Hypoxic hearts overexpressing activated PKC epsilon (aPKCe) have decreased cardiac function on exposure to fatty acid perfusate

2008 ◽  
Vol 44 (4) ◽  
pp. 761
Author(s):  
J. McCarthy ◽  
A. Lochner ◽  
S. Genade ◽  
P. Ping ◽  
M.F. Essop ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Cardiac Function ◽  
Pkc Epsilon

Caloric restriction limits fatty acid oxidation and improves cardiac function in heart failure associated with obesity

2018 ◽  
Vol 124 ◽  
pp. 99
Author(s):  
Qutuba G. Karwi ◽  
Liyan Zhang ◽  
Abhishek Gupta ◽  
Arata Fukushima ◽  
Vaibhav Patel ◽  
...  
Keyword(s):  
Heart Failure ◽  
Fatty Acid ◽  
Cardiac Function ◽  
Caloric Restriction ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation

scholarly journals Exercise training improves cardiac function in infarcted rabbits: involvement of autophagic function and fatty acid utilization

2010 ◽  
Vol 12 (4) ◽  
pp. 323-330 ◽  
Author(s):  
Ching-Yi Chen ◽  
Hsiu-Ching Hsu ◽  
Bai-Chin Lee ◽  
Hung-Ju Lin ◽  
Ying-Hsien Chen ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Cardiac Function ◽  
Fatty Acid Utilization

scholarly journals Dietary Calanus oil recovers metabolic flexibility and rescues postischemic cardiac function in obese female mice

2019 ◽  
Vol 317 (2) ◽  
pp. H290-H299 ◽  
Author(s):  
Kirsten M. Jansen ◽  
Sonia Moreno ◽  
Pablo M. Garcia-Roves ◽  
Terje S. Larsen
Keyword(s):  
Fatty Acid ◽  
Cardiac Function ◽  
Glucose Oxidation ◽  
Myocardial Metabolism ◽  
Dietary Supplementation ◽  
Left Ventricular ◽  
Lv Function ◽  
Marine Oil ◽  
Normal Chow ◽  
Postischemic Recovery

The aim of this study was to find out whether dietary supplementation with Calanus oil (a novel marine oil) or infusion of exenatide (an incretin mimetic) could counteract obesity-induced alterations in myocardial metabolism and improve postischemic recovery of left ventricular (LV) function. Female C57bl/6J mice received high-fat diet (HFD, 45% energy from fat) for 12 wk followed by 8-wk feeding with nonsupplemented HFD, HFD supplemented with 2% Calanus oil, or HFD plus exenatide infusion (10 µg·kg−1·day−1). A lean control group was included, receiving normal chow throughout the whole period. Fatty acid and glucose oxidation was measured in ex vivo perfused hearts during baseline conditions, while LV function was assessed with an intraventricular fluid-filled balloon before and after 20 min of global ischemia. HFD-fed mice receiving Calanus oil or exenatide showed less intra-abdominal fat deposition than mice receiving nonsupplemented HFD. Both treatments prevented the HFD-induced decline in myocardial glucose oxidation. Somewhat surprising, recovery of LV function was apparently better in hearts from mice fed nonsupplemented HFD relative to hearts from mice fed normal chow. More importantly however, postischemic recovery of hearts from mice receiving HFD with Calanus oil was superior to that of mice receiving nonsupplemented HFD and mice receiving HFD with exenatide, as expressed by better pressure development, contractility, and relaxation properties. In summary, dietary Calanus oil and administration of exenatide counteracted obesity-induced derangements of myocardial metabolism. Calanus oil also protected the heart from ischemia, which could have implications for the prevention of obesity-related cardiac disease. NEW & NOTEWORTHY This article describes for the first time that dietary supplementation with a low amount (2%) of a novel marine oil (Calanus oil) in mice is able to prevent the overreliance of fatty acid oxidation for energy production during obesity. The same effect was observed with infusion of the incretin mimetic, exanatide. The improvement in myocardial metabolism in Calanus oil-treated mice was accompanied by a significantly better recovery of cardiac performance following ischemia-reperfusion. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/dietary-calanus-oil-energy-metabolism-and-cardiac-function/ .

scholarly journals L-carnitine Improved the Cardiac Function via the Effect on Myocardial Fatty Acid Metabolism in a Hemodialysis Patient

2018 ◽  
Vol 57 (24) ◽  
pp. 3593-3596 ◽  
Author(s):  
Mai Kaneko ◽  
Hirotaka Fukasawa ◽  
Kento Ishibuchi ◽  
Hiroki Niwa ◽  
Hideo Yasuda ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Cardiac Function ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Hemodialysis Patient ◽  
Myocardial Fatty Acid ◽  
Myocardial Fatty Acid Metabolism

scholarly journals Exercise training impacts the myocardial metabolism of older individuals in a gender-specific manner

