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Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Novel remodeling of the mouse heart mitochondrial proteome in response to acute insulin stimulation.
BACKGROUND AND AIM: Mitochondrial dysfunction contributes to the pathophysiology of diabetic cardiomyopathy. The aim of this study was to investigate the acute changes in the mitochondrial proteome in response to insulin stimulation.
METHODS AND RESULTS: Cardiac mitochondria from C57BL/6 mice after insulin stimulation were analyzed using two-dimensional fluorescence difference gel electrophoresis. MALDI-TOF MS/MS was utilized to identify differences. Two enzymes involved in metabolism and four structural proteins were identified. Succinyl-CoA ligase [ADP forming] subunit beta was identified as one of the differentially regulated proteins. Upon insulin stimulation, a relatively more acidic isoform of this protein was increased by 53% and its functional activity was decreased by ∼32%.
CONCLUSIONS: This proteomic remodeling in response to insulin stimulation may play an important role in the normal and diabetic heart.
METHODS AND RESULTS: Cardiac mitochondria from C57BL/6 mice after insulin stimulation were analyzed using two-dimensional fluorescence difference gel electrophoresis. MALDI-TOF MS/MS was utilized to identify differences. Two enzymes involved in metabolism and four structural proteins were identified. Succinyl-CoA ligase [ADP forming] subunit beta was identified as one of the differentially regulated proteins. Upon insulin stimulation, a relatively more acidic isoform of this protein was increased by 53% and its functional activity was decreased by ∼32%.
CONCLUSIONS: This proteomic remodeling in response to insulin stimulation may play an important role in the normal and diabetic heart.
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