The influence of sleep restriction (SR) during pregnancy on blood pressure and renal function among female adult offspring was investigated. Pregnant Wistar rats were distributed into control and SR groups. The SR was performed between the 14th and 20th days of pregnancy (multiple platforms method for 20 h/day). At 2 months of age, half of the offspring from both groups were subjected to an ovariectomy (ovx), and the other half underwent sham surgery. The groups were as follows: control sham (Csham), control ovx (Covx), SR sham (SR sham), and SR ovx (SR ovx). Renal function markers and systolic blood pressure (BPi, indirect method) were evaluated at 4, 6, and 8 months. Subsequently, the rats were euthanized, kidneys were removed, and processed for morphological analyses of glomerular area (GA), number of glomeruli per mm3 (NG), and kidney mass (KM). Increased BPi was observed in the Covx, SR sham, and SR ovx groups compared to Csham at all ages. Increased plasma creatinine concentration and decreased creatinine clearance were observed in the SR sham and SR ovx groups compared to the Csham and Covx groups. The SR ovx group showed higher BPi and reduced creatinine clearance compared to all other groups. The SR ovx group showed reduced values of GA and KM, as well as increased NG, macrophage infiltration, collagen deposit, and ACE1 expression at the renal cortex. Therefore, SR during pregnancy might be an additional risk factor for developing renal dysfunction and increasing BP in female adult offspring. The absence of female hormones exacerbates the changes caused by SR.
Testosterone esters are hormones commonly used for affirming gender identity in transmen. The present study evaluates the effect of testosterone on renal morphology and function in an animal model submitted to cross-sex hormone therapy used for transmen. Two-month-old Wistar rats were divided into three groups: male con-How to cite this article: Lichtenecker DCK, Argeri R, Castro CHdM, Dias-da-Silva MR, Gomes GN. Cross-sex testosterone therapy modifies the renal morphology and function in female rats and might underlie increased systolic pressure. Clin Exp
The Barker hypothesis strongly supported the influence of fetal environment on the development of chronic diseases in later life. Multiple experimental and human studies have identified that the deleterious effect of fetal programming commonly leads to alterations in renal development. The interplay between environmental insults and fetal genome can induce epigenetic changes and lead to alterations in the expression of renal phenotype. In this review, we have explored the renal development and its functions, while focusing on the epigenetic findings and functional aspects of the renin-angiotensin system and its components.
Fructose overload is associated with cardiovascular and metabolic disorders. During pregnancy, these alterations may affect the maternal environment and predispose offspring to diseases. Aims: To evaluate the renal morphology and function of offspring of dams that received fructose overload during pregnancy and lactation. Methods: Female Wistar rats were divided into the control (C) and fructose (F) groups. C received food and water ad libitum, and F received food and d-fructose solution (20%) ad libitum. The d-fructose offer started 1 week before mating and continued during pregnancy and lactation. The progeny were designated as control (C) or fructose (F); after weaning, half of the F received water to drink (FW), and half received d-fructose (FF). Blood pressure (BP) and renal function were evaluated. The expression of sodium transporters (NHE3-exchanger, NKCC2 and NCC-cotransporters, and ENaC channels) and markers of renal dysfunction, including ED1 (macrophage), eNOS, 8OHdG (oxidative stress), renin, and ACE 1 and 2, were evaluated. CEUA-UNIFESP: 2757270117. The FF group presented with reduced glomerular filtration rate and urinary osmolarity, increased BP, proteinuria, glomerular hypertrophy, macrophage infiltration, and increased expression of transporters (NHE3, NCC, and ENaC), 8OHdG, renin, and ACE1. The FW group did not show increased BP and renal functional alterations; however, it presented glomerular hypertrophy, macrophage infiltration, and increased expression of the transporters (NHE3, NKCC2, NCC, and ENaC), renin, and ACE1. These data suggest that fructose overload during fetal development alters renal development, resulting in the increased expression of renin, ACE1, and sodium transporters, thus predisposing to hypertension and renal dysfunction.
