Substitution of Casein Dietary Protein with Wheat Gluten Protein Protects Dahl Salt Sensitive Rats from the Development of Maternal Syndrome

Abstract

Previously our group demonstrated that the maternal diet of the Dahl Salt‐Sensitive (SS) rat, specifically the protein source, during gestation and lactation can impact the severity of salt sensitive hypertension and renal damage of the offspring in adulthood. Offspring born from mothers fed a wheat gluten‐based diet exhibited blunted salt‐sensitive hypertension and renal damage when compared to offspring born from casein fed mothers. Utilizing an embryo transfer approach we determined that regardless of whether an embryo originated from parents fed a casein or a wheat gluten‐based diet, the diet of the surrogate mother that determined the severity of salt‐sensitivity in the offspring. In addition to the maternal diet, the in utero environment has been shown to contribute to the programming of lifelong health of offspring. Dahl SS rats maintained on a casein‐based diet (SSC) develop maternal syndrome (hypertension and proteinuria) compared to virgin controls. Since offspring from mothers fed a wheat gluten based diet were protected from SS hypertension and the Dahl SSC rat develops maternal syndrome, we tested the hypothesis that mothers fed a wheat gluten (SSWG) diet will be protected from the development of maternal syndrome. To test this hypothesis Dahl SSWG and SSC rats were studied on their respective diets, which are identical in every aspect except for the protein source. At 8 weeks of age, females were instrumented with radio‐telemeters for continuous measurement of mean arterial pressure (MAP). After a recovery period, baseline MAP was measured as well as an overnight urine collection for markers of renal damage before females were mated with males of the same age and diet. Virgin littermate controls of the same age and diet for each strain were run in parallel. During the baseline period, there was no difference observed in MAP or protein excretion rate among any of the groups. As previously reported, the SSC mated rats develop an increase in MAP (141±3 vs 129±3 mmHg, p<0.05) and protein excretion rate (98±16 vs 46±5 mg/day, p<0.05) at gestational day 20 (GD) compared to virgin controls. Interestingly, there was a significant reduction in MAP in the SSWG mated rats compared to SSWG virgin controls at GD20 (114±4 vs 126±4 mmHg, respectively, p<0.05). Comparing the SSC and SSWG mated rats at GD20, it is evident that the SSWG mated rats are protected from developing maternal syndrome seen in the SSC mated rats (MAP: 114±4 vs 141±3 mmHg, p<0.001, Proteinuria: 52±12 vs 98±16 mg/day, p<0.01). Additionally, uterine artery resistance index, which is utilized as a surrogate marker for placental perfusion, is significantly greater in the SSC rats compared to the SSWG at GD20 (0.9±0.02 vs 0.5±0.04, p<0.01, n=2/group). While the SSWG rat are protected from the development of maternal syndrome compared to the SSC, the exact mechanisms for this protection is unknown. This study demonstrates how environmental factors such as diet can play a protective role in the development of maternal syndrome with associated effects on the health of the offspring.Support or Funding InformationHL116264, 18POST33990140, 15SFRN2391002This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.