Renin inhibition improves metabolic syndrome, and reduces angiotensin II levels and oxidative stress in visceral fat tissues in fructose-fed rats

Chou, Chu Lin; Lin, Heng; Chen, Jin Shuen; Fang, Te-Chao

doi:10.1371/journal.pone.0180712

Cited by 30 publications

(23 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the present study, we evaluated renal function and the role of the kidney RAS in animals submitted to high fructose intake from weaning to adulthood by using in vivo and ex vivo methods in this model. Our results showed that high fructose intake determined metabolic and cardiovascular changes, which were consistent with those observed in others studies ( Farah et al, 2006 , 2007 ; Araujo et al, 2016 ; Chou et al, 2017 ; Xu et al, 2017 ).…”

Section: Discussionsupporting

confidence: 93%

“…However, an increase was observed in their visceral fat. These data are consistent with those of other studies using this model in rodents ( Farah et al, 2007 ; De Angelis et al, 2012 ; Chou et al, 2017 ; Xu et al, 2017 ). High fructose diet also induced glucose intolerance and high fasting blood glucose.…”

Section: Discussionsupporting

confidence: 93%

“…Metabolic syndrome (MS) is a disease of modern civilization, being strongly correlated with lifestyle (diet and physical activity), and increase has been linked to the intake of high-fructose corn syrup associate a cluster of common pathologies ( Zimmet et al, 2001 ; Ferder et al, 2010 ; De Angelis et al, 2012 ; Chou et al, 2017 ). High consumption of fructose, a sugar widely used in the western world, is associated with pathological changes, including MS, obesity, glucose intolerance, type II diabetes, fatty liver and other liver diseases, hypertension, and cardiovascular diseases, in both experimental and clinical studies ( Elliott et al, 2002 ; Malik et al, 2010a ; Morris et al, 2012 ; Madani et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

“…Studies have confirmed the influence of fructose-rich diet introduced in the early weeks after birth to adulthood ( Patel et al, 2009 ). Recently, we have observed that early exposure to high fructose intake caused metabolic changes, such as hyperglycemia, insulin resistance, and dyslipidemia, associated with hypertension and cardiovascular disautonomia when provided to rats from weaning to adulthood ( Araujo et al, 2016 ; Chou et al, 2017 ). These modifications are examples of how metabolic programming can modify the outcome of diseases related to metabolic failure in adult life.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Intra-Renal Angiotensin Levels Are Increased in High-Fructose Fed Rats in the Extracorporeal Renal Perfusion Model

et al. 2018

View full text Add to dashboard Cite

Overconsumption of fructose leads to metabolic syndrome as a result of hypertension, insulin resistance, and hyperlipidemia. In this study, the renal function of animals submitted to high fructose intake was analyzed from weaning to adulthood using in vivo and ex vivo methods, being compared with a normal control group. We investigated in ex vivo model of the role of the renin Angiotensin system (RAS) in the kidney. The use of perfused kidney from animals submitted to 8-week fructose treatment showed that high fructose intake caused metabolic and cardiovascular alterations that were consistent with other studies. Moreover, the isolated perfused kidneys obtained from rats under high fructose diet showed a 33% increase in renal perfusion pressure throughout the experimental period due to increased renal vascular resistance and a progressive fall in the glomerular filtration rate, which reached a maximum of 64% decrease. Analysis of RAS peptides in the high fructose group showed a threefold increase in the renal concentrations of angiotensin I (Ang I) and a twofold increase in angiotensin II (Ang II) levels, whereas no change in angiotensin 1-7 (Ang 1-7) was observed when compared with the control animals. We did not detect changes in angiotensin converting enzyme (ACE) activity in renal tissues, but there is a tendency to decrease. These observations suggest that there are alternative ways of producing Ang II in this model. Chymase the enzyme responsible for Ang II formation direct from Ang I was increased in renal tissues in the fructose group, confirming the alternative pathway for the formation of this peptide. Neprilysin (NEP) the Ang 1-7 forming showed a significant decrease in activity in the fructose vs. control group, and a tendency of reduction in ACE2 activity. Thus, these results suggest that the Ang 1-7 vasodilator peptide formation is impaired in this model contributing with the increase of blood pressure. In summary, rats fed high fructose affect renal RAS, which may contribute to several deleterious effects of fructose on the kidneys and consequently an increase in blood pressure.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Intra-Renal Angiotensin Levels Are Increased in High-Fructose Fed Rats in the Extracorporeal Renal Perfusion Model

et al. 2018

View full text Add to dashboard Cite

show abstract

“…The disturbances in the normal redox status of cells cause an increment in reactive oxygen species (ROS) [ 14 ]. Interestingly, MS development in rats fed with fructose [ 15 ] or a high-calorie diet (HCD) [ 16 ] produces an increment in ROS. Therefore, OS could be the link between MS and cognitive disorders [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Metabolic Syndrome Exacerbates the Recognition Memory Impairment and Oxidative‐Inflammatory Response in Rats with an Intrahippocampal Injection of Amyloid Beta 1–42

Díaz

Escobedo

Treviño

et al. 2018

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

An important worldwide health problem as the result of current lifestyle is metabolic syndrome (MS). It has been shown that MS induced by a high-calorie diet (HCD) in rats produces cognitive deterioration in the novel object recognition test (NORt) and decreases synaptic connections and dendritic order in the hippocampus and temporal cortex. However, it is unknown whether MS induced by an HCD participates in the cognitive process observed with the injection of Aβ1–42 into the hippocampus of rats as a model of Alzheimer disease (AD). The induction of MS in rats produces a deterioration in NORt; however, rats with MS injected with Aβ1–42 show a major deterioration in the cognitive process. This event could be explained by the increment in the oxidative stress in both cases studied (MS and Aβ1–42): together, the hippocampus and temporal cortex produce an enhancer effect. In the same way, we observed an increment in interleukin-1β, TNF-α, and GFAP, indicative of exacerbated inflammatory processes by the combination of MS and Aβ1–42. We can conclude that MS might play a key role in the apparition and development of cognitive disorders, including AD. We propose that metabolic theory is important to explain the apparition of cognitive diseases.

show abstract

Depot-Biased ROS: A Middleman in Adipose-Driven Cardiovascular Disease

Bakkar,

Osman,

Alzaim

et al. 2024

Oxidative Stress in Applied Basic Research and Clinical Practice

View full text Add to dashboard Cite

Renin inhibition improves metabolic syndrome, and reduces angiotensin II levels and oxidative stress in visceral fat tissues in fructose-fed rats

Cited by 30 publications

References 53 publications

Intra-Renal Angiotensin Levels Are Increased in High-Fructose Fed Rats in the Extracorporeal Renal Perfusion Model

Intra-Renal Angiotensin Levels Are Increased in High-Fructose Fed Rats in the Extracorporeal Renal Perfusion Model

Metabolic Syndrome Exacerbates the Recognition Memory Impairment and Oxidative‐Inflammatory Response in Rats with an Intrahippocampal Injection of Amyloid Beta 1–42

Depot-Biased ROS: A Middleman in Adipose-Driven Cardiovascular Disease

Contact Info

Product

Resources

About