Chronic Insulin Infusion Normalizes Blood Pressure and the Gene Expressions of Angiotensin II Type 1 Receptor in Fructose-Fed Rats

Fukui, Tetsuya; Hirano, Tsutomu; Shiraishi, Yuji; Nagashima, Masaharu; Adachi, Mitsuru

doi:10.1291/hypres.31.127

Cited by 6 publications

(4 citation statements)

References 30 publications

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“…Thus, the RAS is a reasonable target for prevention of fructose-induced cardiovascular pathologies. It was shown previously that FRD induces a cluster of abnormalities, including hypertension, hypertriglyceridemia, and glucose intolerance in addition to hyperinsulinemia [20], which is in agreement with our results. The ACE and AT 1 receptor upregulated by FRD in this study have been involved in the insulin resistance, also an early phenotype of metabolic syndrome.…”

supporting

confidence: 94%

“…It was previously demonstrated that FRD affects the expression of ACE in aortas and AT 1 receptor in hearts and aortas of male rats [9]. Other study also showed upregulation of AT 1 receptor mRNA and unchanged AT 2 receptor mRNA in aorta under the 60 % FRD [20]. Prolonged AT 1 receptor activation leads to myocyte hypertrophy, which becomes a major risk factor for congestive heart failure, sudden cardiac death, and overall mortality [21].…”

mentioning

confidence: 93%

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Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol

et al. 2014

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The renin-angiotensin system has been implicated in the development of metabolic syndrome and appears to be a key in the local tissue control of normal cardiac functions. Physiological concentrations of estrogens have been shown to be cardioprotective, especially against the damaging effects of fructose-rich diet. The aim of the study was to investigate the expression of the renin-angiotensin system molecules with potentially deleterious effect on the heart (angiotensin-converting enzyme and angiotensin II type 1 receptor) and those with potentially protective effects, (angiotensin-converting enzyme 2 and angiotensin II type 2 receptor), in ovariectomized fructose fed female rats with 17β-estradiol replacement. Real-time PCR and Western blot analysis were used for quantification of gene and protein expression in the heart. Fructose diet increased the expression of angiotensin-converting enzyme and angiotensin II type 1 receptor and decreased the expression of angiotensin-converting enzyme 2 and angiotensin II type 2 receptor. On the other hand, estradiol replacement seems to undo fructose diet effects on cardiac renin-angiotensin system. Downregulation of angiotensin-converting enzyme and angiotensin II type 1 receptor, and reversion of expression of both potentially protective molecules, angiotensin-converting enzyme 2 and angiotensin II type 2 receptor, to the control level in cardiac tissue took place. Obtained results suggest that estradiol may reverse the harmful effect of fructose-rich diet on the expression of renin-angiotensin system molecules. These findings may also be important in further research of phenotypes like insulin resistance, metabolic syndrome, and following cardiovascular pathology in females.

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confidence: 94%

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confidence: 93%

Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol

et al. 2014

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“…Experimental evidence suggests that in MetS, the RAS axis composed of ACE/AT1r is activated. A high-fructose diet can be used an experimental model to increase systolic blood pressure by activating the ACE/ AT1r axis [7,8]. Through AT1r, angiotensin-II can exert its pro-inflammatory effects.…”

Section: Introductionmentioning

confidence: 99%

Short-term administration of GW501516 improves inflammatory state in white adipose tissue and liver damage in high-fructose-fed mice through modulation of the renin-angiotensin system

