receiving the highest dose. A dose-related increase in serum TCA was detected in both males and females starting at 2 ppm. An in vitro study of liver ALDH confirmed that chloral hydrate was a potent inhibitor, with an IC50 of 8 µM, whereas TCA was weakly inhibitory and trichloroethanol was without effect. Analysis of brain biogenic amines was conducted on a limited number (n = 5) of male rats in the control and high dose groups, and no significant treatment-related changes were detected. Taking into account the effect on the myelin sheath of male rats and the effects on liver ALDH and aniline hydroxylase of both males and females at the highest dose level, the no-observed-effect level (NOEL) was determined to be 20 ppm or 1.89 mg kg,1 day,1 in males and 2.53 mg kg,1 day,1 in females. This NOEL is ca. 1000-fold higher than the highest concentration of chloral hydrate reported in the municipal water supply. Copyright © 2002 Crown in the right of Canada. Published by John Wiley & Sons, Ltd. [source] | ||||||||||