Browsing by Subject "Feeding Behavior"

Now showing 1 - 6 of 6
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    Dissociation between diurnal cycles in locomotor activity, feeding behavior and hepatic PERIOD2 expression in chronic alcohol-fed mice
    (Elsevier, 2015-06) Zhou, Peng; Werner, John H.; Lee, Donghoon; Sheppard, Aaron D.; Liangpunsakul, Suthat; Duffield, Giles E.; Department of Medicine, IU School of Medicine
    Chronic alcohol consumption contributes to fatty liver disease. Our studies revealed that the hepatic circadian clock is disturbed in alcohol-induced hepatic steatosis, and effects of chronic alcohol administration upon the clock itself may contribute to steatosis. We extended these findings to explore the effects of chronic alcohol treatment on daily feeding and locomotor activity patterns. Mice were chronically pair-fed ad libitum for 4 weeks using the Lieber-DeCarli liquid diet, with calorie-controlled liquid and standard chow diets as control groups. Locomotor activity, feeding activity, and real-time bioluminescence recording of PERIOD2::LUCIFERASE expression in tissue explants were measured. Mice on liquid control and chow diets exhibited normal profiles of locomotor activity, with a ratio of 22:78% day/night activity and a peak during early night. This pattern was dramatically altered in alcohol-fed mice, marked by a 49:51% ratio and the absence of a distinct peak. While chow-diet fed mice had a normal 24:76% ratio of feeding activity, with a peak in the early night, this pattern was dramatically altered in both liquid-diet groups: mice had a 43:57% ratio, and an absence of a distinct peak. Temporal differences were also observed between the two liquid-diet groups during late day. Cosinor analysis revealed a ∼4-h and ∼6-h shift in the alcohol-fed group feeding and locomotor activity rhythms, respectively. Analysis of hepatic PER2 expression revealed that the molecular clock in alcohol-fed and control liquid-diet mice was shifted by ∼11 h and ∼6 h, respectively. No differences were observed in suprachiasmatic nucleus explants, suggesting that changes in circadian phase in the liver were generated independently from the central clock. These results suggest that chronic alcohol consumption and a liquid diet can differentially modulate the daily rhythmicity of locomotor and feeding behaviors, aspects that might contribute to disturbances in the circadian timing system and development of hepatic steatosis.
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    Use of an Episodic Food Intake Monitoring System to Evaluate Feeding Behavior in Mice
    (Office of the Vice Chancellor for Research, 2016-04-08) Engle, Staci E.; Bansal, Ruchi; Berbari, Nicolas F.
    The measurement of food consumption in laboratory animals is critical to studies in metabolism and obesity. Unfortunately, feeding behavior is very sensitive to the environment. Many factors such as the change of cages, diet, and human interactions can introduce undesired experimental variation. Here we describe our experiences with a commercially available episodic food intake monitoring system, the BioDAQ Monitor. This system is designed to quantitatively record feeding behavior in mice. It continuously monitors the weight of the food and uses this information to determine bout length and size. Bouts that occur soon after one another can then be defined as meals. When an animal jostles the food hopper while eating, the weight of the hopper fluctuates and eating is considered to be in progress. Once the hopper weight has been stable for a specified time, that period of feeding is considered to be concluded. The system also has the capability to assess either food or liquid choice paradigms and to directly measure the administration of orally available drugs in either the feed or the water. In addition to these functions, the system uses an environment monitor to record temperature, humidity and lighting of the room every five minutes. Here we present data showing measurements taken in hyperphagic mutant mice, altered feeding paradigms, and under different drug and protein hormone treatments. Future studies using this system will continue to focus on the hyperphagia associated obesity phenotype observed in mice upon conditional disruption of primary cilia.
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