et al. 2015

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High activation of the angiotensin-converting enzyme (ACE)/(angiotensin-II type 1 receptor) AT1r axis is closely linked to pro-inflammatory effects and liver damage. The aim of this study was to evaluate the effects of the short-term administration of GW501516 on pro-inflammatory markers in white adipose tissue (WAT) and hepatic stellate cells (HSCs), lipogenesis and insulin resistance in the liver upon high-fructose diet (HFru)-induced ACE/AT1r axis activation. Three-month-old male C57Bl/6 mice were fed a standard chow diet or a HFru for 8 weeks. Then, the animals were separated randomly into four groups and treated with GW501516 for 3 weeks. Morphological variables, systolic blood pressure, and plasma determinations were analyzed. In the WAT, the ACE/AT1r axis and pro-inflammatory cytokines were assessed, and in the liver, the ACE/AT1r axis, HSCs, fatty acid oxidation, insulin resistance, and AMPK activation were evaluated. The HFru group displayed a high activation of the ACE/AT1r axis in both the WAT and liver; consequently, we detected inflammation and liver damage. Although GW501516 abolished the increased activation of the ACE/AT1r axis in the WAT, no differences were found in the liver. GW501516 blunted the inflammatory state in the WAT and reduced HSC activation in the liver. In addition, GW501516 alleviates damage in the liver by increasing the expression of the genes that regulate beta-oxidation and decreasing the expression of the genes and proteins that are involved in lipogenesis and gluconeogenesis. We conclude that GW501516 may serve as a therapeutic option for the treatment of a highly activated ACE/AT1r axis in WAT and liver.

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“…Numerous studies have already shown that fructose rich diet increases AngII level in the plasma (Giani et al 2010;Zhou et al 2012;Tran et al 2014;Kobayashi et al 1993;Farah et al 2006;Fukui et al 2008;Tran et al 2009). It was shown in earlier studies that AngII induces nuclear sequestration of AT1 receptor from the plasma membrane, in brain neurons and vascular smooth muscle cells (Lu et al 1998;Bkaily et al 2003).…”

Section: R a F Tmentioning

confidence: 97%

Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue

Bundalo

Djordjević

Bursać

et al. 2017

Appl. Physiol. Nutr. Metab.

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The adipose tissue renin-angiotensin system (RAS) is proposed to be a pathophysiological link between adipose tissue dysregulation and metabolic disorders induced by a fructose-rich diet (FRD). RAS can act intracellularly. We hypothesized that adipocyte nuclear membranes possess angiotensin receptor types 1 and 2 (AT1R and AT2R), which couple to nuclear signaling pathways and regulate oxidative gene expression under FRD conditions. We analyzed the effect of consumption of 10% fructose solution for 9 weeks on biochemical parameters, adipocyte morphology, and expression of AT1R, AT2R, AT1R-associated protein (ATRAP), NADPH oxidase 4 (NOX4), matrix metalloproteinase-9 (MMP-9), and manganese superoxide dismutase (MnSOD) in adipose tissue of Wistar rats. We detected AT1R and AT2R in the nuclear fraction. FRD reduced the level of angiotensin receptors in the nucleus, while increased AT1R and decreased AT2R levels were observed in the plasma membrane. FRD increased the ATRAP mRNA level and decreased MnSOD mRNA and protein levels. No significant differences were observed for MMP-9 and NOX4 mRNA levels. These findings coincided with hyperleptinemia, elevated blood pressure and triglycerides, and unchanged visceral adipose tissue mass and morphology in FRD rats. Besides providing evidence for nuclear localization of angiotensin receptors in visceral adipose tissue, this study demonstrates the different effects of FRD on AT1R expression in different cellular compartments. Elevated blood pressure and decreased antioxidant capacity in visceral fat of fructose-fed rats were accompanied by an increased AT1R level in the plasma membrane, while upregulation of ATRAP and a decrease of nuclear membrane AT1R suggest an increased capacity for attenuation of excessive AT1R signaling and visceral adiposity.

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Chronic Insulin Infusion Normalizes Blood Pressure and the Gene Expressions of Angiotensin II Type 1 Receptor in Fructose-Fed Rats

Cited by 6 publications

References 30 publications

Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol

Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol

Short-term administration of GW501516 improves inflammatory state in white adipose tissue and liver damage in high-fructose-fed mice through modulation of the renin-angiotensin system

Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue

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