Omega-3 polyunsaturated fatty acids preserve retinal function in type 2 diabetic mice

Objective: Diabetic retinopathy (DR) is associated with hyperglycemia-driven microvascular pathology and neuronal compromise in the retina. However, DR is also linked to dyslipidemia. As omega-3 (ω-3) polyunsaturated fatty acids (PUFAs) are protective in proliferative retinopathy, we investigated th...

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Veröffentlicht in:Nutrition & diabetes 2012-07, Vol.2 (7), p.e36-e36
Hauptverfasser: Sapieha, P, Chen, J, Stahl, A, Seaward, M R, Favazza, T L, Juan, A M, Hatton, C J, Joyal, J-S, Krah, N M, Dennison, R J, Tang, J, Kern, T S, Akula, J D, Smith, L E H
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container_end_page e36
container_issue 7
container_start_page e36
container_title Nutrition & diabetes
container_volume 2
creator Sapieha, P
Chen, J
Stahl, A
Seaward, M R
Favazza, T L
Juan, A M
Hatton, C J
Joyal, J-S
Krah, N M
Dennison, R J
Tang, J
Kern, T S
Akula, J D
Smith, L E H
description Objective: Diabetic retinopathy (DR) is associated with hyperglycemia-driven microvascular pathology and neuronal compromise in the retina. However, DR is also linked to dyslipidemia. As omega-3 (ω-3) polyunsaturated fatty acids (PUFAs) are protective in proliferative retinopathy, we investigated the capacity of ω-3PUFAs to preserve retinal function in a mouse model of type 2 diabetes mellitus (T2DM). Design: Male leptin-receptor-deficient ( db/db ) mice were maintained for 22 weeks (4 weeks–26 weeks of life) on calorically and compositionally matched diets, except for 2% enrichment in either ω-3 or ω-6PUFAs. Visual function was assessed at 9, 14 and 26 weeks by electroretinography. Retinal capillary and neuronal integrity, as well as glucose challenge responses, were assessed on each diet. Results: The ω-3PUFA diet significantly preserved retinal function in the mouse model of T2DM to levels similar to those observed in nondiabetic control mice on normal chow. Conversely, retinal function gradually deteriorated in db/db mice on a ω-6PUFA-rich diet. There was also an enhanced ability of ω-3PUFA-fed mice to respond to glucose challenge. The protection of visual function appeared to be independent of cytoprotective or anti-inflammatory effects of ω-3PUFAs. Conclusion: This study identifies beneficial effects of dietary ω-3PUFAs on visual function in T2DM. The data are consistent with dyslipidemia negatively impacting retinal function. As ω-3PUFA lipid dietary interventions are readily available, safe and inexpensive, increasing ω-3PUFA intake in diabetic patients may slow the progression of vision loss in T2DM.
