Mitochondrial and Metabolic Dysfunction in Renal Convoluted Tubules of Obese Mice: Protective Role of Melatonin

Obesity is a common and complex health problem, which impacts crucial organs; it is also considered an independent risk factor for chronic kidney disease. Few studies have analyzed the consequence of obesity in the renal proximal convoluted tubules, which are the major tubules involved in reabsorpti...

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Vydáno v:	PloS one Ročník 9; číslo 10; s. e111141
Hlavní autoři:	Stacchiotti, Alessandra, Favero, Gaia, Giugno, Lorena, Lavazza, Antonio, Reiter, Russel J., Rodella, Luigi Fabrizio, Rezzani, Rita
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Public Library of Science 27.10.2014 Public Library of Science (PLoS)
Témata:	Analysis Animal models Animals Antioxidants Apoptosis Body weight Cristae Damage assessment Damage prevention Drinking behavior Drinking water Ethanol GTP Phosphohydrolases - genetics GTP Phosphohydrolases - metabolism Health risks Kidney Tubules - drug effects Kidney Tubules - metabolism Kidney Tubules - pathology Kidneys Laboratories Male Medicine and Health Sciences Melatonin Melatonin - pharmacology Melatonin - therapeutic use Metabolic disorders Mice Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondria - pathology Mitochondrial DNA Obesity Obesity - complications Obesity - metabolism Organs Proximal tubules Renal failure Renal function Renal Insufficiency - etiology Renal Insufficiency - prevention & control Research and Analysis Methods Risk factors Rodents Supplements Italy
ISSN:	1932-6203, 1932-6203
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Abstract	Obesity is a common and complex health problem, which impacts crucial organs; it is also considered an independent risk factor for chronic kidney disease. Few studies have analyzed the consequence of obesity in the renal proximal convoluted tubules, which are the major tubules involved in reabsorptive processes. For optimal performance of the kidney, energy is primarily provided by mitochondria. Melatonin, an indoleamine and antioxidant, has been identified in mitochondria, and there is considerable evidence regarding its essential role in the prevention of oxidative mitochondrial damage. In this study we evaluated the mechanism(s) of mitochondrial alterations in an animal model of obesity (ob/ob mice) and describe the beneficial effects of melatonin treatment on mitochondrial morphology and dynamics as influenced by mitofusin-2 and the intrinsic apoptotic cascade. Melatonin dissolved in 1% ethanol was added to the drinking water from postnatal week 5-13; the calculated dose of melatonin intake was 100 mg/kg body weight/day. Compared to control mice, obesity-related morphological alterations were apparent in the proximal tubules which contained round mitochondria with irregular, short cristae and cells with elevated apoptotic index. Melatonin supplementation in obese mice changed mitochondria shape and cristae organization of proximal tubules, enhanced mitofusin-2 expression, which in turn modulated the progression of the mitochondria-driven intrinsic apoptotic pathway. These changes possibly aid in reducing renal failure. The melatonin-mediated changes indicate its potential protective use against renal morphological damage and dysfunction associated with obesity and metabolic disease.
AbstractList	Obesity is a common and complex health problem, which impacts crucial organs; it is also considered an independent risk factor for chronic kidney disease. Few studies have analyzed the consequence of obesity in the renal proximal convoluted tubules, which are the major tubules involved in reabsorptive processes. For optimal performance of the kidney, energy is primarily provided by mitochondria. Melatonin, an indoleamine and antioxidant, has been identified in mitochondria, and there is considerable evidence regarding its essential role in the prevention of oxidative mitochondrial damage. In this study we evaluated the mechanism(s) of mitochondrial alterations in an animal model of obesity (ob/ob mice) and describe the beneficial effects of melatonin treatment on mitochondrial morphology and dynamics as influenced by mitofusin-2 and the intrinsic apoptotic cascade. Melatonin dissolved in 1% ethanol was added to the drinking water from postnatal week 5-13; the calculated dose of melatonin intake was 100 mg/kg body weight/day. Compared to control mice, obesity-related morphological alterations were apparent in the proximal tubules which contained round mitochondria with irregular, short cristae and cells with elevated apoptotic index. Melatonin supplementation in obese mice changed mitochondria shape and cristae organization of proximal tubules, enhanced mitofusin-2 expression, which in turn modulated the progression of the mitochondria-driven intrinsic apoptotic pathway. These changes possibly aid in reducing renal failure. The melatonin-mediated changes indicate its potential protective use against renal morphological damage and dysfunction associated with obesity and metabolic disease. Obesity is a common and complex health problem, which impacts crucial organs; it is also considered an independent risk factor for chronic kidney disease. Few studies have analyzed the consequence of obesity in the renal proximal convoluted tubules, which are the major tubules involved in reabsorptive processes. For optimal performance of the kidney, energy is primarily provided by mitochondria. Melatonin, an indoleamine and antioxidant, has been identified in mitochondria, and there is considerable evidence regarding its essential role in the prevention of oxidative mitochondrial damage. In this study we evaluated the mechanism(s) of mitochondrial alterations in an