scholarly journals 4,4,16‐Trifluoropalmitate: Design, Synthesis, Tritiation, Radiofluorination and Preclinical PET Imaging Studies on Myocardial Fatty Acid Oxidation

ChemMedChem ◽  
2020 ◽  
Vol 15 (23) ◽  
pp. 2317-2331
Author(s):  
Alessandro Colombano ◽  
Sergio Dall'Angelo ◽  
Lee Kingston ◽  
Gunnar Grönberg ◽  
Claudia Correia ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Pet Imaging ◽  
Acid Oxidation ◽  
Imaging Studies ◽  
Myocardial Fatty Acid ◽  
Design Synthesis ◽  
Preclinical Pet

379-P: Aldose Reductase Inhibition by AT-001 Prevents Diabetic Cardiomyopathy via Reducing Myocardial Fatty Acid Oxidation Rates

Diabetes ◽  
2021 ◽  
Vol 70 (Supplement 1) ◽  
pp. 379-P
Author(s):  
KESHAV GOPAL ◽  
QUTUBA G. KARWI ◽  
SEYED AMIRHOSSEIN TABATABAEI DAKHILI ◽  
CORY S. WAGG ◽  
RICCARDO PERFETTI ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Aldose Reductase ◽  
Diabetic Cardiomyopathy ◽  
Acid Oxidation ◽  
Myocardial Fatty Acid ◽  
Aldose Reductase Inhibition ◽  
Oxidation Rates

scholarly journals Uncoupling protein 3 deficiency impairs myocardial fatty acid oxidation and contractile recovery following ischemia/reperfusion

2018 ◽  
Vol 113 (6) ◽  
Author(s):  
Kristin S. Edwards ◽  
Sadia Ashraf ◽  
Tyler M. Lomax ◽  
Jessica M. Wiseman ◽  
Michael E. Hall ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Uncoupling Protein ◽  
Ischemia Reperfusion ◽  
Acid Oxidation ◽  
Myocardial Fatty Acid ◽  
Uncoupling Protein 3 ◽  
Contractile Recovery

Myocardial fatty acid oxidation during ischemia and reperfusion

1992 ◽  
pp. 103-109
Author(s):  
René Lerch ◽  
Christian Tamm ◽  
Irene Papageorgiou ◽  
Richard H. Benzi
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Ischemia And Reperfusion ◽  
Myocardial Fatty Acid

scholarly journals Assessment of myocardial metabolic flexibility and work efficiency in human type 2 diabetes using 16-[18F]fluoro-4-thiapalmitate, a novel PET fatty acid tracer

2016 ◽  
Vol 310 (6) ◽  
pp. E452-E460 ◽  
Author(s):  
K. J. Mather ◽  
G. D. Hutchins ◽  
K. Perry ◽  
W. Territo ◽  
R. Chisholm ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Oxygen Consumption ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Metabolic Flexibility ◽  
Work Efficiency ◽  
Myocardial Fatty Acid ◽  
Fuel Selection

Altered myocardial fuel selection likely underlies cardiac disease risk in diabetes, affecting oxygen demand and myocardial metabolic flexibility. We investigated myocardial fuel selection and metabolic flexibility in human type 2 diabetes mellitus (T2DM), using positron emission tomography to measure rates of myocardial fatty acid oxidation {16-[18F]fluoro-4-thia-palmitate (FTP)} and myocardial perfusion and total oxidation ([11C]acetate). Participants underwent paired studies under fasting conditions, comparing 3-h insulin + glucose euglycemic clamp conditions (120 mU·m−2·min−1) to 3-h saline infusion. Lean controls ( n = 10) were compared with glycemically controlled volunteers with T2DM ( n = 8). Insulin augmented heart rate, blood pressure, and stroke index in both groups (all P < 0.01) and significantly increased myocardial oxygen consumption ( P = 0.04) and perfusion ( P = 0.01) in both groups. Insulin suppressed available nonesterified fatty acids ( P < 0.0001), but fatty acid concentrations were higher in T2DM under both conditions ( P < 0.001). Insulin-induced suppression of fatty acid oxidation was seen in both groups ( P < 0.0001). However, fatty acid oxidation rates were higher under both conditions in T2DM ( P = 0.003). Myocardial work efficiency was lower in T2DM ( P = 0.006) and decreased in both groups with the insulin-induced increase in work and shift in fuel utilization ( P = 0.01). Augmented fatty acid oxidation is present under baseline and insulin-treated conditions in T2DM, with impaired insulin-induced shifts away from fatty acid oxidation. This is accompanied by reduced work efficiency, possibly due to greater oxygen consumption with fatty acid metabolism. These observations suggest that improved fatty acid suppression, or reductions in myocardial fatty acid uptake and retention, could be therapeutic targets to improve myocardial ischemia tolerance in T2DM.

Myocardial fatty acid oxidation: Evidence for an albumin-receptor-mediated membrane transfer of fatty acids

1984 ◽  
Vol 79 (3) ◽  
pp. 274-282 ◽  
Author(s):  
J. F. Hütter ◽  
H. M. Piper ◽  
P. G. Spieckermann
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Myocardial Fatty Acid ◽  
Albumin Receptor ◽  
Membrane Transfer

scholarly journals Thyroid Hormone Reverses Aging-Induced Myocardial Fatty Acid Oxidation Defects and Improves the Response to Acutely Increased Afterload

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e65532 ◽  
Author(s):  
Dolena Ledee ◽  
Michael A. Portman ◽  
Masaki Kajimoto ◽  
Nancy Isern ◽  
Aaron K. Olson
Keyword(s):  
Fatty Acid ◽  
Thyroid Hormone ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Myocardial Fatty Acid

Malonyl CoA control of fatty acid oxidation in the newborn heart in response to increased fatty acid supply

2006 ◽  
Vol 84 (11) ◽  
pp. 1215-1222 ◽  
Author(s):  
Arzu Onay-Besikci ◽  
Nandakumar Sambandam
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Acetyl Coa Carboxylase ◽  
Myocardial Fatty Acid ◽  
Acetyl Coa ◽  
Tissue Levels ◽  
Post Surgery ◽  
Malonyl Coa

The concentration of fatty acids in the blood or perfusate is a major determinant of the extent of myocardial fatty acid oxidation. Increasing fatty acid supply in adult rat increases myocardial fatty acid oxidation. Plasma levels of fatty acids increase post-surgery in infants undergoing cardiac bypass operation to correct congenital heart defects. How a newborn heart responds to increased fatty acid supply remains to be determined. In this study, we examined whether the tissue levels of malonyl CoA decrease to relieve the inhibition on carnitine palmitoyltransferase (CPT) I when the myocardium is exposed to higher concentrations of long-chain fatty acids in newborn rabbit heart. We then tested the contribution of the enzymes that regulate tissue levels of malonyl CoA, acetyl CoA carboxylase (ACC), and malonyl CoA decarboxylase (MCD). Our results showed that increasing fatty acid supply from 0.4 mmol/L (physiological) to 1.2 mmol/L (pathological) resulted in an increase in cardiac fatty acid oxidation rates and this was accompanied by a decrease in tissue malonyl CoA levels. The decrease in malonyl CoA was not related to any alterations in total and phosphorylated acetyl CoA carboxylase protein or the activities of acetyl CoA carboxylase and malonyl CoA decarboxylase. Our results suggest that the regulatory role of malonyl CoA remained when the hearts were exposed to high levels of fatty acids.

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