Abstract 241: Influence of Dietary Salt and Renin-angiotensin System activity on plasma Retinol-binding Protein 4 in Healthy Human Subjects

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Qaiser Shafiq ◽  
Jonathan S Williams

Introduction: Retinol-binding protein 4 (RBP-4) is a circulating adipokine associated with insulin resistance, obesity and cardiovascular risk. Previous evidence suggests a negative impact on insulin sensitivity via an interaction with the insulin-stimulated glucose transporter (GLUT-4), specifically in adipocytes. Since angiotensin-2 (ANG-2) impairs GLUT-4 presentation and insulin sensitivity, we hypothesized that renin-angiotensin system (RAS) activity might affect RBP-4 expression as well. Furthermore, both RAS activity and insulin sensitivity are affected by dietary salt, but the relationship between these factors and RBP-4 expression is unknown. We hypothesized that liberal salt diet, via suppression of RAS activity, would be associated with reduced RBP-4 levels compared to salt restriction. METHODS: Healthy subjects (7 men, 7 women, mean age 24 yr, BMI 22.6) were studied on low salt (LS 10 mmol Na/day) diet and then liberal salt (HS 200 mmol Na/day) diet for 1 week each. Samples were drawn after overnight rest in the supine position for plasma renin activity (PRA), serum Aldosterone (Aldo) and plasma RBP-4 and again after ANG-2 infusion (3ng/kg/min x 45 mins). Results: Salt manipulation predictably modified RAS activity (HS v. LS Aldo, 4.5 ± 3.8 v. 19.5 ± 8.5 ng/dl [p<0.01]; HS v. LS PRA, 0.5 ± 0.4 v. 2.7 ± 1.4 ng/ml/hr [p<0.01]). RBP-4 was significantly lower on a HS compared to LS diet (35.4 ± 6.6 v. 38.6 ± 7.9 mg/L, p= 0.017). No significant change was observed in RBP-4 level after ANG-2 infusion on either diet. Fasting insulin levels trended lower on HS compared to LS (3.9 ± 6.8 v. 4.4 ± 1.2 μIU/ml, p=0.09), but there was no difference in fasting glucose (81.9 ± 6.8 v. 82.1 ± 4.7 mg/dl, p=0.92). Conclusion: RBP-4 levels are modified by dietary salt intake. RBP-4 levels were lower under HS conditions (suppressed RAS) as compared to LS conditions. Acute administration of ANG-2 does not increase RBP-4 levels in this healthy population. Insulin response was similar to prior reports suggesting that the connection between RAS activity, dietary salt and insulin sensitivity may include RBP-4. Future work exploring the relationship between RBP-4, GLUT-4 and insulin sensitivity should take into consideration the effect of dietary salt intake.

Hypertension ◽  
2012 ◽  
Vol 60 (1) ◽  
pp. 98-105 ◽  
Author(s):  
Chris Tikellis ◽  
Raelene J. Pickering ◽  
Despina Tsorotes ◽  
Olivier Huet ◽  
Jaye Chin-Dusting ◽  
...  

2007 ◽  
Vol 10 (10A) ◽  
pp. 1151-1155 ◽  
Author(s):  
Julian Segura ◽  
Luis M Ruilope

AbstractAbdominal obesity is a risk factor for cardiovascular disease worldwide, and it is becoming a dramatic issue for national health systems. Overweight and obesity are highly associated with multiple comorbidities, elevated blood pressure values, dyslipidaemia, reduced insulin sensitivity and alterations of large and minor vessels.Activation of the renin–angiotensin system (RAS) in adipose tissue may represent an important link between obesity and hypertension. Angiotensin II has been shown to play a role in adipocyte growth and differentiation. Adipocytes also secrete adiponectin, enhancing insulin sensitivity and preventing atherosclerosis. Blockade of the RAS with either an angiotensin-converting enzyme inhibitor or an angiotensin II receptor blocker results in a substantial increase in adiponectin levels and improved insulin sensitivity. Obesity-related hypertension needs a comprehensive approach to treatment including both weight loss and pharmacological therapies. Antihypertensive drugs prescription should be based on guidelines recommendations for management of hypertension, taking into account the growing evidences about the relationship between some antihypertensive drugs and the development of new-onset diabetes.This review discusses the role of RAS in the relationship between obesity, essential hypertension and insulin resistance.


