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.

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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.

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.