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The aim was evaluate if the alterations promoted by the insertion of a western diet during the perinatal period can be transgenerational. 4 female rats mated in the ratio 2:1. After pregnancy confirmation, a western on control diet was offered until the weaning of the pups. Pups of both groups were accompanied until complete 90 days, and then were placed to mate. After pregnancy confirmation, all rats were fed with a standard rodent diet. After weaning, rats were divided in 2 groups: second‐generation control offspring (2ºCO) and second‐generation western offspring (2ºWO), both fed with the same standard diet. Offspring body weight (BW) was measured weakly until the 90th day, dietary intake (DI) and calorie consumption (CC) was accompanied during a period of 10 days between the 30th and 40th day (young stage ‐YS) and the 60th and 70th day (adult stage ‐ AS). Offspring fasting glucose was evaluated with 30, 60 and 90 days. 2ºWO pups born with increased BW (2ºCO 5.41 ± 0.08 vs 2ºWO 6.82 ± 0.11) and maintained higher until 90th day(2ºCO 222 ± 5.11 vs 2ºWO 277 ± 4.6). In addition, 2ºWO pups had increased DI and CC in both periods, YS (DI: 2ºCO 121.3 ± 2.75 vs 2ºWO 132.6 ± 3.12) ‐ (CC: 2ºCO 552.14 ± 12.48 vs 2ºWO 603.42 ± 8.24) and AS (DI: 2ºCO 202.1 ± 6.42 vs 2ºWO 220 ± 2.64) ‐ (CC: 2ºCO 641.01 ± 21.11 vs 2ºWO 700.38 ± 14.11). In relation to fasting glucose, no change was observed in any of the periods (30 days: 2ºCO 84.83 ± 2.01 vs 2ºWO 89.5 ± 1.87; 60 days: 2ºCO 87.83 ± 3.88 vs 2ºWO 82.67 ± 2.60; 90 days: 2ºCO 93.83 ± 2.54 vs 2ºWO 82.66 ± 1.87). In conclusion, these findings suggests that dietary patterns influence directly the feeding behavior of future generations.

Dexamethasone is the most clinically used glucocorticoid with an established role in the treatment of a wide spectrum of inflammatory‐related diseases. While the therapeutic actions are well known, dexamethasone treatment causes a number of cardiovascular side effects, which are complex, frequent and, in some particular cases, clinically unnoticeable. Thus, we investigated whether a therapeutic regimen of dexamethasone affects cardiac arrhythmogenesis and/or promote cardiac remodeling, focusing on the contribution of reactive oxygen species (ROS). Male Wistar rats were treated with dexamethasone (2 mg/kg, i.p.) for 7 days. Afterward, hemodynamic measurements, autonomic modulation, left ventricular function, cardiac fibrosis, superoxide (O2·−) generation, superoxide dismutase (SOD) activity, lipid peroxidation (TBARS) and arrhythmias were evaluated. Here, we show that dexamethasone increases blood pressure, associated with enhanced cardiac and vascular sympathetic modulation. Moreover, a marked increase in the cardiac O2·− generation was observed, whereas the enhanced SOD activity did not prevent the higher levels of lipid peroxidation in dexamethasone group. Although preserved ventricular contractility and β‐adrenergic responsiveness, we found that dexamethasone‐treated rats display greater interstitial and perivascular fibrosis than control. Besides that, despite the absence of arrhythmias at basal condition, we demonstrated by in vivo and ex vivo approaches that dexamethasone‐treated rats are more susceptible to develop harmful forms of ventricular arrhythmias, when challenged with pharmacological drugs or burst pacing‐induced arrhythmias. Notably, concomitant treatment with apocynin, an inhibitor of NADPH oxidase, prevented these ectopic ventricular events. Taken together, our data revealed that the dexamethasone treated rats were hypertensive and their hearts become arrthymogenic, in addition, our results uncover the pivotal role of ROS‐generating NADPH oxidases in the arrhythmias vulnerability.Support or Funding InformationFapitec/SE ; CAPES ; CNPq and Estácio UniversityThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.