A very-low-protein diet ameliorates advanced diabetic nephropathy through autophagy induction by suppression of the mTORC1 pathway in Wistar fatty rats, an animal model of type 2 diabetes and obesity
Aims/hypothesis The efficacy of a low-protein diet (LPD) on diabetic nephropathy is controversial. We aimed to investigate the renoprotective effects of an LPD and the underlying molecular mechanism in a rat model of type 2 diabetes and obesity. Methods Diabetic male Wistar fatty ( fa / fa ) rats (W...
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| Veröffentlicht in: | Diabetologia 2016-06, Vol.59 (6), p.1307-1317 |
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| creator | Kitada, Munehiro Ogura, Yoshio Suzuki, Taeko Sen, Shi Lee, Seon Myeong Kanasaki, Keizo Kume, Shinji Koya, Daisuke |
| description | Aims/hypothesis
The efficacy of a low-protein diet (LPD) on diabetic nephropathy is controversial. We aimed to investigate the renoprotective effects of an LPD and the underlying molecular mechanism in a rat model of type 2 diabetes and obesity.
Methods
Diabetic male Wistar fatty (
fa
/
fa
) rats (WFRs) were treated with a standard diet (23.84% protein) or an LPD (5.77% protein) for 20 weeks from 24 weeks of age. We investigated the effect of the LPD on renal function, fibrosis, tubular cell damage, inflammation, mitochondrial morphology of proximal tubular cells (PTCs), apoptosis, autophagy and activation of mammalian target of rapamycin complex 1 (mTORC1).
Results
Kidney weight, albuminuria, excretion of urinary liver-type fatty acid binding protein, levels of plasma cystatin C and changes in renal histology, including fibrosis, tubular cell damage and inflammation, were aggravated in WFRs compared with non-diabetic Wistar lean rats (WLRs). Fragmented and swelling mitochondria accumulated in PTCs and apoptosis were enhanced in the kidney of WFRs. Immunohistochemical staining of p62 and p-S6 ribosomal protein (p-S6RP) in the tubular lesions of WFRs was increased compared with WLRs. The LPD intervention clearly ameliorated damage as shown by the assessment of renal function and histology, particularly tubulointerstitial damage in diabetic kidneys. Additionally, the 5.77% LPD, but not the 11.46% LPD, significantly suppressed p-S6RP levels and increased microtubule-associated protein light chain 3-II levels in the renal cortex. The LPD intervention partially decreased HbA
1c
levels in WFRs, and no differences in mean BP were observed among any of the groups.
Conclusions/interpretation
A very-low-protein diet improved advanced diabetic renal injuries, including tubulointerstitial damage, by restoring autophagy through the suppression of the mTORC1 pathway. |
| doi_str_mv | 10.1007/s00125-016-3925-4 |
| format | Article |
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The efficacy of a low-protein diet (LPD) on diabetic nephropathy is controversial. We aimed to investigate the renoprotective effects of an LPD and the underlying molecular mechanism in a rat model of type 2 diabetes and obesity.
Methods
Diabetic male Wistar fatty (
fa
/
fa
) rats (WFRs) were treated with a standard diet (23.84% protein) or an LPD (5.77% protein) for 20 weeks from 24 weeks of age. We investigated the effect of the LPD on renal function, fibrosis, tubular cell damage, inflammation, mitochondrial morphology of proximal tubular cells (PTCs), apoptosis, autophagy and activation of mammalian target of rapamycin complex 1 (mTORC1).
Results
Kidney weight, albuminuria, excretion of urinary liver-type fatty acid binding protein, levels of plasma cystatin C and changes in renal histology, including fibrosis, tubular cell damage and inflammation, were aggravated in WFRs compared with non-diabetic Wistar lean rats (WLRs). Fragmented and swelling mitochondria accumulated in PTCs and apoptosis were enhanced in the kidney of WFRs. Immunohistochemical staining of p62 and p-S6 ribosomal protein (p-S6RP) in the tubular lesions of WFRs was increased compared with WLRs. The LPD intervention clearly ameliorated damage as shown by the assessment of renal function and histology, particularly tubulointerstitial damage in diabetic kidneys. Additionally, the 5.77% LPD, but not the 11.46% LPD, significantly suppressed p-S6RP levels and increased microtubule-associated protein light chain 3-II levels in the renal cortex. The LPD intervention partially decreased HbA
1c
levels in WFRs, and no differences in mean BP were observed among any of the groups.
