Taking Diabetes to Heart—Deregulation of Myocardial Lipid Metabolism in Diabetic Cardiomyopathy

Bayeva, Marina; Sawicki, Konrad Teodor; Ardehali, Hossein

doi:10.1161/jaha.113.000433

Cited by 127 publications

(99 citation statements)

References 251 publications

(235 reference statements)

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“…A highly significant decrease in HR, LVDP and +dp/dt was recorded in both groups signifying that isolated hearts from diabetic rats exhibited a certain degree of DCM. Our results are in agreement with the work of other researchers who reported similar findings in diabetic rats [24,25]. Indeed, alterations of diastolic and systolic function are widely reported in uncomplicated diabetic subjects and often predict the development of other chronic diabetic complications [26].…”

Section: Discussionsupporting

confidence: 94%

Effect of Diabetes Mellitus and Its Control on Myocardial Contractile Function in Rats

Alsawy

El-Damarawi

2014

Open Access Maced J Med Sci

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Competing Interests: The authors have declared that no competing interests exist. Abstract AIM:This work was done to study the effect of both types of diabetes mellitus (DM) on myocardial contractility in rats. Also, we investigated the role of treatment of DM with insulin and rosiglitazone (used as treatment for type 1 and type 2 DM respectively) in improvement of myocardial dysfunction in diabetic rats. METHODS:The study included 50 male Wistar albino rats, divided into 5 groups: control (group I), streptozotocin induced type 1 DM (group II), fructose induced type 2 DM (group III), insulin treated type 1 diabetic rats (group IV) and rosiglitazone treated type 2 diabetic rats (group V). At the end of the study, retro-orbital blood samples were withdrawn and blood glucose, plasma triglyceride (TG), total cholesterol (TC) and thyroid hormones levels were measured. Rats were then anesthetized and their hearts were excised and connected to Langendorff apparatus to perform mechanical cardiac performance tests including heart rate (HR), left ventricular developed pressure (LVDP) and maximum rate of pressure rise (+dp/dt). RESULTS:Data of the study showed that relative to control group, there was significant increase in blood glucose, plasma TG and TC levels while, thyroid hormones and myocardial performance parameters showed significant decrease in both type 1 and type 2 diabetic rats. Treatment of type 1 diabetic rats with insulin and type 2 with rosiglitazone resulted in significant decrease in blood glucose, plasma TG and TC levels associated with significant improvement in thyroid hormones and myocardial performance parameters. The results also showed that insulin treatment of type 1 was more effective in ameliorating all parameters than treatment of type 2 by rosiglitazone. CONCLUSION:We concluded that the induction of both types of diabetes resulted in decreased myocardial performance parameters. The treatment of type 1 and type 2 diabetes by insulin and oral rosiglitazone respectively improved to a great extent the altered metabolism and mechanical myocardial parameters, with more improving effect of insulin in type 1 than rosiglitazone in type 2 DM.

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Section: Discussionsupporting

confidence: 94%

Effect of Diabetes Mellitus and Its Control on Myocardial Contractile Function in Rats

Alsawy

El-Damarawi

2014

Open Access Maced J Med Sci

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“…It is known that glucose utilization as a source of energy by the cardiomyocyte is impaired in diabetes (23) and that the diabetic heart depends almost completely on fatty acid oxidation for ATP (24,25). This lack of energy flexibility is considered to be one of the factors that lead to diabetic cardiomyopathy (26,27). ApoA-I may thus provide a favorable shift in the balance of energy use toward increased glucose metabolism.…”

Section: Discussionmentioning

confidence: 99%

Dual Actions of Apolipoprotein A-I on Glucose-Stimulated Insulin Secretion and Insulin-Independent Peripheral Tissue Glucose Uptake Lead to Increased Heart and Skeletal Muscle Glucose Disposal

et al. 2016

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Apolipoprotein A-I (apoA-I) of HDL is central to the transport of cholesterol in circulation. ApoA-I also provides glucose control with described in vitro effects of apoA-I on β-cell insulin secretion and muscle glucose uptake. In addition, apoA-I injections in insulin-resistant diet-induced obese (DIO) mice lead to increased glucose-stimulated insulin secretion (GSIS) and peripheral tissue glucose uptake. However, the relative contribution of apoA-I as an enhancer of GSIS in vivo and as a direct stimulator of insulin-independent glucose uptake is not known. Here, DIO mice with instant and transient blockade of insulin secretion were used in glucose tolerance tests and in positron emission tomography analyses. Data demonstrate that apoA-I to an equal extent enhances GSIS and acts as peripheral tissue activator of insulin-independent glucose uptake and verify skeletal muscle as an apoA-I target tissue. Intriguingly, our analyses also identify the heart as an important target tissue for the apoA-I–stimulated glucose uptake, with potential implications in diabetic cardiomyopathy. Explorations of apoA-I as a novel antidiabetic drug should extend to treatments of diabetic cardiomyopathy and other cardiovascular diseases in patients with diabetes.

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“…Although HF could develop secondary to increased susceptibility to atherosclerosis, dyslipidemia, hypertension, and the prothrombotic state, 121 epidemiological studies have shown increased development of cardiomyopathy even in the absence of underlying coronary artery disease or hypertension. This susceptibility to impaired LV function in diabetic patients has been termed diabetic cardiomyopathy.…”

Section: Diabetic Cardiomyopathy and Chronic Inflammationmentioning

confidence: 99%

Chronic Heart Failure and Inflammation

Dick

Epelman

2016

Circulation Research

499

380

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As a greater proportion of patients survive their initial cardiac insult, medical systems worldwide are being faced with an ever-growing need to understand the mechanisms behind the pathogenesis of chronic heart failure (HF). There is a wealth of information about the role of inflammatory cells and pathways during acute injury and the reparative processes that are subsequently activated. We discuss the different causes that lead to chronic HF development and how the sum of initial inflammatory and reparative responses only sets the trajectory for disease progression. Unfortunately, comparatively little is known about the contribution of the immune system once the trajectory has been set, and chronic HF has been established—which clinically represents the majority of patients. It is known that chronic HF is associated with circulating inflammatory cytokines that can predict clinical outcomes, yet the causative role inflammation plays in disease progression is not well defined, and the majority of clinical trials that target aspects of inflammation in patients with chronic HF have largely been negative. This review will present what is currently known about inflammation in chronic HF in both humans and animal models as a means to highlight the gap in our knowledge base that requires further examination.

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Taking Diabetes to Heart—Deregulation of Myocardial Lipid Metabolism in Diabetic Cardiomyopathy

Cited by 127 publications

References 251 publications

Effect of Diabetes Mellitus and Its Control on Myocardial Contractile Function in Rats

Effect of Diabetes Mellitus and Its Control on Myocardial Contractile Function in Rats

Dual Actions of Apolipoprotein A-I on Glucose-Stimulated Insulin Secretion and Insulin-Independent Peripheral Tissue Glucose Uptake Lead to Increased Heart and Skeletal Muscle Glucose Disposal

Chronic Heart Failure and Inflammation

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