Recombinant Glucagon-Like Peptide-1 Increases Myocardial Glucose Uptake and Improves Left Ventricular Performance in Conscious Dogs With Pacing-Induced Dilated Cardiomyopathy

Nikolaidis, Lazaros A.; Elahi, Dariush; Hentosz, Teresa; Doverspike, Aaron; Huerbin, Rhonda; Zourelias, Lee; Stolarski, Carol; Shen, You‐Tang; Shannon, Richard P.

doi:10.1161/01.cir.0000139339.85840.dd

Cited by 462 publications

(355 citation statements)

References 32 publications

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“…Each data point represents the mean ± SEM for 8-10 experiments; statistical analysis performed using two-way repeated measures ANOVA (P = NS). both GLP-1(7-36)amide and GLP-1(9-36)amide significantly improved left ventricular function [9]. Similarly, Sonne et al demonstrated that both exendin-4 (1-39) and GLP-1(9-36)amide were able to augment left ventricular performance in a rat heart ischaemia-reperfusion model [28].…”

Section: Discussionmentioning

confidence: 95%

“…Recent studies report wide-ranging cardiovascular actions of GLP-1 such as modulation of heart rate, blood pressure and cardiac structure and function [3][4][5][6][7][8]. Furthermore, GLP-1 has been shown to improve cardiovascular function in experimental heart failure [9,10] and in both diabetic and non-diabetic heart failure patients [11,12]. Chronic GLP-1 treatment has also been found to improve cardiovascular risk factors, such as HDL cholesterol, triglycerides and diastolic blood pressure, in patients with type 2 diabetes [13].…”

Section: T R a C Tmentioning

confidence: 99%

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GLP-1 and related peptides cause concentration-dependent relaxation of rat aorta through a pathway involving KATP and cAMP

Green

Hand

Dougan

et al. 2008

Archives of Biochemistry and Biophysics

136

132

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a b s t r a c tIncreasing evidence from both clinical and experimental studies indicates that the insulin-releasing hormone, glucagon-like peptide-1 (GLP-1) may exert additional protective/reparative effects on the cardiovascular system. The aim of this study was to examine vasorelaxant effects of GLP-1(7-36)amide, three structurally-related peptides and a non-peptide GLP-1 agonist in rat aorta. Interestingly, all GLP-1 compounds, including the established GLP-1 receptor antagonist, exendin (9-39) caused concentrationdependent relaxation. Mechanistic studies employing hyperpolarising concentrations of potassium or glybenclamide revealed that these relaxant effects are mediated via specific activation of ATP-sensitive potassium channels. Further experiments using a specific membrane-permeable cyclic AMP (cAMP) antagonist, and demonstration of increased cAMP production in response to GLP-1 illustrated the critical importance of this pathway. These data significantly extend previous observations suggesting that GLP-1 may modulate vascular function, and indicate that this effect may be mediated by the GLP-1 receptor. However, further studies are required in order to establish whether GLP-1 related agents may confer additional cardiovascular benefits to diabetic patients.

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Section: Discussionmentioning

confidence: 95%

Section: T R a C Tmentioning

confidence: 99%

GLP-1 and related peptides cause concentration-dependent relaxation of rat aorta through a pathway involving KATP and cAMP

Green

Hand

Dougan

et al. 2008

Archives of Biochemistry and Biophysics

136

132

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“…Nikolaidis et al 17 infused GLP-1 over 48 hours in escalating doses (1.5 to 20 pmol/kg/min) in a group of conscious control dogs to determine hemodynamic effects of GLP-1 on normal hearts (measured for 48 hours after infusion was complete). There was no effect on LV systolic pressure, LV end-diastolic pressure (LVEDP), LV dP/dt, heart rate or mean arterial pressure.…”

Section: Experimental Studies Of Glp-1 In Non-ischemic Dilated Cardiomentioning

confidence: 99%

Glucagon‐like Peptide‐1 and Myocardial Protection: More than Glycemic Control

Fields

Patterson

Karnik

et al. 2009

Clinical Cardiology

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Pharmacologic intervention for the failing heart has traditionally targeted neurohormonal activation and ventricular remodeling associated with cardiac dysfunction. Despite the multitude of agents available for the treatment of heart failure, it remains a highly prevalent clinical syndrome with substantial morbidity and mortality, necessitating alternative strategies of targeted management. One such area of interest is the ability to modulate myocardial glucose uptake and its impact on cardioprotection. Glucose‐insulin‐potassium (GIK) infusions have been studied for decades, with conflicting results regarding benefit in acute myocardial infarction. Based on the same concepts, glucagon‐like peptide‐1‐[7–36] amide (GLP‐1) has recently been demonstrated to be a more effective alternative in left ventricular (LV) systolic dysfunction. This paper provides a review on the current evidence supporting the use of GLP‐1 in both animal models and humans with ischemic and nonischemic cardiomyopathy. Copyright © 2009 Wiley Periodicals, Inc.

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“…Although chronic HF is a multifactorial disease, altered energy metabolism has been suggested as one of the most important causes of HF [3]. In fact, several studies have shown that interventions for cardiac metabolic change improve cardiac function and prevent the progression of cardiac dysfunction [67][68][69]. Elucidation of the mechanisms by which RNF207 plays a role in energy metabolism in HF may uncover new therapeutic strategies for HF.…”

Section: Discussionmentioning

confidence: 99%

The novel heart-specific RING finger protein 207 is involved in energy metabolism in cardiomyocytes

Mizushima

Takahashi

Watanabe

et al. 2016

Journal of Molecular and Cellular Cardiology

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A failing heart shows severe energy insufficiency, and it is presumed that this energy shortage plays a critical role in the development of cardiac dysfunction. However, little is known about the mechanisms that cause energy metabolic alterations in the failing heart. Here, we show that the novel RING-finger protein 207 (RNF207), which is specifically expressed in the heart, plays a role in cardiac energy metabolism. Depletion of RNF207 in neonatal rat cardiomyocytes (NRCs) leads to a reduced cellular concentration of adenosine triphosphate (ATP) and mitochondrial dysfunction.Consistent with this result, we observed here that the expression of RNF207 was significantly reduced in mice with common cardiac diseases including heart failure.Intriguingly, proteomic approaches revealed that RNF207 interacts with the voltage-dependent anion channel (VDAC), which is considered to be a key regulator of mitochondria function, as an RNF207-interacting protein. Our findings indicate that RNF207 is involved in ATP production by cardiomyocytes, suggesting that RNF207 plays an important role in the development of heart failure.3 Highlights l RNF207 is specifically expressed in the heart. l RNF207 enhances activity of the tricarboxylic acid cycle in cardiomyocytes.l RNF207 directly interacts with VDAC1 through its coiled-coil domain.l Heart failure significantly reduces the expression of RNF207 in mice.4

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Recombinant Glucagon-Like Peptide-1 Increases Myocardial Glucose Uptake and Improves Left Ventricular Performance in Conscious Dogs With Pacing-Induced Dilated Cardiomyopathy

Cited by 462 publications

References 32 publications

GLP-1 and related peptides cause concentration-dependent relaxation of rat aorta through a pathway involving KATP and cAMP

GLP-1 and related peptides cause concentration-dependent relaxation of rat aorta through a pathway involving KATP and cAMP

Glucagon‐like Peptide‐1 and Myocardial Protection: More than Glycemic Control

The novel heart-specific RING finger protein 207 is involved in energy metabolism in cardiomyocytes

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