Female Mice are not Protected from Elevation in Blood Pressure due to High Fructose Consumption

Abstract

High salt and high fructose (HSHF) diet can cause hypertension as well as comorbidities related to metabolic syndrome. Sex differences resulting from high salt and high fructose diets have been reported. Previously, we reported that female mice, like age‐matched male mice, do not demonstrate increased blood pressure upon a 30‐day period of high salt consumption (Rouch A., et al FASEB J. 1135.1, 2014). We also found no sex differences in blood pressure in mice under normal dietary conditions (Waturuocha C., et al FASEB J. 855.2, 2017). Interestingly, under HSHF consumption, male and female mice showed elevated blood pressure and the increase occurred faster in females (Fan L., et al FASEB J. 30, 731.6, 2016). Moreover, RT‐qPCR analysis under HSHF condition showed higher expression of key sodium transporters in females. Our purpose of this study was to determine if sex differences occur in mice under a high fructose diet. Four‐week old intact male and female CD‐1 mice were purchased from Envigo, Inc. (Indianapolis, IN). Mice (n= 6/group) were placed in metabolic cages and consumed standard chow (0.25% salt) and water for 5 days, followed by 30 days of the standard chow and a drinking solution of 20% fructose. Mice then consumed the standard chow and water for a recovery period of 8 days. Daily measurements included body weight, sodium intake and excretion. Mean arterial pressure (MAP, mmHg) was measured 5 days per week via the tail‐cuff technique (Kent Scientific, CODA System). Separate mice on the same dietary protocol were maintained in bins and used for RT‐qPCR expression of renal sodium transporters. These mice (n= 4/group) were euthanized and sacrificed at the end of the first, third, fifth and sixth week. Kidneys were removed and renal cortical tissue samples were processed for total RNA, first‐strand cDNA synthesis and RT‐qPCR. Results showed that baseline MAP in females was not different compared to males (83.4 ± 4.6 and 84 ± 3.2, respectively). During high fructose consumption, average MAP exceeded baseline values in both females and males (90 ± 2.3 and 94 ± 1.3, respectively, p< 0.05). Males had significantly higher MAP than females in week three (94 ± 3.2 and 83 ± 3.3 respectively, p< 0.04). However, there was no significant difference in MAP in all other weeks. During the recovery phase, MAP returned to values not different from baseline in females and males (87 ± 5.1 and 88 ± 3.9 respectively). All mice reduced their food intake upon drinking fructose solution. The average sodium intake, normalized to body weight, was not different between the sexes. There were no measured sex differences regarding renal sodium handling, i.e., sodium excretion or retention. While molecular expression analysis of renal transporters is ongoing, based on the results indicating essentially no sex differences in blood pressure or in renal sodium handling, we conclude that female mice are not protected from high fructose‐induced blood pressure. Future studies of a longer duration (3 – 6 months) should be conducted to investigate further the possible sex differences under high fructose consumption.Support or Funding InformationOSU‐CHSThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.