GSE173256: Increased cardiac fatty acid oxidation in a mouse model with decreased malonyl-CoA sensitivity of CPT1B

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GROUP CONDITION SAMPLES
heart
GSM5264386 GSM5264393 GSM5264396 GSM5264397
GSM5264385 GSM5264387 GSM5264388 GSM5264389 GSM5264391
GSM5264390 GSM5264392 GSM5264394 GSM5264395
Description

Submission Date: Apr 25, 2021

Summary: Mitochondrial fatty acid oxidation (FAO) is an important energy provider for cardiac work and changes in cardiac substrate preference are associated with different heart diseases. Carnitine palmitoyltransferase 1B (CPT1B) is thought to perform the rate limiting enzyme step in FAO and is inhibited by malonyl-CoA. The role of CPT1B in cardiac metabolism has been addressed by inhibiting or decreasing CPT1B protein or after modulation of tissue malonyl-CoA metabolism. We assessed the role of CPT1B malonyl-CoA sensitivity in cardiac metabolism.

GEO Accession ID: GSE173256

PMID: 29635338

Description

Submission Date: Apr 25, 2021

Summary: Mitochondrial fatty acid oxidation (FAO) is an important energy provider for cardiac work and changes in cardiac substrate preference are associated with different heart diseases. Carnitine palmitoyltransferase 1B (CPT1B) is thought to perform the rate limiting enzyme step in FAO and is inhibited by malonyl-CoA. The role of CPT1B in cardiac metabolism has been addressed by inhibiting or decreasing CPT1B protein or after modulation of tissue malonyl-CoA metabolism. We assessed the role of CPT1B malonyl-CoA sensitivity in cardiac metabolism.

GEO Accession ID: GSE173256

PMID: 29635338

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