Cardiac energy dependence on glucose increases metabolites related to glutathione and activates metabolic genes controlled by mechanistic target of rapamycin
Background Long chain acyl‐CoA synthetases (ACSL) catalyze long‐chain fatty acids (FA)
conversion to acyl‐CoAs. Temporal ACSL 1 inactivation in mouse hearts (Acsl1 H−/−)
impaired FA oxidation and dramatically increased glucose uptake, glucose oxidation, and
mTOR activation, resulting in cardiac hypertrophy. We used unbiased metabolomics and
gene expression analyses to elucidate the cardiac cellular response to increased glucose
use in a genetic model of inactivated FA oxidation. Methods and Results Metabolomics …
conversion to acyl‐CoAs. Temporal ACSL 1 inactivation in mouse hearts (Acsl1 H−/−)
impaired FA oxidation and dramatically increased glucose uptake, glucose oxidation, and
mTOR activation, resulting in cardiac hypertrophy. We used unbiased metabolomics and
gene expression analyses to elucidate the cardiac cellular response to increased glucose
use in a genetic model of inactivated FA oxidation. Methods and Results Metabolomics …
P663 Cardiac energy dependence on glucose increases metabolites related to glutathione and activates metabolic genes controlled by mTOR.
J Schisler, T Grevengoed, J Ellis… - Cardiovascular …, 2014 - search.ebscohost.com
Long chain acyl-CoA synthetases (ACSL) catalyze long chain fatty acids (FA) conversion to
acyl-CoAs. Temporal ACSL1 inactivation in mouse hearts (Acsl1H-/-) impaired FA oxidation
(FAO) and dramatically increased glucose uptake, glucose oxidation, and mTOR activation,
resulting in cardiac hypertrophy. Our objective was to elucidate the cardiac cellular response
to increased glucose utilization in response to the genetic inactivation of FAO using
metabolomics and gene expression analyses. Using metabolomics analysis, we identified …
acyl-CoAs. Temporal ACSL1 inactivation in mouse hearts (Acsl1H-/-) impaired FA oxidation
(FAO) and dramatically increased glucose uptake, glucose oxidation, and mTOR activation,
resulting in cardiac hypertrophy. Our objective was to elucidate the cardiac cellular response
to increased glucose utilization in response to the genetic inactivation of FAO using
metabolomics and gene expression analyses. Using metabolomics analysis, we identified …
以上显示的是最相近的搜索结果。 查看全部搜索结果