animal model of obesity (ob/ob mice) and describe the beneficial effects of melatonin treatment on mitochondrial morphology and dynamics as influenced by mitofusin-2 and the intrinsic apoptotic cascade. Melatonin dissolved in 1% ethanol was added to the drinking water from postnatal week 5-13; the calculated dose of melatonin intake was 100 mg/kg body weight/day. Compared to control mice, obesity-related morphological alterations were apparent in the proximal tubules which contained round mitochondria with irregular, short cristae and cells with elevated apoptotic index. Melatonin supplementation in obese mice changed mitochondria shape and cristae organization of proximal tubules, enhanced mitofusin-2 expression, which in turn modulated the progression of the mitochondria-driven intrinsic apoptotic pathway. These changes possibly aid in reducing renal failure. The melatonin-mediated changes indicate its potential protective use against renal morphological damage and dysfunction associated with obesity and metabolic disease.Obesity is a common and complex health problem, which impacts crucial organs; it is also considered an independent risk factor for chronic kidney disease. Few studies have analyzed the consequence of obesity in the renal proximal convoluted tubules, which are the major tubules involved in reabsorptive processes. For optimal performance of the kidney, energy is primarily provided by mitochondria. Melatonin, an indoleamine and antioxidant, has been identified in mitochondria, and there is considerable evidence regarding its essential role in the prevention of oxidative mitochondrial damage. In this study we evaluated the mechanism(s) of mitochondrial alterations in an animal model of obesity (ob/ob mice) and describe the beneficial effects of melatonin treatment on mitochondrial morphology and dynamics as influenced by mitofusin-2 and the intrinsic apoptotic cascade. Melatonin dissolved in 1% ethanol was added to the drinking water from postnatal week 5-13; the calculated dose of melatonin intake was 100 mg/kg body weight/day. Compared to control mice, obesity-related morphological alterations were apparent in the proximal tubules which contained round mitochondria with irregular, short cristae and cells with elevated apoptotic index. Melatonin supplementation in obese mice changed mitochondria shape and cristae organization of proximal tubules, enhanced mitofusin-2 expression, which in turn modulated the progression of the mitochondria-driven intrinsic apoptotic pathway. These changes possibly aid in reducing renal failure. The melatonin-mediated changes indicate its potential protective use against renal morphological damage and dysfunction associated with obesity and metabolic disease.
Audience	Academic
Author	Lavazza, Antonio Favero, Gaia Reiter, Russel J. Stacchiotti, Alessandra Rezzani, Rita Rodella, Luigi Fabrizio Giugno, Lorena
AuthorAffiliation	3 Department of Cellular and Structural Biology, UT Health Science Center San Antonio, San Antonio, Texas, United States of America 2 Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, OIE Reference Laboratory for RHD, Brescia, Italy The University of Manchester, United Kingdom 1 Anatomy and Physiopathology Division, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy
AuthorAffiliation_xml	– name: 1 Anatomy and Physiopathology Division, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy – name: The University of Manchester, United Kingdom – name: 3 Department of Cellular and Structural Biology, UT Health Science Center San Antonio, San Antonio, Texas, United States of America – name: 2 Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, OIE Reference Laboratory for RHD, Brescia, Italy
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BackLink	https://www.ncbi.nlm.nih.gov/pubmed/25347680$$D View this record in MEDLINE/PubMed
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Copyright	COPYRIGHT 2014 Public Library of Science 2014 Stacchiotti 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. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2014 Stacchiotti et al 2014 Stacchiotti et al
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: AS GF RJR LFR RR. Performed the experiments: AS GF LG AL. Analyzed the data: AS GF RJR LFR RR. Contributed reagents/materials/analysis tools: AS GF LG AL RJR LFR RR. Contributed to the writing of the manuscript: AS GF RJR LFR RR.
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Snippet	Obesity is a common and complex health problem, which impacts crucial organs; it is also considered an independent risk factor for chronic kidney disease. Few...
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SubjectTerms	Analysis Animal models Animals Antioxidants Apoptosis Body weight Cristae Damage assessment Damage prevention Drinking behavior Drinking water Ethanol GTP Phosphohydrolases - genetics GTP Phosphohydrolases - metabolism Health risks Kidney Tubules - drug effects Kidney Tubules - metabolism Kidney Tubules - pathology Kidneys Laboratories Male Medicine and Health Sciences Melatonin Melatonin - pharmacology Melatonin - therapeutic use Metabolic disorders Mice Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondria - pathology Mitochondrial DNA Obesity Obesity - complications Obesity - metabolism Organs Proximal tubules Renal failure Renal function Renal Insufficiency - etiology Renal Insufficiency - prevention & control Research and Analysis Methods Risk factors Rodents Supplements
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Title	Mitochondrial and Metabolic Dysfunction in Renal Convoluted Tubules of Obese Mice: Protective Role of Melatonin
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Volume	9
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