Loss of Renal Tubular PGC-1α Exacerbates Diet-Induced Renal Steatosis and Age-Related Urinary Sodium Excretion in Mice
The kidney has a high energy demand and is dependent on oxidative metabolism for ATP production. Accordingly, the kidney is rich in mitochondria, and mitochondrial dysfunction is a common denominator for several renal diseases. While the mitochondrial master regulator peroxisome proliferator-activat...
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| Veröffentlicht in: | PloS one 2016-07, Vol.11 (7), p.e0158716 |
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| description | The kidney has a high energy demand and is dependent on oxidative metabolism for ATP production. Accordingly, the kidney is rich in mitochondria, and mitochondrial dysfunction is a common denominator for several renal diseases. While the mitochondrial master regulator peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is highly expressed in kidney, its role in renal physiology is so far unclear. Here we show that PGC-1α is a transcriptional regulator of mitochondrial metabolic pathways in the kidney. Moreover, we demonstrate that mice with an inducible nephron-specific inactivation of PGC-1α in the kidney display elevated urinary sodium excretion, exacerbated renal steatosis during metabolic stress but normal blood pressure regulation. Overall, PGC-1α seems largely dispensable for basal renal physiology. However, the role of PGC-1α in renal mitochondrial biogenesis indicates that activation of PGC-1α in the context of renal disorders could be a valid therapeutic strategy to ameliorate renal mitochondrial dysfunction. |
| doi_str_mv | 10.1371/journal.pone.0158716 |
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Accordingly, the kidney is rich in mitochondria, and mitochondrial dysfunction is a common denominator for several renal diseases. While the mitochondrial master regulator peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is highly expressed in kidney, its role in renal physiology is so far unclear. Here we show that PGC-1α is a transcriptional regulator of mitochondrial metabolic pathways in the kidney. Moreover, we demonstrate that mice with an inducible nephron-specific inactivation of PGC-1α in the kidney display elevated urinary sodium excretion, exacerbated renal steatosis during metabolic stress but normal blood pressure regulation. Overall, PGC-1α seems largely dispensable for basal renal physiology. However, the role of PGC-1α in renal mitochondrial biogenesis indicates that activation of PGC-1α in the context of renal disorders could be a valid therapeutic strategy to ameliorate renal mitochondrial dysfunction.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0158716</identifier><identifier>PMID: 27463191</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Age ; Animals ; Biology and Life Sciences ; Blood pressure ; Deactivation ; Diet ; Diet, High-Fat ; Drinking water ; Energy demand ; Enzymes ; Excretion ; Experiments ; Fatty acids ; Gene expression ; Homeostasis ; Hypertension ; Inactivation ; Inflammation ; Kidney Diseases - metabolism ; Kidney Diseases - urine ; Kidney Tubules - metabolism ; Kidneys ; Lipid Metabolism ; Lipids ; Medicine and Health Sciences ; Metabolic pathways ; Metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria ; Musculoskeletal system ; Oxidative metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism ; Phenotype ; Physiology ; Proteins ; Renal function ; Rodents ; Sodium ; Sodium - urine ; Steatosis ; Transcription ; Urine</subject><ispartof>PloS one, 2016-07, Vol.11 (7), p.e0158716</ispartof><rights>2016 Svensson et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Accordingly, the kidney is rich in mitochondria, and mitochondrial dysfunction is a common denominator for several renal diseases. While the mitochondrial master regulator peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is highly expressed in kidney, its role in renal physiology is so far unclear. Here we show that PGC-1α is a transcriptional regulator of mitochondrial metabolic pathways in the kidney. Moreover, we demonstrate that mice with an inducible nephron-specific inactivation of PGC-1α in the kidney display elevated urinary sodium excretion, exacerbated renal steatosis during metabolic stress but normal blood pressure regulation. Overall, PGC-1α seems largely dispensable for basal renal physiology. 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Accordingly, the kidney is rich in mitochondria, and mitochondrial dysfunction is a common denominator for several renal diseases. While the mitochondrial master regulator peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is highly expressed in kidney, its role in renal physiology is so far unclear. Here we show that PGC-1α is a transcriptional regulator of mitochondrial metabolic pathways in the kidney. Moreover, we demonstrate that mice with an inducible nephron-specific inactivation of PGC-1α in the kidney display elevated urinary sodium excretion, exacerbated renal steatosis during metabolic stress but normal blood pressure regulation. Overall, PGC-1α seems largely dispensable for basal renal physiology. 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| subjects | Age Animals Biology and Life Sciences Blood pressure Deactivation Diet Diet, High-Fat Drinking water Energy demand Enzymes Excretion Experiments Fatty acids Gene expression Homeostasis Hypertension Inactivation Inflammation Kidney Diseases - metabolism Kidney Diseases - urine Kidney Tubules - metabolism Kidneys Lipid Metabolism Lipids Medicine and Health Sciences Metabolic pathways Metabolism Mice Mice, Inbred C57BL Mice, Knockout Mitochondria Musculoskeletal system Oxidative metabolism Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism Phenotype Physiology Proteins Renal function Rodents Sodium Sodium - urine Steatosis Transcription Urine |
| title | Loss of Renal Tubular PGC-1α Exacerbates Diet-Induced Renal Steatosis and Age-Related Urinary Sodium Excretion in Mice |
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