Metabolic abnormalities of the heart in type II diabetes

Amaral, Nelson; Okonko, Darlington O.

doi:10.1177/1479164115580936

Cited by 40 publications

(39 citation statements)

References 116 publications

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“…Apart from the coexistence of myocardial ischaemia and hypertension, the excessive myocardial free fatty acid uptake and metabolism in diabetes cause lower left ventricular function, increase mitochondrial reactive oxygen stress, and exert lipotoxic effects in myocardial cells. 33,34 In addition, excessive deposition of advanced glycation end products initiates inflammatory signalling and propagates apoptosis, fibrotic remodelling and immune cell infiltration, 35 and also constitutes a driving factor for cardiomyocyte stiffness and myocardial collagen deposition. 36 Accompanying autonomic dysfunction and subsequent activation of the neuro-hormonal compensatory systems led to the progressive loss of cardiac myocytes and a downward spiral of cardiac failure.…”

Section: Discussionmentioning

confidence: 99%

Risk of heart failure in a population with type 2 diabetes versus a population without diabetes with and without coronary heart disease

Chen

Ho²,

2018

Diabetes Obesity Metabolism

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Diabetes mellitus may increase the risk of HF in both men and women, as well as in all age groups, especially in young people. People with type 2 diabetes without CHD had a similarly increased risk of HF to that of control subjects with CHD. Certain coronary revascularization procedures and CHDs, including percutaneous transluminal coronary angiography, coronary artery bypass surgery and acute myocardial infarction, were found to greatly increase risk of HF in people with type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Risk of heart failure in a population with type 2 diabetes versus a population without diabetes with and without coronary heart disease

Chen

Ho²,

2018

Diabetes Obesity Metabolism

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“…The myocardial contractile dysfunction has been attributed to the detrimental effects of prolonged hyperglycemia on cardiomyocytes. These include enhanced dependence on fatty acid metabolism, reduced myofilament Ca ++ sensitivity, mitochondrial dysfunction, oxidative stress, and apoptosis/necrosis [4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 98%

Cardiomyocyte–fibroblast interaction contributes to diabetic cardiomyopathy in mice: Role of HMGB1/TLR4/IL-33 axis

Tao

Song

Lan

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Diabetic cardiomyopathy (DiCM) is characterized by myocardial fibrosis and dysfunction. In rodent models of diabetes myocardial HMGB1 increases while IL-33 decreases. The major cardiac cell type expressing HMGB1 is the myocyte while the primary IL-33 expressing cell is the fibroblast. The aim of this study was to delineate the extracellular communication pathway(s) between cardiomyocytes and fibroblasts that contributes to murine DiCM. The streptozotocin (STZ)-induced murine model of diabetes and a cardiomyocyte/fibroblast co-culture challenged with high glucose were used. In STZ mice, myocardial HMGB1 expression was increased while IL-33 expression decreased (immunofluorescence and Western blot). In addition, STZ mice had an increased myocardial collagen deposition and myocardial dysfunction (pressure-volume loop analysis). An HMGB1 inhibitor (A-box) or exogenous IL-33 prevented the myocardial collagen deposition and dysfunction. In the cardiomyocyte/fibroblast co-culture model, HG increased cardiomyocyte HMGB1 secretion, decreased fibroblast IL-33 expression, and increased fibroblast collagen I production. Further, using A-box and HMGB1 shRNA transfected myocytes, we found that cardiomyocyte-derived HMGB1 dramatically potentiated the HG-induced down-regulation of IL-33 and the increase in collagen I expression in the fibroblasts. The potentiating effects of the cardiomyocytes was diminished when toll-like receptor 4 deficient (TLR4(-/-)) fibroblasts were co-cultured with wild-type myocytes. Finally, TLR4(-/-) mice with diabetes had increased myocardial expression of HMGB1, but failed to down-regulate IL-33. The diabetes-induced myocardial collagen deposition and cardiac dysfunction were significantly attenuated in TLR4(-/-) mice. In conclusion, our findings support a role for "cardiomyocyte HMGB1-fibroblast TLR4/IL-33 axis" in the development of myocardial fibrosis and dysfunction in a murine model of diabetes.

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“…HF is a common complication in patients with T2D, and the prognosis of patients with both T2D and HF is poor, with a median survival time of approximately 4 years . T2D is associated with cardiac remodeling that can lead to diabetic cardiomyopathy, characterized by myocardial structural and functional abnormalities in the absence of coronary artery disease, hypertension, congenital heart disease or valvular disease . T2D‐related metabolic abnormalities, including hyperglycaemia, lipotoxicity and hyperinsulinaemia, can lead to restrictive diabetic cardiomyopathy, also known as HF with preserved left ventricular ejection fraction …”

Section: Mechanisms Of CV and Renal Protection With Sglt‐2 Inhibitorsmentioning

confidence: 99%

Effects of sodium‐glucose cotransporter‐2 inhibitors on the cardiovascular and renal complications of type 2 diabetes

Chilton

2019

Diabetes Obesity Metabolism

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Sodium‐glucose cotransporter‐2 inhibitors (SGLT‐2is) have been shown to mitigate the risks of cardiovascular (CV) and renal complications in patients with type 2 diabetes (T2D) and CV risk factors or CV disease (CVD). In CV outcomes trials (CVOTs) of patients with T2D and established CVD or multiple CV risk factors, empagliflozin and canagliflozin were associated with significant reductions in the risks of major adverse CV events (MACE), hospitalization for heart failure (HF) and kidney disease progression. In the DECLARE–TIMI 58 study, in which the majority of patients did not have established CVD, dapagliflozin was associated with significant reductions in the composite end point of CV death or hospitalization for HF and was noninferior to placebo with regard to MACE; although patients had relatively good renal function, dapagliflozin also showed renal benefits similar to those seen with empagliflozin and canagliflozin. This article reviews the increased risk of CVD and renal disease in patients with T2D and discusses the potential mechanisms of the cardioprotective and renoprotective effects of SGLT‐2i therapy. The observed improvements in CV and renal outcomes with SGLT‐2is in CVOTs suggest a class effect in this patient population and have influenced treatment guidelines for the way add‐on therapy to metformin is initiated in patients with T2D and high CV risk. The overall cardioprotective and renoprotective effects of SGLT‐2is in patients with T2D and high CV risk are most likely attributable to multiple mechanisms, including cardiac, haemodynamic, metabolic, anti‐inflammatory and renal effects.

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Metabolic abnormalities of the heart in type II diabetes

Cited by 40 publications

References 116 publications

Risk of heart failure in a population with type 2 diabetes versus a population without diabetes with and without coronary heart disease

Risk of heart failure in a population with type 2 diabetes versus a population without diabetes with and without coronary heart disease

Cardiomyocyte–fibroblast interaction contributes to diabetic cardiomyopathy in mice: Role of HMGB1/TLR4/IL-33 axis

Effects of sodium‐glucose cotransporter‐2 inhibitors on the cardiovascular and renal complications of type 2 diabetes

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