Conclusions/interpretation
A very-low-protein diet improved advanced diabetic renal injuries, including tubulointerstitial damage, by restoring autophagy through the suppression of the mTORC1 pathway.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-016-3925-4</identifier><identifier>PMID: 27020449</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Apoptosis ; Autophagy ; Autophagy - genetics ; Autophagy - physiology ; Diabetes ; Diabetes Mellitus, Type 2 - diet therapy ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - pathology ; Diabetic Nephropathies - diet therapy ; Diabetic Nephropathies - metabolism ; Diabetic Nephropathies - pathology ; Diabetic nephropathy ; Diet, Protein-Restricted ; Disease Models, Animal ; Fatty acids ; Histology ; Human Physiology ; Immunohistochemistry ; Internal Medicine ; Kidneys ; Male ; Malnutrition ; Mechanistic Target of Rapamycin Complex 1 ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Microscopy, Electron, Transmission ; Multiprotein Complexes - genetics ; Multiprotein Complexes - metabolism ; Obesity ; Obesity - diet therapy ; Obesity - metabolism ; Obesity - pathology ; Proteins ; Rats ; Rats, Wistar ; Real-Time Polymerase Chain Reaction ; TOR Serine-Threonine Kinases - genetics ; TOR Serine-Threonine Kinases - metabolism</subject><ispartof>Diabetologia, 2016-06, Vol.59 (6), p.1307-1317</ispartof><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c481t-76114f389a706b2004dd1213f039687a3651849ebc08313d572693ef107e65583</citedby><cites>FETCH-LOGICAL-c481t-76114f389a706b2004dd1213f039687a3651849ebc08313d572693ef107e65583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00125-016-3925-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00125-016-3925-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27020449$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kitada, Munehiro</creatorcontrib><creatorcontrib>Ogura, Yoshio</creatorcontrib><creatorcontrib>Suzuki, Taeko</creatorcontrib><creatorcontrib>Sen, Shi</creatorcontrib><creatorcontrib>Lee, Seon Myeong</creatorcontrib><creatorcontrib>Kanasaki, Keizo</creatorcontrib><creatorcontrib>Kume, Shinji</creatorcontrib><creatorcontrib>Koya, Daisuke</creatorcontrib><title>A very-low-protein diet ameliorates advanced diabetic nephropathy through autophagy induction by suppression of the mTORC1 pathway in Wistar fatty rats, an animal model of type 2 diabetes and obesity</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Aims/hypothesis
The efficacy of a low-protein diet (LPD) on diabetic nephropathy is controversial. We aimed to investigate the renoprotective effects of an LPD and the underlying molecular mechanism in a rat model of type 2 diabetes and obesity.
Methods
Diabetic male Wistar fatty (
fa
/
fa
) rats (WFRs) were treated with a standard diet (23.84% protein) or an LPD (5.77% protein) for 20 weeks from 24 weeks of age. We investigated the effect of the LPD on renal function, fibrosis, tubular cell damage, inflammation, mitochondrial morphology of proximal tubular cells (PTCs), apoptosis, autophagy and activation of mammalian target of rapamycin complex 1 (mTORC1).
Results
Kidney weight, albuminuria, excretion of urinary liver-type fatty acid binding protein, levels of plasma cystatin C and changes in renal histology, including fibrosis, tubular cell damage and inflammation, were aggravated in WFRs compared with non-diabetic Wistar lean rats (WLRs). Fragmented and swelling mitochondria accumulated in PTCs and apoptosis were enhanced in the kidney of WFRs. Immunohistochemical staining of p62 and p-S6 ribosomal protein (p-S6RP) in the tubular lesions of WFRs was increased compared with WLRs. The LPD intervention clearly ameliorated damage as shown by the assessment of renal function and histology, particularly tubulointerstitial damage in diabetic kidneys. Additionally, the 5.77% LPD, but not the 11.46% LPD, significantly suppressed p-S6RP levels and increased microtubule-associated protein light chain 3-II levels in the renal cortex. The LPD intervention partially decreased HbA
1c
levels in WFRs, and no differences in mean BP were observed among any of the groups.
