Effect of valsartan, an angiotensin II receptor blocker, on markers of oxidation and glycation in Japanese type 2 diabetic subjects: Blood pressure-independent effect of valsartan

Saisho, Yoshifumi; Komiya, Naoko; Hara, Hiroshi

doi:10.1016/j.diabres.2006.04.015

Cited by 43 publications

(24 citation statements)

References 12 publications

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“…In addition, Ang II infusion increased RAGE expression in retinas via ROS generation [43] (RAS → AGE-RAGE). Consistent with these findings, treatment with low-dose valsartan, an AT1R antagonist, decreased serum AGE levels in association with reduced oxidative stress generation in type-2 diabetic patients [44] (RAS → AGE-RAGE). Therefore, ramipril could inhibit the AGE-RAGE system by suppression the RAS (Figure 3).…”

Section: Discussionmentioning

confidence: 64%

Ramipril inhibits AGE-RAGE-induced matrix metalloproteinase-2 activation in experimental diabetic nephropathy

Fukami

Yamagishi

Coughlan

et al. 2014

Diabetol Metab Syndr

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BackgroundAdvanced glycation end products (AGE)-receptor for AGE (RAGE) axis and renin-angiotensin system (RAS) play a role in diabetic nephropathy (DN). Matrix metalloproteinase-2 (MMP-2) activation also contributes to DN. However, the pathological interaction among AGE-RAGE, RAS and MMP-2 in DN remains unknown. We examined here the involvement of AGE and RAS in MMP-2 activation in streptozotocin (STZ)-induced diabetic rats and in AGE-exposed rat renal proximal tubular cells (RPTCs).MethodsExperimental diabetes was induced in 6-week-old male Sprague–Dawley (SD) rats by intravenous injection of STZ. Diabetic rats received ramipril (3 mg/kg body weight/day) or vehicle for 32 weeks. AGE-modified rat serum albumin (AGE-RSA) or RSA was intraperitoneally administrated to 6-week-old male SD rats for 16 weeks. RPTCs were stimulated with 100 μg/ml AGE-modified bovine serum albumin (AGE-BSA) or BSA in the presence or absence of 10-7 M ramiprilat, an inhibitor of angiotensin-converting enzyme or 100 nM BAY11-7082, an IκB-α phosphorylation inhibitor.ResultsAGE and RAGE expression levels and MMP-2 activity in the tubules of diabetic rats was significantly increased in association with increased albuminuria, all of which were blocked by ramipril. AGE infusion induced tubular MMP-2 activation and RAGE gene expression in SD rats. Ramiprilat or BAY11-7082 inhibited the AGE-induced MMP-2 activation or reactive oxygen species generation in RPTCs. Angiotensin II increased MMP-2 gene expression in RPTCs, which was blocked by BAY11-7082.ConclusionsOur present study suggests the involvement of AGE-RAGE-induced, RAS-mediated MMP-2 activation in experimental DN. Blockade of AGE-RAGE axis by ramipril may protect against DN partly via suppression of MMP-2.

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Section: Discussionmentioning

confidence: 64%

Ramipril inhibits AGE-RAGE-induced matrix metalloproteinase-2 activation in experimental diabetic nephropathy

Fukami

Yamagishi

Coughlan

et al. 2014

Diabetol Metab Syndr

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“…Among the angiotensin II receptor blockers, olmesartan (43) and valsartan (44,45) decrease AGE concentrations, whereas irbesartan does not (46,47). Despite losartan’s known effect on AGE concentrations in an animal model (48), in the current study, losartan treatment did not affect the relationship between AGE/OP concentrations and RFL or renal structural lesions, suggesting the absence of a class effect.…”

Section: Discussionmentioning

confidence: 99%

Advanced Glycation End Products Predict Loss of Renal Function and Correlate With Lesions of Diabetic Kidney Disease in American Indians With Type 2 Diabetes

et al. 2016

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We examined associations of advanced glycation end products (AGEs) with renal function loss (RFL) and its structural determinants in American Indians with type 2 diabetes. Data were from a 6-year clinical trial that assessed renoprotective efficacy of losartan. Participants remained under observation after the trial concluded. Glomerular filtration rate (GFR) was measured annually. Kidney biopsies were performed at the end of the trial. Five AGEs were measured in serum collected at enrollment and at kidney biopsy. RFL was defined as ≥40% decline of measured GFR from baseline. Of 168 participants (mean baseline age 41 years, HbA1c 9.2%, GFR 164 mL/min, and albumin-to-creatinine ratio 31 mg/g), 104 reached the RFL end point during median follow-up of 8.0 years. After multivariable adjustment, each doubling of carboxyethyl lysine (hazard ratio [HR] 1.60 [95% CI 1.08–2.37]) or methylglyoxal hydroimidazolone (HR 1.30 [95% CI 1.02–1.65]) concentration was associated with RFL. Carboxyethyl lysine, carboxymethyl lysine, and methylglyoxal hydroimidazolone correlated positively with cortical interstitial fractional volume (partial r = 0.23, P = 0.03; partial r = 0.25, P = 0.02; and partial r = 0.31, P = 0.003, respectively). Glyoxyl hydroimidazolone and methylglyoxal hydroimidazolone correlated negatively with total filtration surface per glomerulus (partial r = −0.26, P = 0.01; and partial r = −0.21, P = 0.046, respectively). AGEs improve prediction of RFL and its major structural correlates.

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“…It has been shown that multifactorial intervention for coronary risk factors effectively reduces the incidence of CVD and all-cause mortality [129]. Antihypertensives and statins have also been reported to reduce oxidative stress [130,131,132,133]. Thus, to improve CVD outcomes and mortality in patients with diabetes, a multifactorial approach appropriately managing each coronary risk factor is necessary.…”

Section: Discussionmentioning

confidence: 99%

Glycemic Variability and Oxidative Stress: A Link between Diabetes and Cardiovascular Disease?

Saisho

2014

IJMS

Self Cite

159

134

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Diabetes is associated with a two to three-fold increase in risk of cardiovascular disease. However, intensive glucose-lowering therapy aiming at reducing HbA1c to a near-normal level failed to suppress cardiovascular events in recent randomized controlled trials. HbA1c reflects average glucose level rather than glycemic variability. In in vivo and in vitro studies, glycemic variability has been shown to be associated with greater reactive oxygen species production and vascular damage, compared to chronic hyperglycemia. These findings suggest that management of glycemic variability may reduce cardiovascular disease in patients with diabetes; however, clinical studies have shown conflicting results. This review summarizes the current knowledge on glycemic variability and oxidative stress, and discusses the clinical implications.

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Effect of valsartan, an angiotensin II receptor blocker, on markers of oxidation and glycation in Japanese type 2 diabetic subjects: Blood pressure-independent effect of valsartan

Cited by 43 publications

References 12 publications

Ramipril inhibits AGE-RAGE-induced matrix metalloproteinase-2 activation in experimental diabetic nephropathy

Ramipril inhibits AGE-RAGE-induced matrix metalloproteinase-2 activation in experimental diabetic nephropathy

Advanced Glycation End Products Predict Loss of Renal Function and Correlate With Lesions of Diabetic Kidney Disease in American Indians With Type 2 Diabetes

Glycemic Variability and Oxidative Stress: A Link between Diabetes and Cardiovascular Disease?

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