1997 ◽  
Vol 29 (Supplement) ◽  
pp. 19
Author(s):  
D. R. Dengel ◽  
R. V. Hogikyan ◽  
M. D. Brown ◽  
S. G. Glickman ◽  
M. A. Supiano

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4534
Author(s):  
Darwish Mohd Mohd Isa ◽  
Suzana Shahar ◽  
Feng J. He ◽  
Hazreen Abdul Majid

Health literacy has been recognized as a significant social determinant of health, defined as the ability to access, understand, appraise, and apply health-related information across healthcare, disease prevention, and health promotion. This systematic review aims to understand the relationship between health literacy, blood pressure, and dietary salt intake. A web-based search of PubMed, Web of Science, CINAHL, ProQuest, Scopus, Cochrane Library, and Prospero was performed using specified search/MESH terms and keywords. Two reviewers independently performed the data extraction and analysis, cross-checked, reviewed, and resolved any discrepancies by the third reviewer. Twenty out of twenty-two studies met the inclusion criteria and were rated as good quality papers and used in the final analysis. Higher health literacy had shown to have better blood pressure or hypertension knowledge. However, the relationship between health literacy with dietary salt intake has shown mixed and inconsistent findings. Studies looking into the main four domains of health literacy are still limited. More research exploring the links between health literacy, blood pressure, and dietary salt intake in the community is warranted. Using appropriate and consistent health literacy tools to evaluate the effectiveness of salt reduction as health promotion programs is required.


2013 ◽  
Vol 126 (2) ◽  
pp. 147-154 ◽  
Author(s):  
Renata Libianto ◽  
George Jerums ◽  
Que Lam ◽  
Angela Chen ◽  
Sara Baqar ◽  
...  

Although low dietary salt intake has beneficial effects on BP (blood pressure), low 24hUNa (24 h urinary sodium excretion), the most accurate estimate of dietary salt intake, is associated with increased mortality in people with diabetes. In the non-diabetic population, low salt intake is associated with increased RAAS (renin–angiotensin–aldosterone system) activity. In this cross-sectional study, we examined the relationship between 24hUNa, PRA (plasma renin activity), serum aldosterone and BNP (brain natriuretic peptide) in patients with diabetes. Clinical characteristics, 24hUNa, PRA, serum aldosterone and BNP were recorded in 222 consecutive patients (77% with Type 2 diabetes) attending a diabetes clinic at a tertiary hospital. The relationship between 24hUNa, serum aldosterone, PRA, BNP, urinary potassium excretion, serum potassium, serum sodium, eGFR (estimated glomerular filtration rate), urinary albumin excretion and HbA1c (glycated haemoglobin) was examined by a multivariable regression model. Levels of 24hUNa significantly predicted serum aldosterone in a linear fashion (R2=0.20, P=0.002). In the subgroup of patients (n=46) not taking RAAS-modifying agents, this relationship was also observed (R2=0.10, P=0.03), and the effect of 24hUNa on serum aldosterone was found to be more pronounced than in the whole cohort (coefficient=−0.0014, compared with −0.0008). There was no demonstrable relationship between 24hUNa and PRA or BNP. Low 24hUNa is associated with increased serum aldosterone in people with diabetes, in the presence and absence of RAAS-modifying agents. This raises the possibility that stimulation of the RAAS may be a mechanism that contributes to adverse outcomes observed in patients with low 24hUNa.


2004 ◽  
Vol 286 (2) ◽  
pp. F267-F277 ◽  
Author(s):  
Hiroyuki Suzuki ◽  
Tatsuo Yamamoto ◽  
Naoki Ikegaya ◽  
Akira Hishida

Dietary salt intake modulates the renin-angiotensin system (RAS); however, little is known about the effect of salt intake on the progression of glomerulonephritis. We investigated the glomerular expression of TGF-β1 type I (TβRI) and II (TβRII) TGF-β receptors and RAS components in rats with antithymocyte serum (ATS) nephritis on normal (NSI)-, low (LSI)-, and high-salt intake (HSI) and on HSI rats receiving candesartan cilexetil (CC) and LSI rats receiving PD-123319. Glomerular lesions were less severe in rats on LSI and aggravated in those on HSI compared with those on NSI. Intrarenal renin and glomerular ANG II levels were significantly higher in LSI and lower in HSI rats. In ATS nephritis, HSI increased glomerular TβRI, TβRII, and ANG II type 1 receptor (AT1R), and decreased glomerular ANG II type 2 receptor (AT2R), whereas LSI decreased glomerular TGF-β1 and TβRI and increased glomerular AT2R. CC ameliorated glomerular lesions, reduced glomerular TGF-β1 and TβRII, and increased glomerular AT2R. PD-123319 aggravated glomerular lesions and increased glomerular TGF-β1 and TβRII. Our results suggest that dietary salt intake influences progression of ATS nephritis by modulating glomerular TGF-β1 and TβR expression resulting, at least in part, from altered glomerular AT1R and AT2R expression.


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