Conclusions/interpretation
A very-low-protein diet improved advanced diabetic renal injuries, including tubulointerstitial damage, by restoring autophagy through the suppression of the mTORC1 pathway.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Autophagy - genetics</subject><subject>Autophagy - physiology</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - diet therapy</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diabetic Nephropathies - diet therapy</subject><subject>Diabetic Nephropathies - metabolism</subject><subject>Diabetic Nephropathies - pathology</subject><subject>Diabetic nephropathy</subject><subject>Diet, Protein-Restricted</subject><subject>Disease Models, Animal</subject><subject>Fatty acids</subject><subject>Histology</subject><subject>Human Physiology</subject><subject>Immunohistochemistry</subject><subject>Internal Medicine</subject><subject>Kidneys</subject><subject>Male</subject><subject>Malnutrition</subject><subject>Mechanistic Target of Rapamycin Complex 1</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Microscopy, Electron, Transmission</subject><subject>Multiprotein Complexes - genetics</subject><subject>Multiprotein Complexes - metabolism</subject><subject>Obesity</subject><subject>Obesity - diet therapy</subject><subject>Obesity - metabolism</subject><subject>Obesity - pathology</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>TOR Serine-Threonine Kinases - genetics</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kV2L1TAQhoMo7rr6A7yRgDdeWM1Xk_RyOfgFCwuyonclbabnZGmTmqS79Bf6t0w9RxFBCGSGed6ZSV6EnlPyhhKi3iZCKKsrQmXFmxKIB-icCs4qIph-iM63ckW1_HaGnqR0SwjhtZCP0RlThBEhmnP04xLfQVyrMdxXcwwZnMfWQcZmgtGFaDIkbOyd8T3YUjEdZNdjD_Mhhtnkw4pziZb9AZslh_lg9it23i59dsHjbsVpmecIKW1pGAoNeLq5_ryjeJPfmw3HX13KJuLB5LziMjS9xsaX4yYz4ilYGH9p1xkwO22x7eUtDh0kl9en6NFgxgTPTvcF-vL-3c3uY3V1_eHT7vKq6oWmuVKSUjFw3RhFZMcIEdZSRvlAeCO1MlzWVIsGup5oTrmtFZMNh4ESBbKuNb9Ar459y2d9XyDldnKph3E0HsKSWqq0ZkxSzgr68h_0NizRl-02SinSMC4KRY9UH0NKEYZ2juXVcW0paTeX26PLbXG53VxuN82LU-elm8D-Ufy2tQDsCKRS8nuIf43-b9efrH6z2Q</recordid><startdate>20160601</startdate><enddate>20160601</enddate><creator>Kitada, Munehiro</creator><creator>Ogura, Yoshio</creator><creator>Suzuki, Taeko</creator><creator>Sen, Shi</creator><creator>Lee, Seon Myeong</creator><creator>Kanasaki, Keizo</creator><creator>Kume, Shinji</creator><creator>Koya, Daisuke</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20160601</creationdate><title>A very-low-protein diet ameliorates advanced diabetic nephropathy through autophagy induction by suppression of the mTORC1 pathway in Wistar fatty rats, an animal model of type 2 diabetes and obesity</title><author>Kitada, Munehiro ; Ogura, Yoshio ; Suzuki, Taeko ; Sen, Shi ; Lee, Seon Myeong ; Kanasaki, Keizo ; Kume, Shinji ; Koya, Daisuke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-76114f389a706b2004dd1213f039687a3651849ebc08313d572693ef107e65583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Autophagy - genetics</topic><topic>Autophagy - physiology</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - diet therapy</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diabetic Nephropathies - diet therapy</topic><topic>Diabetic Nephropathies - metabolism</topic><topic>Diabetic Nephropathies - pathology</topic><topic>Diabetic nephropathy</topic><topic>Diet, Protein-Restricted</topic><topic>Disease Models, Animal</topic><topic>Fatty acids</topic><topic>Histology</topic><topic>Human Physiology</topic><topic>Immunohistochemistry</topic><topic>Internal Medicine</topic><topic>Kidneys</topic><topic>Male</topic><topic>Malnutrition</topic><topic>Mechanistic Target of Rapamycin Complex 1</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Microscopy, Electron, Transmission</topic><topic>Multiprotein Complexes - genetics</topic><topic>Multiprotein Complexes - metabolism</topic><topic>Obesity</topic><topic>Obesity - diet therapy</topic><topic>Obesity - metabolism</topic><topic>Obesity - pathology</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>TOR Serine-Threonine Kinases - genetics</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kitada, Munehiro</creatorcontrib><creatorcontrib>Ogura, Yoshio</creatorcontrib><creatorcontrib>Suzuki, Taeko</creatorcontrib><creatorcontrib>Sen, Shi</creatorcontrib><creatorcontrib>Lee, Seon Myeong</creatorcontrib><creatorcontrib>Kanasaki, Keizo</creatorcontrib><creatorcontrib>Kume, Shinji</creatorcontrib><creatorcontrib>Koya, Daisuke</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kitada, Munehiro</au><au>Ogura, Yoshio</au><au>Suzuki, Taeko</au><au>Sen, Shi</au><au>Lee, Seon Myeong</au><au>Kanasaki, Keizo</au><au>Kume, Shinji</au><au>Koya, Daisuke</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A very-low-protein diet ameliorates advanced diabetic nephropathy through autophagy induction by suppression of the mTORC1 pathway in Wistar fatty rats, an animal model of type 2 diabetes and obesity</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2016-06-01</date><risdate>2016</risdate><volume>59</volume><issue>6</issue><spage>1307</spage><epage>1317</epage><pages>1307-1317</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aims/hypothesis
The efficacy of a low-protein diet (LPD) on diabetic nephropathy is controversial. We aimed to investigate the renoprotective effects of an LPD and the underlying molecular mechanism in a rat model of type 2 diabetes and obesity.
Methods
Diabetic male Wistar fatty (
fa
/
fa
) rats (WFRs) were treated with a standard diet (23.84% protein) or an LPD (5.77% protein) for 20 weeks from 24 weeks of age. We investigated the effect of the LPD on renal function, fibrosis, tubular cell damage, inflammation, mitochondrial morphology of proximal tubular cells (PTCs), apoptosis, autophagy and activation of mammalian target of rapamycin complex 1 (mTORC1).
Results
Kidney weight, albuminuria, excretion of urinary liver-type fatty acid binding protein, levels of plasma cystatin C and changes in renal histology, including fibrosis, tubular cell damage and inflammation, were aggravated in WFRs compared with non-diabetic Wistar lean rats (WLRs). Fragmented and swelling mitochondria accumulated in PTCs and apoptosis were enhanced in the kidney of WFRs. Immunohistochemical staining of p62 and p-S6 ribosomal protein (p-S6RP) in the tubular lesions of WFRs was increased compared with WLRs. The LPD intervention clearly ameliorated damage as shown by the assessment of renal function and histology, particularly tubulointerstitial damage in diabetic kidneys. Additionally, the 5.77% LPD, but not the 11.46% LPD, significantly suppressed p-S6RP levels and increased microtubule-associated protein light chain 3-II levels in the renal cortex. The LPD intervention partially decreased HbA
1c
levels in WFRs, and no differences in mean BP were observed among any of the groups.
Conclusions/interpretation
A very-low-protein diet improved advanced diabetic renal injuries, including tubulointerstitial damage, by restoring autophagy through the suppression of the mTORC1 pathway.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>27020449</pmid><doi>10.1007/s00125-016-3925-4</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animals Apoptosis Autophagy Autophagy - genetics Autophagy - physiology Diabetes Diabetes Mellitus, Type 2 - diet therapy Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - pathology Diabetic Nephropathies - diet therapy Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology Diabetic nephropathy Diet, Protein-Restricted Disease Models, Animal Fatty acids Histology Human Physiology Immunohistochemistry Internal Medicine Kidneys Male Malnutrition Mechanistic Target of Rapamycin Complex 1 Medicine Medicine & Public Health Metabolic Diseases Microscopy, Electron, Transmission Multiprotein Complexes - genetics Multiprotein Complexes - metabolism Obesity Obesity - diet therapy Obesity - metabolism Obesity - pathology Proteins Rats Rats, Wistar Real-Time Polymerase Chain Reaction TOR Serine-Threonine Kinases - genetics TOR Serine-Threonine Kinases - metabolism |
| title | A very-low-protein diet ameliorates advanced diabetic nephropathy through autophagy induction by suppression of the mTORC1 pathway in Wistar fatty rats, an animal model of type 2 diabetes and obesity |
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