Increased exposure to sodium during pregnancy and lactation changes basal and induced behavioral and neuroendocrine responses in adult male offspring

Silva, Márcia S; Lucio-Oliveira, F.; Mecawi, André Souza; Almeida, Lucas Ferreira de; Ruginsk, Sílvia Graciela; Greenwood, Michael; Vivas, Laura; Elias, Lucila Leico Kagohara; Murphy, David

doi:10.14814/phy2.13210

Cited by 6 publications

(2 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies in rodents that used dietary or water salt supplementation (2–8%) confirm these findings, reporting impaired cognition, aggravation of cerebral ischemic injury, and high-stress responsivity ( Ge et al, 2017 ; Faraco et al, 2018 , 2019 ; Mitchell et al, 2018 ; Gilman et al, 2019a ; Zhang et al, 2020 ). Importantly, preclinical studies suggest that the maternal high-salt diet can also induce changes in locomotion, inhibition, and anxiety in the offspring, when fed in the preconception, gestation, or lactation periods ( Mcbride et al, 2008 ; Mecawi and Almeida, 2017 ; Dingess et al, 2018 ). During these periods, the offspring is highly susceptible to dietary salt, which may impact on development, potentially leading to lifelong changes in metabolism and behavior.…”

Section: Introductionmentioning

confidence: 99%

High-Salt Diet in the Pre- and Postweaning Periods Leads to Amygdala Oxidative Stress and Changes in Locomotion and Anxiety-Like Behaviors of Male Wistar Rats

Leal

Silva

Rocha-Gomes

et al. 2022

Front. Behav. Neurosci.

View full text Add to dashboard Cite

High-salt (HS) diets have recently been linked to oxidative stress in the brain, a fact that may be a precursor to behavioral changes, such as those involving anxiety-like behavior. However, to the best of our knowledge, no study has evaluated the amygdala redox status after consuming a HS diet in the pre- or postweaning periods. This study aimed to evaluate the amygdala redox status and anxiety-like behaviors in adulthood, after inclusion of HS diet in two periods: preconception, gestation, and lactation (preweaning); and only after weaning (postweaning). Initially, 18 females and 9 male Wistar rats received a standard (n = 9 females and 4 males) or a HS diet (n = 9 females and 5 males) for 120 days. After mating, females continued to receive the aforementioned diets during gestation and lactation. Weaning occurred at 21-day-old Wistar rats and the male offspring were subdivided: control-control (C-C)—offspring of standard diet fed dams who received a standard diet after weaning (n = 9–11), control-HS (C-HS)—offspring of standard diet fed dams who received a HS diet after weaning (n = 9–11), HS-C—offspring of HS diet fed dams who received a standard diet after weaning (n = 9–11), and HS-HS—offspring of HS diet fed dams who received a HS diet after weaning (n = 9–11). At adulthood, the male offspring performed the elevated plus maze and open field tests. At 152-day-old Wistar rats, the offspring were euthanized and the amygdala was removed for redox state analysis. The HS-HS group showed higher locomotion and rearing frequency in the open field test. These results indicate that this group developed hyperactivity. The C-HS group had a higher ratio of entries and time spent in the open arms of the elevated plus maze test in addition to a higher head-dipping frequency. These results suggest less anxiety-like behaviors. In the analysis of the redox state, less activity of antioxidant enzymes and higher levels of the thiobarbituric acid reactive substances (TBARS) in the amygdala were shown in the amygdala of animals that received a high-salt diet regardless of the period (pre- or postweaning). In conclusion, the high-salt diet promoted hyperactivity when administered in the pre- and postweaning periods. In animals that received only in the postweaning period, the addition of salt induced a reduction in anxiety-like behaviors. Also, regardless of the period, salt provided amygdala oxidative stress, which may be linked to the observed behaviors.

show abstract

Section: Introductionmentioning

confidence: 99%

High-Salt Diet in the Pre- and Postweaning Periods Leads to Amygdala Oxidative Stress and Changes in Locomotion and Anxiety-Like Behaviors of Male Wistar Rats

Leal

Silva

Rocha-Gomes

et al. 2022

Front. Behav. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Infants exposed to foods higher in sodium displayed more acceptance for salty foods at six months and preschool age [ 18 , 19 ]. It has been proposed that such increases in sodium preference that result from early dietary NaCl exposure may be due to changes in salt taste processing or changes in systems regulating sodium balance [ 20 ]. These studies are suggestive of a direct link between dietary sodium and salt taste preference; a relationship that is maintained in adulthood.…”

Section: The Drive To Consume Sodium and Salt Tastementioning

confidence: 99%

Sodium Intake and Disease: Another Relationship to Consider

et al. 2023

View full text Add to dashboard Cite

Sodium (Na+) is crucial for numerous homeostatic processes in the body and, consequentially, its levels are tightly regulated by multiple organ systems. Sodium is acquired from the diet, commonly in the form of NaCl (table salt), and substances that contain sodium taste salty and are innately palatable at concentrations that are advantageous to physiological homeostasis. The importance of sodium homeostasis is reflected by sodium appetite, an “all-hands-on-deck” response involving the brain, multiple peripheral organ systems, and endocrine factors, to increase sodium intake and replenish sodium levels in times of depletion. Visceral sensory information and endocrine signals are integrated by the brain to regulate sodium intake. Dysregulation of the systems involved can lead to sodium overconsumption, which numerous studies have considered causal for the development of diseases, such as hypertension. The purpose here is to consider the inverse—how disease impacts sodium intake, with a focus on stress-related and cardiometabolic diseases. Our proposition is that such diseases contribute to an increase in sodium intake, potentially eliciting a vicious cycle toward disease exacerbation. First, we describe the mechanism(s) that regulate each of these processes independently. Then, we highlight the points of overlap and integration of these processes. We propose that the analogous neural circuitry involved in regulating sodium intake and blood pressure, at least in part, underlies the reciprocal relationship between neural control of these functions. Finally, we conclude with a discussion on how stress-related and cardiometabolic diseases influence these circuitries to alter the consumption of sodium.

show abstract