Cardiac Metabolism in Diabetes Mellitus

Yoshimura, Michihiro; Anzawa, Ryuko; Mochizuki, Seibu

doi:10.2174/138161208786071263

Cited by 19 publications

(15 citation statements)

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“…The other chronic features of DM include progressive development of retinopathy, nephropathy with a risk of foot ulcers, and reproductive dysfunction (Liu et al 2013;Smolek et al 2013). People with DM are at increased risk of developing cardiovascular, peripheral vascular, and cerebrovascular diseases (Bell 2008;Yoshimura et al 2008). Unfortunately, this disease remains incurable and it only can be controlled with drugs depending on its type.…”

Section: Introductionmentioning

confidence: 99%

Moringa oleiferaleaf extract ameliorates alloxan-induced diabetes in rats by regeneration of β cells and reduction of pyruvate carboxylase expression

Latif

Bialy

Mahboub

et al. 2014

Biochem. Cell Biol.

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Moringa oleifera Lam. contains many active ingredients with nutritional and medicinal values. It is commonly used in folk medicine as an antidiabetic agent. The present study was designed to investigate how an aqueous extract from the leaves of M. oleifera reveals hypoglycemia in diabetic rats. M. oleifera leaf extract counteracted the alloxan-induced diabetic effects in rats as it normalized the elevated serum levels of glucose, triglycerides, cholesterol, and malondialdehyde, and normalized mRNA expression of the gluconeogenic enzyme pyruvate carboxylase in hepatic tissues. It also increased live body weight gain and normalized the reduced mRNA expression of fatty acid synthase in the liver of diabetic rats. Moreover, it restored the normal histological structure of the liver and pancreas damaged by alloxan in diabetic rats. This study revealed that the aqueous extract of M. oleifera leaves possesses potent hypoglycemic effects through the normalization of elevated hepatic pyruvate carboxylase enzyme and regeneration of damaged hepatocytes and pancreatic β cells via its antioxidant properties.

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Section: Introductionmentioning

confidence: 99%

Moringa oleiferaleaf extract ameliorates alloxan-induced diabetes in rats by regeneration of β cells and reduction of pyruvate carboxylase expression

Latif

Bialy

Mahboub

et al. 2014

Biochem. Cell Biol.

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“…Chronic exposure to excessive circulating nutrients, glucose and insulin (INS), promote INS resistance, and the underlying chronic conditions (i.e., obesity, diabetes, and hypertension) exacerbates CV risk. Attenuations of INS-mediated vascular relaxation and glucose transport in CV and skeletal muscle tissue in conditions of INS resistance are major contributing factors responsible for development of these comorbidities (1,31,48,70,76,80,109).Diet-induced obesity (DIO) also induces activation of systemic and tissue renin-angiotensin system (RAS) that results in chronic exposure of CV tissue to excess ANG II, a vasoconstrictive, progrowth/inflammatory hormone (25,36,50). ANG II promotes both INS resistance and CVD via ANG II-mediated activation of ANG II type 1 receptor (AT1R) (3,5,13,34,43,53,56,81,100,104).…”

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confidence: 99%

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confidence: 99%

Adaptive mechanisms to compensate for overnutrition-induced cardiovascular abnormalities

