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Plos Biology : Pgc-1Α Deficiency Causes Multi-system Energy Metabolic Derangements ; Muscle Dysfunction, Abnormal Weight Control and Hepatic Steatosis, Volume 3

By Vidal-puig, Antonio

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Book Id: WPLBN0003924118
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos Biology : Pgc-1Α Deficiency Causes Multi-system Energy Metabolic Derangements ; Muscle Dysfunction, Abnormal Weight Control and Hepatic Steatosis, Volume 3  
Author: Vidal-puig, Antonio
Volume: Volume 3
Language: English
Subject: Journals, Science, Biology
Collections: Periodicals: Journal and Magazine Collection, PLoS Biology
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Publisher: Plos

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Vidal-Puig, A. (n.d.). Plos Biology : Pgc-1Α Deficiency Causes Multi-system Energy Metabolic Derangements ; Muscle Dysfunction, Abnormal Weight Control and Hepatic Steatosis, Volume 3. Retrieved from http://netlibrary.net/


Description
Description : The gene encoding the transcriptional coactivator peroxisome proliferator-activated receptor-c coactivator-1a (PGC-1a) was targeted in mice. PGC-1a null (PGC-1a / ) mice were viable. However, extensive phenotyping revealed multi-system abnormalities indicative of an abnormal energy metabolic phenotype. The postnatal growth of heart and slow-twitch skeletal muscle, organs with high mitochondrial energy demands, is blunted in PGC-1a / mice. With age, the PGC-1a / mice develop abnormally increased body fat, a phenotype that is more severe in females. Mitochondrial number and respiratory capacity is diminished in slow-twitch skeletal muscle of PGC-1a / mice, leading to reduced muscle performance and exercise capacity. PGC-1a / mice exhibit a modest diminution in cardiac function related largely to abnormal control of heart rate. The PGC-1a / mice were unable to maintain core body temperature following exposure to cold, consistent with an altered thermogenic response. Following short-term starvation, PGC-1a / mice develop hepatic steatosis due to a combination of reduced mitochondrial respiratory capacity and an increased expression of lipogenic genes. Surprisingly, PGC-1a / mice were less susceptible to diet-induced insulin resistance than wild-type controls. Lastly, vacuolar lesions were detected in the central nervous system of PGC-1a / mice. These results demonstrate that PGC-1a is necessary for appropriate adaptation to the metabolic and physiologic stressors of postnatal life.

 

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