Cardiac Glucose and Fatty Acid Oxidation in the Streptozotocin-Induced Diabetic Spontaneously Hypertensive Rat

Hypertension ◽  
1995 ◽  
Vol 25 (2) ◽  
pp. 235-241 ◽  
Author(s):  
Michael E. Christe ◽  
Robert L. Rodgers
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Spontaneously Hypertensive Rat ◽  
Acid Oxidation ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat

scholarly journals Longitudinal Evaluation of Fatty Acid Metabolism in Normal and Spontaneously Hypertensive Rat Hearts with Dynamic MicroSPECT Imaging

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Bryan W. Reutter ◽  
Ronald H. Huesman ◽  
Kathleen M. Brennan ◽  
Rostyslav Boutchko ◽  
Stephen M. Hanrahan ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Spontaneously Hypertensive Rat ◽  
Projection Data ◽  
Ct Scanner ◽  
Pinhole Spect ◽  
Time Activity ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat

The goal of this project is to develop radionuclide molecular imaging technologies using a clinical pinhole SPECT/CT scanner to quantify changes in cardiac metabolism using the spontaneously hypertensive rat (SHR) as a model of hypertensive-related pathophysiology. This paper quantitatively compares fatty acid metabolism in hearts of SHR and Wistar-Kyoto normal rats as a function of age and thereby tracks physiological changes associated with the onset and progression of heart failure in the SHR model. The fatty acid analog, 123I-labeled BMIPP, was used in longitudinal metabolic pinhole SPECT imaging studies performed every seven months for 21 months. The uniqueness of this project is the development of techniques for estimating the blood input function from projection data acquired by a slowly rotating camera that is imaging fast circulation and the quantification of the kinetics of 123I-BMIPP by fitting compartmental models to the blood and tissue time-activity curves.

Fatty acid oxidation and its impact on response of spontaneously hypertensive rat hearts to an adrenergic stress: benefits of a medium-chain fatty acid

2005 ◽  
Vol 288 (3) ◽  
pp. H1425-H1436 ◽  
Author(s):  
François Labarthe ◽  
Maya Khairallah ◽  
Bertrand Bouchard ◽  
William C. Stanley ◽  
Christine Des Rosiers
Keyword(s):  
Fatty Acid ◽  
Energy Production ◽  
Spontaneously Hypertensive Rat ◽  
Chain Fatty Acid ◽  
Acid Oxidation ◽  
Adrenergic Stimulation ◽  
Exogenous Fatty Acid ◽  
Spontaneously Hypertensive ◽  
Lactate Dehydrogenase Release ◽  
Rat Hearts

The spontaneously hypertensive rat (SHR) is a model of cardiomyopathy characterized by a restricted use of exogenous long-chain fatty acid (LCFA) for energy production. The aims of the present study were to document the functional and metabolic response of the SHR heart under conditions of increased energy demand and the effects of a medium-chain fatty acid (MCFA; octanoate) supplementation in this situation. Hearts were perfused ex vivo in a working mode with physiological concentrations of substrates and hormones and subjected to an adrenergic stimulation (epinephrine, 10 μM). 13C-labeled substrates were used to assess substrate selection for energy production. Compared with control Wistar rat hearts, SHR hearts showed an impaired response to the adrenergic stimulation as reflected by 1) a smaller increase in contractility and developed pressure, 2) a faster decline in the aortic flow, and 3) greater cardiac tissue damage (lactate dehydrogenase release: 1,577 ± 118 vs. 825 ± 44 mU/min, P < 0.01). At the metabolic level, SHR hearts presented 1) a reduced exogenous LCFA contribution to the citric acid cycle flux (16 ± 1 vs. 44 ± 4%, P < 0.001) and an enhanced contribution of endogenous substrates (20 ± 4 vs. 1 ± 4%, P < 0.01); and 2) an increased lactate production from glycolysis, with a greater lactate-to-pyruvate production ratio. Addition of 0.2 mM octanoate reduced lactate dehydrogenase release (1,145 ± 155 vs. 1,890 ± 89 mU/min, P < 0.001) and increased exogenous fatty acid contribution to energy metabolism (23.7 ± 1.3 vs. 15.8 ± 0.8%, P < 0.01), which was accompanied by an equivalent decrease in unlabeled endogenous substrate contribution, possibly triglycerides (11.6 ± 1.5 vs. 19.0 ± 1.2%, P < 0.01). Taken altogether, these results demonstrate that the SHR heart shows an impaired capacity to withstand an acute adrenergic stress, which can be improved by increasing the contribution of exogenous fatty acid oxidation to energy production by MCFA supplementation.

Abstract 485: Mito-Targeted Antioxidant Superior to Non-Targeted Isoform in Modulating Energy Metabolism and Preventing Cardiovascular Remodelling in Spontaneously Hypertensive Rat

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Sherin Saheera ◽  
Ajay Godwin Potnuri ◽  
Raunak R Nair
Keyword(s):  
Fatty Acid ◽  
Energy Metabolism ◽  
Spontaneously Hypertensive Rat ◽  
Heart Diseases ◽  
Left Ventricular ◽  
Metabolic Switch ◽  
Spontaneously Hypertensive ◽  
Beneficial Effects ◽  
Hypertensive Rat ◽  
2D Echocardiography

Hypertension induced left ventricular hypertrophy (LVH) augments the risk of cardiovascular anomalies. Oxidative stress leads to the activation of the hypertrophic program with a metabolic switch from fatty acid to glucose oxidation. Mitochondria, the major source of free radicals, exhibit alterations in hypertensive heart diseases. Targeted antioxidants are expected to reduce mitochondrial reactive oxygen species more effectively than general antioxidants. This study was designed to assess whether mito-targeted antioxidant, MitoTempol is more effective than general oxidant, Tempol on hypertension, hypertrophy and cardiac energy metabolism. Spontaneously Hypertensive Rat were administered either Tempol (20mg/kg/day) or Mito Tempol (2mg/kg/day) orally for 30 days. Post treatment, animals were subjected to 2D-echocardiography. The Myocardial lysates were subjected to Insolution digestion followed by RPLC - LTQ-Orbitrap-MS analysis. Mid-ventricular sections were probed for markers of energy metabolism and fibrosis. The beneficial effect on cardiovascular structure and function was significantly higher for Mito Tempol. Increase in mitochondrial antioxidants and stimulation of fatty acid metabolism with significant improvement in cardiovascular function was apparent in SHR treated with Mito Tempol. The study indicates that Mito Tempol is superior to its non- targeted isoform in preventing hypertension induced LVH, and the beneficial effects on heart are possibly mediated by reversal of metabolic remodelling.

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