High-fat diet changes the behavioural and hormonal responses to water deprivation in male Wistar rats.

NEW FINDINGS: What is the central question of this study? What is the effect of an obesogenic diet on the control of hydromineral balance in rats? What is the main finding and its importance? The results showed that, when dehydrated, rats fed a high-fat diet drink less water than their control-diet-fed counterparts. Changes in aquaporin-7 and peroxisome proliferator-activated receptor α expression in the white adipose tissue might be involved. ABSTRACT: High-fat diet (HFD) increases fat accumulation, glycaemia and blood triglycerides and is used as a model to study obesity. Besides the metabolic changes, obesity likely affects water intake. We assessed the effects of HFD on behavioural and hormonal responses to water deprivation. Additionally, we measured if the adipose tissue is differentially affected by water deprivation in control and HFD-fed rats. HFD rats showed a decreased basal water intake when compared to control-fed rats. When subjected to 48 h of water deprivation, as expected, both control and HFD rats drank more water than the hydrated rats. However, the increase in water intake was lessened in HFD dehydrated rats. Similarly, the increase in haematocrit in dehydrated rats was less pronounced in HFD dehydrated rats. These results suggest that HFD diminishes drinking behaviour. White adipose tissue weight, glycaemia and plasma glycerol concentration were increased in HFD rats; however, after 48 h of water deprivation, these parameters were significantly decreased in dehydrated HFD rats, when compared to controls. The increase in adipose tissue caused by HFD may mitigate the effects of dehydration, possibly through the increased production of metabolic water caused by lipolysis in the adipocytes. Oxytocin possibly mediates the lipolytic response, since both its secretion and receptor expression are affected by dehydration in both control and HFD rats, which suggests that oxytocin signalling is maintained in these conditions. Changes in mediators of lipolysis, such as aquaporin-7 and peroxisome proliferator-activated receptor α, might contribute to the different effects observed in control and HFD rats.

Sex-specific influence of maternal exposure to bisphenol A on sodium and fluid balance in response to dipsogenic challenges in rats.

The plasticizer bisphenol A (BPA) is one of the highest volume chemicals produced worldwide. Human exposure to BPA occurs almost constantly. BPA is an endocrine disruptor that interferes in estrogen receptor functions. This is important for the developing brain, which is particularly sensitive to the estrogenic effects of BPA. Body fluid balance is maintained by a complex network of systems that regulate sodium and water intakes and electrolyte excretion. The development of these control systems occurs during early life and therefore, may be susceptible to changes in the uterine environment. The aim of this work was to study the effects of two low BPA doses in the dam, during pregnancy and lactation, on adult offspring drinking and sodium and urine excretion after dipsogenic challenge. Dams were exposed to BPA in drinking water to mimic the most likely route of human exposure. The results showed that BPA did not disrupt spontaneous fluid balance, but altered sodium and fluid intakes in the BPA offspring under osmotic challenges. In experiments, both 24h fluid deprivation and sodium depletion modified fluid ingestive response in BPA offspring compared to control offspring. The increased preference for 2.7% NaCl solution in male BPA offspring is similar to female control offspring, altered ingestive behavior appears to be due to feminization of males and "hyperfeminization" of female BPA offspring, as they drink more than female control offspring. Our results indicate that exposure to low doses of BPA in early life may disrupt the development of sex-specific drinking behaviors by altering the steroid programming of the brain, and this disruption affects males and females differently.

Chronic exposure to low doses of bisphenol A alters hydromineral responses in rats.

Bisphenol A (BPA) is a chemical commonly used in the industrial sectors, hence humans are exposed to the compound repetitively. BPA is an endocrine disruptor and has been anticipated to interfere on chemical estrogen receptor functions and other nuclear hormone receptors. Estrogens are steroid hormones that, in addition to their neuroendocrine roles, affect water and salt intakes in numerous species, including humans and rodents. Changes in the hydrosaline balance produce compensatory behavioral and physiological responses, which serve to preserve or restore osmolarity and blood volume to optimal levels, thus preventing cardiovascular disease. The aim of the present work was to determine for first time the effect of long-term and low-dose BPA treatment on thirst and sodium appetite. Wistar rats were exposed to BPA via drinking water to mimic the most likely route of human exposure, and different dipsogenic and natriorexigenic stimuli were assessed. The BPA-treated rats tend to drink less water that control rats following 24-h fluid restriction, but there was no statistically significant decrease. Perhaps the BPA dose does not have enough estrogenic potency to affect water intake. In the extracellular fluid depletion test, the control rats significantly increased 2.7% NaCl solution intake on repeated testing, showing sodium appetite sensitization, i.e. the capacity to enhance sodium intake produced by stimulus repetition; whereas BPA-treated rats did not. In this study, fluid and electrolyte balance in BPA-treated rats is generally adequate but impaired in osmotic challenges, for example by sodium depletion. Thus, neuroendocrine systems involved in maintaining body fluid and electrolyte homeostasis were altered in BPA-treated rats.

The endocannabinoid system and the neuroendocrine control of hydromineral balance.

Endocannabinoids (ECBs) are ubiquitous lipophilic agents, and this characteristic is consistent with the wide range of homeostatic functions attributed to the ECB system. There is an increasing number of studies showing that the ECB system affects neurotransmission within the hypothalamic neurohypophyseal system. We provide an overview of the primary roles of ECBs in the modulation of neuroendocrine function and, specifically, in the control of hydromineral homeostasis. Accordingly, the general aspects of ECB-mediated signalling, as well as the specific contributions of the central component of the ECB system to the integration of behavioural and endocrine responses that control body fluid homeostasis, are discussed.