High Fructose‐Induced Hypertension and Renal Damage Are Exaggerated in Dahl Salt‐Sensitive Rats via Renal Renin‐Angiotensin System Activation

Xu, Li; Hu, Gaizun; Qiu, Jiahe; Fan, Yuxuan; Ma, Yixuan; Miura, Tetsuji; Kohzuki, Masahiro; Itoh, Osamu

doi:10.1161/jaha.120.016543

Cited by 10 publications

(14 citation statements)

References 45 publications

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“…However, this group received fructose until the end of the experimental period; therefore, the alterations of the transporters may be due to the direct effect of fructose in addition to the effect of maternal fructose intake. Similar results were observed in rats treated with fructose by Xu et al (2017) and Ares et al (2019) and may be linked to changes in the renal expression of RAS components ( Xu et al, 2017 ; Ares et al, 2019 ; Xu et al, 2021 ). In the FW group, the expression of all sodium transporters, including NKCC2, increased.…”

Section: Discussionsupporting

confidence: 81%

Effects of maternal fructose intake on the offspring’s kidneys

et al. 2022

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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.

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Section: Discussionsupporting

confidence: 81%

Effects of maternal fructose intake on the offspring’s kidneys

et al. 2022

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“…In addition, Ex with treadmill for 8 wk attenuated the high salt-induced glomerular sclerosis in DS rats, although it did not affect blood pressure ( 20 , 22 ). An antihypertensive treatment with hydralazine, which lowered blood pressure to the control levels, did not ameliorate renal dysfunction and damage in the HFr-fed DS rats ( 18 ). These results suggest that the renal protective effects of Ex are not mediated through its antihypertensive effects in DS rats.…”

Section: Discussionmentioning

confidence: 95%

“…On the last day of the experiments, all rats were housed in an individual metabolic cage, and urine samples were collected on ice for 24 h. Urinary albumin and creatinine were measured (Oriental Yeast Co., Ltd., Nagahama, Japan). The urinary liver type-fatty acid binding protein (L-FABP) ( 27 ), a biomarker of proximal tubular stress and tubulointerstitial disorder and has a correlation with urine albumin excretion in diabetic kidney disease and CKD patients, was also measured as previously described ( 18 ). It can help predict the progression of diabetic kidney disease on renal damage at very early stage.…”

Section: Methodsmentioning

confidence: 99%

“…Moreover, using a genetic model of hypertension and kidney disease, Dahl salt-sensitive (DS) rats exhibited further exaggeration in the HFr-induced hypertension and renal damage than Sprague-Dawley rats. We recently reported that HFr elevates blood pressure in DS rats, but not in Dahl salt-resistant (DR) rats, and HFr-induced urinary albumin excretion, glomerular injury, and renal interstitial fibrosis are exaggerated in DS rats ( 18 ). HFr also increases the renal expression of AGT, renin, ACE, and AT1R.…”

mentioning

confidence: 99%

“…HFr also increases the renal expression of AGT, renin, ACE, and AT1R. RAS inhibitors attenuate the HFr-induced hypertension and renal damage in DS rats ( 18 ).…”

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confidence: 99%

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Exercise Training Prevents High Fructose-Induced Hypertension and Renal Damages in Male Dahl Salt-Sensitive Rats

Qiu

et al. 2022

Medicine &Amp; Science in Sports &Amp; Exercise

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IntroductionHigh-fructose diet (HFr) causes metabolic syndrome, and HFr-induced hypertension and renal damage are exaggerated in Dahl salt-sensitive (DS) rats. Exercise training (Ex) has antihypertensive and renal protective effects in rats fed HFr; however, there has been little discussion about the DS rats, which exhibit metabolic disturbances. This study thus examined the effects of Ex on DS rats fed HFr.MethodsMale DS rats were divided into three groups. The control group was fed a control diet, and both the HFr group and the HFr–Ex group were fed an HFr (60% fructose). The HFr–Ex group also underwent treadmill running (20 m·min−1, 60 min·d−1, 5 d·wk−1). After 12 wk, renal function, histology, and renin–angiotensin system were examined.ResultsHFr increased blood pressure, urinary albumin, and creatinine clearance, and Ex inhibited these increases. HFr induced glomerular sclerosis, podocyte injury, afferent arteriole thickening, and renal interstitial fibrosis, and Ex ameliorated them. HFr reduced plasma renin activity, and Ex further reduced the activity. HFr also increased the expression of angiotensinogen, renin, angiotensin-converting enzyme (ACE), and angiotensin II type 1 receptor, and Ex restored the ACE expression to the control levels. HFr decreased the expression of ACE2, angiotensin II type 2 receptor, and Mas receptor, and Ex restored the ACE2 and Mas receptor expressions to the control levels and further decreased the angiotensin II type 2 receptor expression. HFr increased the ACE activity and decreased the ACE2 activity, and Ex restored these activities to the control levels.ConclusionsEx prevents HFr-induced hypertension and renal damages in DS rats. The changes in renal renin–angiotensin system may be involved in the mechanism of the antihypertensive and renal protective effects of Ex.

