Control of whole body energy homeostasis by microRNA regulation
AssigneesBoard of Regents, The University of Texas System, Miragen Therapeutics, Inc.
InventorsEva van Rooij, Eric Olson, Chad Grueter, Rusty Montgomery
Life of this patent
Estimating the term…
Abstract
The disclosure provides a method of regulating fatty acid or glucose metabolism in a cell by contacting the cell with a modulator of miR-208a and/or miR-208b activity or expression. The disclosure also provides a method of treating or preventing a metabolic disorder, such as obesity, diabetes, or metabolic syndrome, in a subject by administering to the subject an inhibitor of miR-208a and/or miR-208b activity or expression. Also provided is a method of enhancing or improving mitochondrial function and/or redox-homeostasis in a subject by administering to the subject an inhibitor of miR-208a and/or miR-208b activity or expression.
Claims19
A method of treating obesity, hypercholesterolemia, type 2 diabetes, hepatic steatosis, hyperlipidemia, insulin resistance, a glycogen storage disease, or aberrant glucose uptake and/or utilization in a subject in need thereof comprising administering to the subject an inhibitor of miR-208a and/or miR-208b, wherein the inhibitor is an antisense oligonucleotide, wherein the antisense oligonucleotide comprises a sequence that is at least partially complementary to a mature sequence of miR-208a and/or miR-208b, and wherein the expression or activity of miR-208a and/or miR-208b is reduced in the cells of the subject following administration.
A method of regulating fatty acid or glucose metabolism in a subject in need thereof comprising administering an inhibitor of miR-208a and/or miR-208b expression or activity to the subject, wherein the inhibitor of miR-208a and/or miR-208b is an antisense oligonucleotide comprising a sequence that is at least partially complementary to a mature sequence of miR-208a and/or miR-208b.
A method of enhancing mitochondrial function or redox-homeostasis in a subject in need thereof comprising administering to the subject an antisense oligonucleotide comprising a sequence that is at least partially complementary to a miR-208a or miR-208b sequence, wherein the expression or activity of milt-208a or miR-208b is reduced in the cells of the subject following administration of the antisense oligonucleotide.
Dependencies are inferred from the claim text.