The consumption of foods that have fructose in its formulations has grown in the last decades. Nevertheless, increased consumption of this sugar has been related to the development of diseases such as obesity, diabetes and others. Many physiological changes occur during pregnancy and lactation and high consumption of fructose in these periods can interfere with maternal health. Thus, this study aims to evaluate the effects of increased fructose consumption on gestation and lactation on blood pressure and renal function. Methods Females Wistar rats were randomly assigned to groups: Control (C) and Fructose (F). The group C received food and drinking water ad libitum, and F received food and D‐fructose solution (20%) for drinking ad libitum. In F, the offer of D‐fructose solution begun 1week before mating and continued during pregnancy and lactation. Renal function was evaluated 21 days after offspring birth. Indirect measurement of systolic blood pressure (BPi), body weight, arterial blood pH, glycemia, ureia concentration in plasma, glomerular filtration rate ‐ GFR (creatinine clearance), excreted load of sodium (ENa+) and potassium (EK+) were measured. Ethic Committee on Animal Use of the Federal University of Sao Paulo approval number 757270117. Results Compared with C group, F presented higher values of BPi (129.7±1.4 vs 118.4±1.9 mmHg; p=0.0012), body weight (281.7±4.9 vs 232.7± 22.9 g; p=0.0245) and urinary flow (33.4±3.6 vs 14.6±2.1 mL; p=0.0035). F also had decreased GFR (3.8±0.4 vs 6.0± 0.5 mL/min/kg; p=0.0082), ENa+ (0.88±0.12 vs 1.42±0.25 mEq/24h; p=0.0350) and EK+ (2.24±0.38 vs 3.73±0.51 mEq/24h, p=0.0350). There were no significant differences between the groups regarding the arterial blood pH (7.40±0.01 vs 7.39±0.02; p=0.7599), glycemia (160.7± 3.5 vs 146.7±4.7 mg/dL; p=0.0565) and ureia concentration in plasma (36.7±1.2 vs 34.9±1.1 mg/dL; p=0.4645). Values presented as mean ± sem, Mann‐Whitney test, p ≤ 0.05; number of animals: C=6, F=7. Conclusions The results suggest that in rats, fructose overload during pregnancy and lactation can lead to maternal renal dysfunction (reduced GFR and sodium excretion), changes probably related to the increase in blood pressure observed in these animals. Support or Funding Information FAPESP, CNPq This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
After lactation, many children consume fructose-rich processed foods. However, overconsumption of these foods can predispose individuals to non-communicable chronic diseases, which can have different repercussions depending on the sex. Thus, we evaluated the effects of fructose overload introduced after weaning on the renal function of young rats of both sexes.Methods: After weaning, male and female offspring of Wistar rats were assigned to drink water (the male/water and female/water groups) or 20% D-fructose solution (male/fructose and female/fructose groups). Food and water or fructose solution was offered ad libitum. Rats were evaluated at 4 months. Parameters analyzed: blood pressure, body weight, triglyceride levels, glomerular filtration rate, sodium, potassium, calcium, and magnesium excretion, macrophage infiltration, and eNOS and 8OHdG expression in renal tissue. CEUA-UNIFESP: 2757270117.Results: Fructose intake affected the blood pressure, body weight, and plasma triglyceride in all rats. Glomerular filtration rate was significantly reduced in males that received fructose when compared to that of the control group. Sodium and potassium excretion decreased in all fructose-treated rats; however, the excreted load of these ions was significantly higher in females than in males. In the female control group, calcium excretion was higher than that of the male control group. Fructose overload increased magnesium excretion in females, and also increased macrophage infiltration and reduced eNOS expression in both males and females.Conclusion: Fructose overload introduced after weaning caused metabolic and renal changes in rats. Renal function was more affected in males; however, several significant alterations were also observed in the female-fructose group.
Testosterone esters are used in clinical conditions such as male hypogonadism. Additionally, it has been used to improve sports performance, increasing muscle mass in both genders, and to affirm gender identity by transgender men. However, few experimental studies have been carried out to evaluate the repercussion of testosterone on female rodents on renal function and blood pressure. Thus, the present study aims to evaluate the blood pressure and renal function in female rats subjected chronically to testosterone therapy. Adult female Wistar rats weighing 200 ± 20 g were randomly assigned to receive testosterone (T) or vehicle (control group ‐ C). Group T received testosterone cypionate (3.0 mg/kg, i.m.) and C received vehicle oil every 10 days for 4 months. Renal function and blood pressure were evaluated at 6 months of age. Urine was collected in metabolic cages for 24 h. Plasma and urine concentrations of urea, creatinine, sodium, potassium, osmolality, and glomerular filtration rate (GFR) were measured. The kidneys were weighed, paraffin‐embedded, and histological sections were prepared to evaluate the glomerular area. When compared to C, the group T had higher values of BP [C: 119±1.0; T: 131±1.4; mmHg], lower GFR [C: 0.78±0.02; T: 0.67±0.03; ml/min/g kidney weight], increased proteinuria [C: 2.9±0.2; T: 6.2±0.9 mg/24 h], increased kidney weight [C: 1.8±0.04; T: 2.2±0.06; g] and glomerular hypertrophy [C: 7884±112.8; T: 8917±152.4; µm2]. Urinary osmolality and sodium and potassium excretion were similar in both groups. Testosterone therapy in female rats increased blood pressure and induced renal changes that may be related to adaptations caused by the hormonal treatment that carried female rats close to male physiological conditions.
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