AMPK stimulation and PGC-1 alpha suppression in peroxisome deficient hepatocytes favor catabolic over anabolic carbohydrate metabolism
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Emiel Ver Loren van Themaat
PROVIDER: E-GEOD-27720 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
Carbohydrate metabolism is perturbed in peroxisome-deficient hepatocytes due to mitochondrial dysfunction, AMP-activated protein kinase (AMPK) activation, and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) suppression.
Peeters Annelies A Fraisl Peter P van den Berg Sjoerd S van den Berg Sjoerd S Ver Loren van Themaat Emiel E Van Kampen Antoine A Rider Mark H MH Takemori Hiroshi H van Dijk Ko Willems KW Van Veldhoven Paul P PP Carmeliet Peter P Baes Myriam M
The Journal of biological chemistry 20111014 49
Hepatic peroxisomes are essential for lipid conversions that include the formation of mature conjugated bile acids, the degradation of branched chain fatty acids, and the synthesis of docosahexaenoic acid. Through unresolved mechanisms, deletion of functional peroxisomes from mouse hepatocytes (L-Pex5(-/-) mice) causes severe structural and functional abnormalities at the inner mitochondrial membrane. We now demonstrate that the peroxisomal and mitochondrial anomalies trigger energy deficits, as ...[more]
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