scholarly journals Defective Fatty Acid Uptake in the Spontaneously Hypertensive Rat Is a Primary Determinant of Altered Glucose Metabolism, Hyperinsulinemia, and Myocardial Hypertrophy

2001 ◽  
Vol 276 (26) ◽  
pp. 23661-23666 ◽  
Author(s):  
Tahar Hajri ◽  
Azeddine Ibrahimi ◽  
Chris T. Coburn ◽  
F. F. Knapp ◽  
Ted Kurtz ◽  
...  
1984 ◽  
Vol 102 (3) ◽  
pp. 381-386 ◽  
Author(s):  
R. Gross ◽  
P. Mialhe

ABSTRACT To elucidate the hypolipacidaemic effect of insulin in ducks, its action on the uptake of free fatty acids (FFA) by duck hepatocytes was determined. At low doses (10 mu./l) insulin stimulated FFA uptake. This effect was not observed with higher doses of insulin (20, 30 and 50 mu./l). Growth hormone at physiological concentrations and corticosterone (14·4 nmol/l) decreased basal activity, probably by reducing glucose metabolism and consequently α-glycerophosphate (α-GP) supply. Insulin was able to reverse the inhibition induced by GH and corticosterone on both FFA uptake and α-GP production. These results therefore suggest that the hypolipacidaemic effect of insulin may be partly mediated by its action on hepatic FFA uptake. J. Endocr. (1984) 102, 381–386


Placenta ◽  
1998 ◽  
Vol 19 (5-6) ◽  
pp. 403-408 ◽  
Author(s):  
R.M. Lewis ◽  
N.S. Bassett ◽  
B.M. Johnston ◽  
S.J.M. Skinner

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Bryan W. Reutter ◽  
Ronald H. Huesman ◽  
Kathleen M. Brennan ◽  
Rostyslav Boutchko ◽  
Stephen M. Hanrahan ◽  
...  

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.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 150-OR
Author(s):  
ANNE-MARIE CARREAU ◽  
CHRISTOPHE NOLL ◽  
BRIGITTE GUERIN ◽  
LAURENT BIERTHO ◽  
ERIC E. TURCOTTE ◽  
...  

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Sherin Saheera ◽  
Ajay Godwin Potnuri ◽  
Raunak R Nair

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.


2003 ◽  
Vol 278 (46) ◽  
pp. 45209-45215 ◽  
Author(s):  
Michal Pravenec ◽  
Ludmila Kazdová ◽  
Vladimír Landa ◽  
Václav Zídek ◽  
Petr Mlejnek ◽  
...  

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