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Ayanna S. Augustus

Researcher at Columbia University

Publications -  9
Citations -  968

Ayanna S. Augustus is an academic researcher from Columbia University. The author has contributed to research in topics: Lipoprotein lipase & Triglyceride. The author has an hindex of 9, co-authored 9 publications receiving 923 citations. Previous affiliations of Ayanna S. Augustus include Thomas Jefferson University.

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Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathy

TL;DR: Lipoprotein lipase expressed on the surface of cardiomyocytes can increase lipid uptake and produceCardiomyopathy, and an alpha-myosin heavy-chain promoter upstream of a human lipop protein lipase minigene construct with a glycosylphosphatidylinositol anchoring sequence on the carboxyl terminal region is placed.
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Routes of FA delivery to cardiac muscle: modulation of lipoprotein lipolysis alters uptake of TG-derived FA.

TL;DR: The data suggest that the heart is especially effective in removal of circulating TG and core lipids and that this is due to LPL hydrolysis and not its bridging function.
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Loss of Lipoprotein Lipase-derived Fatty Acids Leads to Increased Cardiac Glucose Metabolism and Heart Dysfunction

TL;DR: Long term reduction of lipoprotein FA uptake is associated with impaired cardiac function despite a compensatory increase in glucose utilization, and hearts unable to obtain FA from lipop protein TG were able to compensate by increasing glucose uptake, glycolysis, and glucose oxidation.
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Cardiac-specific knock-out of lipoprotein lipase alters plasma lipoprotein triglyceride metabolism and cardiac gene expression

TL;DR: The loss of LpL in the heart leads to defective plasma metabolism of TG, and fatty acids derived from lipoprotein TG and not just albumin-associated fatty acids are important for cardiac lipid metabolism and gene regulation.
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Peroxisome Proliferator-Activated Receptor Agonists Modulate Heart Function in Transgenic Mice with Lipotoxic Cardiomyopathy

TL;DR: Overall, PPAR activators exhibit differential effects in this model of lipotoxic dilated cardiomyopathy, whereas an agonist of PPARα did not improve cardiac lipids and worsened heart function.