Impact of the renin–angiotensin system on cardiac energy metabolism in heart failure

Mori, Jun; Zhang, Liyan; Oudit, Gavin Y.; Lopaschuk, Gary D.

doi:10.1016/j.yjmcc.2013.07.010

Cited by 52 publications

(34 citation statements)

References 129 publications

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“…Meanwhile, the presence of AT1R and AT2R localized to mitochondria has been reported, which indicates the direct effect of RAS on the mitochondria [33]. Dysfunctional mitochondria, in turn, produce excessive amounts of ROS such as superoxide (O 2 À ), hydrogen peroxide (H 2 O 2 ), and peroxynitrite (OONO À ).…”

Section: Discussionmentioning

confidence: 99%

Rcan1-1L overexpression induces mitochondrial autophagy and improves cell survival in angiotensin II-exposed cardiomyocytes

Duan

Yan

et al. 2015

Experimental Cell Research

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Section: Discussionmentioning

confidence: 99%

Rcan1-1L overexpression induces mitochondrial autophagy and improves cell survival in angiotensin II-exposed cardiomyocytes

Duan

Yan

et al. 2015

Experimental Cell Research

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“…Although a considerable number of studies on myocardial metabolism and energetics during cardiovascular diseases are known [18], there remains much to be learned. In addition, over the last several years, a series of studies have been published which have highlighted the power of metabolic profiling to expand our understanding of metabolic disorder in the cardiovascular diseases [26]. Cardiovascular diseases are often accompanied by significant perturbations in cardiac energy metabolism, which can decrease cardiac energy supply and cardiac efficiency [33].…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y damages the integrity of mitochondrial structure and disrupts energy metabolism in cultured neonatal rat cardiomyocytes

Luo

Guo

et al. 2015

Peptides

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“…10 The increased uptake of dietary fatty acids by the heart of AT2R-KO mice on control diet could be due to an increased activation of AT1R and may thus contribute to the deleterious effect of cardiac AT1R activation observed by others. 38 In conclusion, we have shown that adipocyte remodeling occurs before the onset of insulin resistance in the HFHF-STZ mouse model and that AT2R-KO abolishes this early hypertrophic adipocyte remodeling without change in total adiposity. Further studies are needed to determine the molecular mechanisms by which AT2R affects these adaptations to diabetogenic conditions and whether the AT2R could be a relevant target for the prevention of type 2 diabetes.…”

Section: Discussionmentioning

confidence: 57%

Postprandial fatty acid uptake and adipocyte remodeling in angiotensin type 2 receptor-deficient mice fed a high-fat/high-fructose diet

et al. 2015

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The role of the angiotensin type-2 receptor in adipose physiology remains controversial. The aim of the present study was to demonstrate whether genetic angiotensin type-2 receptor-deficiency prevents or worsens metabolic and adipose tissue morphometric changes observed following a 6-week high-fat/high-fructose diet with injection of a small dose of streptozotocin. We compared tissue uptake of nonesterified fatty acid and dietary fatty acid in wild-type and angiotensin type-2 receptor-deficient mice by using the radiotracer 14(R,S)-[ 18 F]-fluoro-6-thia-heptadecanoic acid in mice fed a standard or high-fat diet. Postprandial fatty acid uptake in the heart, liver, skeletal muscle, kidney and adipose tissue was increased in wild-type mice after a high-fat diet and in angiotensin type-2 receptor-deficient mice on both standard and high-fat diets. Compared to the wild-type mice, angiotensin type-2 receptor-deficient mice had a lower body weight, an increase in fasting blood glucose and a decrease in plasma insulin and leptin levels. Mice fed a high-fat diet exhibited increased adipocyte size that was prevented by angiotensin type-2 receptor-deficiency. Angiotensin type-2 receptor-deficiency abolished the early hypertrophic adipocyte remodeling induced by a high-fat diet. The small size of adipocytes in the angiotensin type-2 receptor-deficient mice reflects their inability to store lipids and explains the increase in fatty acid uptake in nonadipose tissues. In conclusion, a genetic deletion of the angiotensin type-2 receptor is associated with metabolic dysfunction of white adipose depots, and indicates that adipocyte remodeling occurs before the onset of insulin resistance in the high-fat fed mouse model.

show abstract

Impact of the renin–angiotensin system on cardiac energy metabolism in heart failure

Cited by 52 publications

References 129 publications

Rcan1-1L overexpression induces mitochondrial autophagy and improves cell survival in angiotensin II-exposed cardiomyocytes

Rcan1-1L overexpression induces mitochondrial autophagy and improves cell survival in angiotensin II-exposed cardiomyocytes

Neuropeptide Y damages the integrity of mitochondrial structure and disrupts energy metabolism in cultured neonatal rat cardiomyocytes

Postprandial fatty acid uptake and adipocyte remodeling in angiotensin type 2 receptor-deficient mice fed a high-fat/high-fructose diet

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