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Sweetened Beverage Intake and Incident Chronic Kidney Disease in the UK Biobank Study

Heo,

Koh,

Park

et al. 2024

JAMA Netw Open

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ImportanceAn increasing body of evidence indicates an association between consuming sugar or its alternatives and cardiometabolic diseases. However, the effects of the consumption of sugar-sweetened beverages, artificially sweetened beverages, and natural juices on kidney health remain unclear.ObjectiveTo investigate the association of the intake of sugar-sweetened beverages, artificially sweetened beverages, and natural juices with the risk of chronic kidney disease (CKD), and the effect of substituting these beverage types for one another on this association.Design, Setting, and ParticipantsThis prospective, population-based cohort study analyzed data from the UK Biobank. Participants without a history of CKD who completed at least 1 dietary questionnaire were included. The follow-up period was from the date of the last dietary questionnaire until October 31, 2022, in England; July 31, 2021, in Scotland; and February 28, 2018, in Wales. Data were analyzed from May 1 to August 1, 2023.ExposuresConsumption of sugar-sweetened beverages, artificially sweetened beverages, and natural juices.Main Outcomes and MeasuresThe primary outcome was incident CKD. Multivariable Cox proportional hazards models were used to estimate the associations between the 3 beverage types and incident CKD. A substitution analysis was used to evaluate the effect on the associations of substituting one beverage type for another.ResultsA total of 127 830 participants (mean [SD] age, 55.2 [8.0] years; 66 180 female [51.8%]) were included in the primary analysis. During a median (IQR) follow-up of 10.5 (10.4-11.2) years, 4459 (3.5%) cases of incident CKD occurred. The consumption of more than 1 serving per day of sugar-sweetened beverages was associated with higher risk of incident CKD (adjusted hazard ratio [AHR], 1.19 [95% CI, 1.05-1.34]) compared with not consuming sugar-sweetened beverages. The AHR for participants consuming more than 0 to 1 serving per day of artificially sweetened beverages was 1.10 (95% CI, 1.01-1.20) and for consuming more than 1 serving per day was 1.26 (95% CI, 1.12-1.43) compared with consuming no artificially sweetened beverages. By contrast, there was no significant association between natural juice intake and incident CKD (eg, for &gt;1 serving per day: HR, 0.99 [95% CI, 0.87-1.11]; P = .10). Substituting sugar-sweetened beverages with artificially sweetened beverages did not show any significant difference in the risk of CKD (HR, 1.03 [95% CI, 0.96-1.10]). Conversely, replacing 1 serving per day of sugar-sweetened beverage with natural juice (HR, 0.93 [95% CI, 0.87-0.97]) or water (HR, 0.93 [95% CI, 0.88-0.99]) or replacing 1 serving per day of artificially sweetened beverage with natural juice (HR, 0.90 [95% CI, 0.84-0.96]) or water (HR, 0.91 [95% CI, 0.86-0.96]) was associated with a reduced risk of incident CKD.Conclusions and RelevanceFindings from this cohort study suggest that lower consumption of sugar-sweetened beverages or artificially sweetened beverages may reduce the risk of developing CKD.

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High Fructose‐Induced Hypertension and Renal Damage Are Exaggerated in Dahl Salt‐Sensitive Rats via Renal Renin‐Angiotensin System Activation

Cited by 10 publications

References 45 publications

Effects of maternal fructose intake on the offspring’s kidneys

Effects of maternal fructose intake on the offspring’s kidneys

Exercise Training Prevents High Fructose-Induced Hypertension and Renal Damages in Male Dahl Salt-Sensitive Rats

Sweetened Beverage Intake and Incident Chronic Kidney Disease in the UK Biobank Study

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