Dehydration-Associated Anorexia: Development and Rapid Reversal

doi:10.1016/S0031-9384(98)00244-3

Physiology & Behavior

Volume 65, Issues 4–5, 15 October 1998, Pages 871-878

https://doi.org/10.1016/S0031-9384(98)00244-3 Get rights and content

Abstract

Dehydration in rats results in anorexia that is proportional to the degree of dehydration. The aims of this study were first, to determine when anorexia develops in response to drinking hypertonic (2.5%) saline for 4 days; and second, to determine the organization of ingestive behaviors after access to water is resumed. Body weights, food, and fluid intake were measured morning and evening before, during, and after a 4-day period of dehydration caused by drinking hypertonic saline. A profile of the behaviors expressed immediately after rehydration was determined. The data make three points. First, dehydration-associated anorexia does not emerge until the second night of dehydration when the composition of the fluid compartments can no longer be homeostatically buffered. Second, dehydration reduces the amount food eaten nocturnally, but leaves diurnal food consumption largely unaffected. Animals very rapidly return to predehydration nocturnal ingestion patterns, whereas the amounts of food and water ingested during the day are significantly increased. Increased diurnal food intake may play a significant role in normalizing metabolism after dehydration. Finally, anorexia is reversed within minutes of rehydration. The data suggest a model where dehydration simultaneously activates two sets of circuits within the brain that will independently stimulate or inhibit feeding. Eating is inhibited during dehydration through the action of a set of inhibitory circuits, which masks the output of circuits that stimulate eating. However, when drinking water resumes, sensory inputs to these circuits rapidly release the inhibition and allow eating to proceed freely.

Section snippets

Methods and materials

Twenty-four adult male Sprague–Dawley rats (225–250 g body weight at the beginning of the experiment) were singly housed and maintained on a 12 L: 12D photoperiod (lights on at 0600 h) with unlimited water and rat chow (Teklad rodent diet 8604), and allowed at least 5 days of acclimation to animal quarters before measurements began. For the first 5 days of the experiment (experimental days 1–5) animals were given water to drink. This was changed to 2.5% saline (w/v) at 1730 h of Day 5, and was

Changes in body weight

Figure 1 shows changes in nocturnal and diurnal body weight measured throughout the experiment. In the predehydration period body weights increased at rate of 15.5 ± 0.4 g/rat/night, and decreased at rate of −8.2 ± 0.3 g/rat/day, resulting in a mean daily weight gain of 8.1 ± 0.2 g/rat/24 h measured from one morning to the next. On the first morning following drinking hypertonic saline, mean body weights were reduced by approximately 2.5% from those measured the previous evening (Fig. 1), but

Discussion

The development of anorexia during dehydration appears to have a relatively slow onset with eating not actively inhibited until the second night of dehydration. During the first night both the amounts consumed and the ratio of food to fluid intake were not significantly different from those seen in the predehydration period. This finding suggests that at this early stage of dehydration the central mechanisms responsible for anorexia do not have a significant influence on eating behavior. We

Acknowledgements

I would like to thank Graciela Sanchez–Watts and Judson Karlen for help with these experiments. This work was supported by grants NS 29728 and KO-4 01833 from NINDS, NIH.

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Citation Excerpt :
Dehydration-induced anorexia involves an important physiological adaptation that limits the intake of osmolytes from food and helps maintain the integrity of fluid compartments [62]. Watts and colleagues found that rats develop profound anorexia from dehydration when given hypertonic saline (2.5 % NaCl) instead of water [63]. They also showed that, in dehydrated rats in comparison with euhydrated rats, gene expression of neuropeptide Y (NPY) in the arcuate nucleus was significantly increased, CRH in the PVN was markedly decreased, and CRH in the lateral hypothalamic area was significantly increased [61].
From its identification and isolation in 1954, arginine vasopressin (AVP) has attracted attention, not only for its peripheral functions such as vasoconstriction and reabsorption of water from kidney, but also for its central effects. As there is now considerable evidence that AVP plays a crucial role in feeding behavior and energy balance, it has become a promising therapeutic target for treating obesity or other obesity-related metabolic disorders. However, the underlying mechanisms for AVP regulation of these central processes still remain largely unknown. In this review, we will provide a brief overview of the current knowledge concerning how AVP controls energy balance and feeding behavior, focusing on physiological aspects including the relationship between AVP, circadian rhythmicity, and glucocorticoids.

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ArticlesDehydration-Associated Anorexia: Development and Rapid Reversal

Abstract

Section snippets

Methods and materials

Changes in body weight

Discussion

Acknowledgements

Physiol. Behav.

Physiol. Behav.

Physiol. Behav.

Peptides

Neuroscience

Neuroscience

Brain Res.

Neuroscience

Front. Neuroendocrinol.

Preoptic-hypothalamic periventricular lesions alter food-associated drinking and circadian rhythms

J. Comp. Physiol. Psychol.

Oropharyngeal control of drinking in rats

J. Comp. Physiol. Psychol.

The lower brainstem and bodily homeostasis

The role of antidiuretic hormone during water deprivation in rats

J. Physiol. (Lond.)

Eating as a regulatory control of drinking in the rat

J. Comp. Physiol. Psychol.

Caudal brainstem participates in the distributed neural control of feeding

Thirst and sodium appetite

Saline drinking effects on food and water intake in rats

Psychol. Rep.

Articles
Dehydration-Associated Anorexia: Development and Rapid Reversal