2008 ◽  
Vol 295 (2) ◽  
pp. H842-H850 ◽  
Author(s):  
Pablo F. Soto ◽  
Pilar Herrero ◽  
Kenneth B. Schechtman ◽  
Alan D. Waggoner ◽  
Jeffrey M. Baumstark ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Cardiac Function ◽  
Myocardial Metabolism ◽  
Older Individuals ◽  
Myocardial Fatty Acid ◽  
Substrate Metabolism ◽  
Specific Manner ◽  
Myocardial Substrate ◽  
Gender Specific

Aging is associated with decreases in aerobic capacity, cardiac function, and insulin sensitivity as well as alterations in myocardial substrate metabolism. Endurance exercise training (EET) improves cardiac function in a gender-specific manner, and EET has been shown to improve whole body glucose tolerance, but its effects on myocardial metabolism are unclear. Accordingly, we studied the effect of EET on myocardial substrate metabolism in older men and women. Twelve healthy older individuals (age: 60–75 yr; 6 men and 6 women) underwent PET with [15O]water, [11C]acetate, [11C]glucose, and [11C]palmitate for the assessment of myocardial blood flow (MBF), myocardial O2 consumption (MV̇o2), myocardial glucose utilization (MGU), and myocardial fatty acid utilization (MFAU), respectively, at rest and during dobutamine infusion (10 μg·kg−1·min−1). Measurements were repeated after 11 mo of EET. Maximal O2 uptake (V̇o2max) increased ( P = 0.005) after EET. MBF was unaffected by training, as was resting MV̇o2; however, posttraining dobutamine MV̇o2 was significantly higher ( P = 0.05), as was MGU ( P < 0.04). Although overall dobutamine MFAU was unchanged, posttraining dobutamine MFAU increased in women ( P = 0.01) but decreased in men ( P = 0.03). Thus, EET in older individuals improves the catecholamine response of myocardial glucose metabolism. Moreover, gender differences exist in the myocardial fatty acid metabolic response to training. These findings suggest a role for altered myocardial substrate metabolism in modulating the cardiovascular benefits of EET in older individuals.

scholarly journals Ketogenic Diet Suppressed T-Regulatory Cells and Promoted Cardiac Fibrosis via Reducing Mitochondria-Associated Membranes and Inhibiting Mitochondrial Function

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Jun Tao ◽  
Hao Chen ◽  
Ya-Jing Wang ◽  
Jun-Xiong Qiu ◽  
Qing-Qi Meng ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Cardiac Function ◽  
Ketogenic Diet ◽  
Mitochondrial Respiration ◽  
Cardiac Fibrosis ◽  
Interstitial Fibrosis ◽  
Diabetic Patients ◽  
T Regulatory Cell ◽  
Metabolic Indices ◽  
And Function

Ketogenic diet (KD) is popular in diabetic patients but its cardiac safety and efficiency on the heart are unknown. The aim of the present study is to determine the effects and the underlined mechanisms of KD on cardiac function in diabetic cardiomyopathy (DCM). We used db/db mice to model DCM, and different diets (regular or KD) were used. Cardiac function and interstitial fibrosis were determined. T-regulatory cell (Treg) number and functions were evaluated. The effects of ketone body (KB) on fatty acid (FA) and glucose metabolism, mitochondria-associated endoplasmic reticulum membranes (MAMs), and mitochondrial respiration were assessed. The mechanisms via which KB regulated MAMs and Tregs were addressed. KD improved metabolic indices in db/db mice. However, KD impaired cardiac diastolic function and exacerbated ventricular fibrosis. Proportions of circulatory CD4+CD25+Foxp3+ cells in whole blood cells and serum levels of IL-4 and IL-10 were reduced in mice fed with KD. KB suppressed the differentiation to Tregs from naive CD4+ T cells. Cultured medium from KB-treated Tregs synergically activated cardiac fibroblasts. Meanwhile, KB inhibited Treg proliferation and productions of IL-4 and IL-10. Treg MAMs, mitochondrial respiration and respiratory complexes, and FA synthesis and oxidation were all suppressed by KB while glycolytic levels were increased. L-carnitine reversed Treg proliferation and function inhibited by KB. Proportions of ST2L+ cells in Tregs were reduced by KB, as well as the production of ST2L ligand, IL-33. Reinforcement expressions of ST2L in Tregs counteracted the reductions in MAMs, mitochondrial respiration, and Treg proliferations and productions of Treg cytokines IL-4 and IL-10. Therefore, despite the improvement of metabolic indices, KD impaired Treg expansion and function and promoted cardiac fibroblast activation and interstitial fibrosis. This could be mainly mediated by the suppression of MAMs and fatty acid metabolism inhibition via blunting IL-33/ST2L signaling.

Sign in / Sign up

Export Citation Format

Share Document