Pulakat

DeMarco

Ardhanari

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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In conditions of overnutrition, cardiac cells must cope with a multitude of extracellular signals generated by changes in nutrient load (glucose, amino acids, and lipids) and the hormonal milieu [increased insulin (INS), ANG II, and adverse cytokine/adipokine profile]. Herein, we review the diverse compensatory/adaptive mechanisms that counter the deleterious effects of excess nutrients and growth factors. We largely focus the discussion on evidence obtained from Zucker obese (ZO) and Zucker diabetic fatty (ZDF) rats, which are useful models to evaluate adaptive and maladaptive metabolic, structural, and functional cardiac remodeling. One adaptive mechanism present in the INS-resistant ZO, but absent in the diabetic ZDF heart, involves an interaction between the nutrient sensor kinase mammalian target of rapamycin complex 1 (mTORC1) and ANG II-type 2 receptor (AT2R). Recent evidence supports a cardioprotective role for the AT2R; for example, suppression of AT2R activation interferes with antihypertrophic/antifibrotic effects of AT1R blockade, and AT2R agonism improves cardiac structure and function. We propose a scenario, whereby mTORC1-signaling-mediated increase in AT2R expression in the INS-resistant ZO heart is a cardioprotective adaptation to overnutrition. In contrast to the ZO rat, heart tissues of ZDF rats do not show activation of mTORC1. We posit that such a lack of activation of the mTOR↔AT2R integrative pathway in cardiac tissue under conditions of obesity-induced diabetes may be a metabolic switch associated with INS deficiency and clinical diabetes.

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“…This leads to cardiac insulin resistance and the activation of mitogen activated protein kinases, which promote fibroblast proliferation while inducing cardiomyocyte fibrosis and apoptosis [31] . The serum level of aldosterone is increased in the prediabetic and diabetic condition and triggers LV hypertrophy, fibrosis and cardiac remodelling [32] . Both angiotensin Ⅱ and aldosterone cause increased production of ROS and the activation of NADPH oxidase, and they therefore increase cytosolic oxidative stress [33] .…”

Section: Impaired Calcium Homeostasis and Dysfunction Of Mitochondriamentioning

confidence: 99%

Is diabetic cardiomyopathy a specific entity?

Letonja

Petrovič

2014

WJC

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Diabetes mellitus (DM) is characterised by hyperglycemia, insulin resistance and metabolic dysregulation leading to diastolic and systolic dysfunction in diabetes. In this review, the pathogenetic and pathomorphological changes leading to diastolic and systolic dysfunction in diabetes are discussed. Changes in metabolic signalling pathways, mediators and effectors contribute to the pathogenesis of cardiac dysfunction in DM called diabetic cardiomyopathy (DC). Echocardiographic studies report on the association between DM and the presence of cardiac hypertrophy and myocardial stiffness that lead to diastolic dysfunction. More recently reported echocardiographic studies with more sensitive techniques, such as strain analysis, also observed systolic dysfunction as an early marker of DC. Depression of systolic and diastolic function is continuum and the line of separation is artificial. To conclude, according to current knowledge, DC is expected to be a common single phenotype that is caused by different pathogenetic and pathomorphological changes leading to diastolic and systolic dysfunction in diabetes.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Diabetes mellitus; Diabetic cardiomyopathy; Pathogenesis; Diastolic dysfunction; Systolic dysfunction; Morphological changes; Apoptosis Core tip: Changes in metabolic signalling pathways via several mediators contribute to the pathogenesis of cardiac dysfunction in diabetes called diabetic cardiomyopathy (DC). In this review, the pathogenetic and pathomorphological changes leading to diastolic and systolic dysfunction in diabetes are discussed. Echocardiographic studies report on the association between diabetes and the presence of cardiac hypertrophy and myocardial stiffness that lead to diastolic dysfunction. More recently reported echocardiographic studies with more sensitive techniques, such as strain analysis, also observed systolic dysfunction as an early marker of DC.Letonja M, Petrovič D. Is diabetic cardiomyopathy a specific entity? World J Cardiol 2014; 6(1): 8-13 Available from: URL:

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Cardiac Metabolism in Diabetes Mellitus

Cited by 19 publications

References 0 publications

Moringa oleiferaleaf extract ameliorates alloxan-induced diabetes in rats by regeneration of β cells and reduction of pyruvate carboxylase expression

Moringa oleiferaleaf extract ameliorates alloxan-induced diabetes in rats by regeneration of β cells and reduction of pyruvate carboxylase expression

Adaptive mechanisms to compensate for overnutrition-induced cardiovascular abnormalities

Is diabetic cardiomyopathy a specific entity?

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