期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 104, 期 12, 页码 5223-5228出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0611623104
关键词
knockout mice; oxidative metabolism; energy metabolism; lipogenesis
资金
- NICHD NIH HHS [5R01 HD027183, R01 HD027183] Funding Source: Medline
- NIDDK NIH HHS [5R37 DK057978, U19 DK062434, R37 DK057978, U19 DK62434-01] Funding Source: Medline
- NIEHS NIH HHS [P42 ES10337, P42 ES010337] Funding Source: Medline
The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator 1 beta (PGC-1 beta) is believed to control mitochondrial oxidative energy metabolism by activating specific target transcription factors including estrogen-related receptors and nuclear respiratory factor 1, yet its physiological role is not yet clearly understood. To define its function in vivo, we generated and characterized mice lacking the functional PGC-1 beta protein [PGC-1 beta knockout (KO) mice]. PGC-1 beta KO mice are viable and fertile and show no overt phenotype under normal laboratory conditions. However, the KO mice displayed an altered expression in a large number of nuclear-encoded genes governing mitochondrial and metabolic functions in multiple tissues including heart, skeletal muscle, brain, brown adipose tissue, and liver. In contrast to PGC-la KO mice that are reportedly hyperactive, PGC-1 beta KO mice show greatly decreased activity during the dark cycle. When acutely exposed to cold, the KO mice developed abnormal hypothermia and morbidity. Furthermore, high-fat feeding induced hepatic steatosis and increased serum triglycericle and cholesterol levels in the KO mice. These results suggest that PGC-1 beta in mouse plays a nonredundant role in controlling mitochondrial oxidative energy metabolism.
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