doi_str_mv 10.1038/nutd.2012.10
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However, DR is also linked to dyslipidemia. As omega-3 (ω-3) polyunsaturated fatty acids (PUFAs) are protective in proliferative retinopathy, we investigated the capacity of ω-3PUFAs to preserve retinal function in a mouse model of type 2 diabetes mellitus (T2DM). Design: Male leptin-receptor-deficient ( db/db ) mice were maintained for 22 weeks (4 weeks–26 weeks of life) on calorically and compositionally matched diets, except for 2% enrichment in either ω-3 or ω-6PUFAs. Visual function was assessed at 9, 14 and 26 weeks by electroretinography. Retinal capillary and neuronal integrity, as well as glucose challenge responses, were assessed on each diet. Results: The ω-3PUFA diet significantly preserved retinal function in the mouse model of T2DM to levels similar to those observed in nondiabetic control mice on normal chow. Conversely, retinal function gradually deteriorated in db/db mice on a ω-6PUFA-rich diet. There was also an enhanced ability of ω-3PUFA-fed mice to respond to glucose challenge. The protection of visual function appeared to be independent of cytoprotective or anti-inflammatory effects of ω-3PUFAs. Conclusion: This study identifies beneficial effects of dietary ω-3PUFAs on visual function in T2DM. The data are consistent with dyslipidemia negatively impacting retinal function. As ω-3PUFA lipid dietary interventions are readily available, safe and inexpensive, increasing ω-3PUFA intake in diabetic patients may slow the progression of vision loss in T2DM.</description><identifier>ISSN: 2044-4052</identifier><identifier>EISSN: 2044-4052</identifier><identifier>DOI: 10.1038/nutd.2012.10</identifier><identifier>PMID: 23448719</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>692/699/2743/137/138 ; 692/699/2743/137/773 ; 692/700/139/1449 ; 692/700/459/1994 ; Clinical Nutrition ; Diabetes ; Epidemiology ; Internal Medicine ; Medicine ; Medicine &amp; Public Health ; Metabolic Diseases ; Original ; original-article</subject><ispartof>Nutrition &amp; diabetes, 2012-07, Vol.2 (7), p.e36-e36</ispartof><rights>The Author(s) 2012</rights><rights>Copyright Nature Publishing Group Jul 2012</rights><rights>Copyright © 2012 Macmillan Publishers Limited 2012 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c516t-67b3f57af820f974363e717b09d19a887c752695f0b22239276d9a40a05c4c983</citedby><cites>FETCH-LOGICAL-c516t-67b3f57af820f974363e717b09d19a887c752695f0b22239276d9a40a05c4c983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408641/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408641/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23448719$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sapieha, P</creatorcontrib><creatorcontrib>Chen, J</creatorcontrib><creatorcontrib>Stahl, A</creatorcontrib><creatorcontrib>Seaward, M R</creatorcontrib><creatorcontrib>Favazza, T L</creatorcontrib><creatorcontrib>Juan, A M</creatorcontrib><creatorcontrib>Hatton, C J</creatorcontrib><creatorcontrib>Joyal, J-S</creatorcontrib><creatorcontrib>Krah, N M</creatorcontrib><creatorcontrib>Dennison, R J</creatorcontrib><creatorcontrib>Tang, J</creatorcontrib><creatorcontrib>Kern, T S</creatorcontrib><creatorcontrib>Akula, J D</creatorcontrib><creatorcontrib>Smith, L E H</creatorcontrib><title>Omega-3 polyunsaturated fatty acids preserve retinal function in type 2 diabetic mice</title><title>Nutrition &amp; diabetes</title><addtitle>Nutr &amp; Diabetes</addtitle><addtitle>Nutr Diabetes</addtitle><description>Objective: Diabetic retinopathy (DR) is associated with hyperglycemia-driven microvascular pathology and neuronal compromise in the retina. 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diabetes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sapieha, P</au><au>Chen, J</au><au>Stahl, A</au><au>Seaward, M R</au><au>Favazza, T L</au><au>Juan, A M</au><au>Hatton, C J</au><au>Joyal, J-S</au><au>Krah, N M</au><au>Dennison, R J</au><au>Tang, J</au><au>Kern, T S</au><au>Akula, J D</au><au>Smith, L E H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Omega-3 polyunsaturated fatty acids preserve retinal function in type 2 diabetic mice</atitle><jtitle>Nutrition &amp; diabetes</jtitle><stitle>Nutr &amp; Diabetes</stitle><addtitle>Nutr Diabetes</addtitle><date>2012-07-23</date><risdate>2012</risdate><volume>2</volume><issue>7</issue><spage>e36</spage><epage>e36</epage><pages>e36-e36</pages><issn>2044-4052</issn><eissn>2044-4052</eissn><abstract>Objective: Diabetic retinopathy (DR) is associated with hyperglycemia-driven microvascular pathology and neuronal compromise in the retina. However, DR is also linked to dyslipidemia. As omega-3 (ω-3) polyunsaturated fatty acids (PUFAs) are protective in proliferative retinopathy, we investigated the capacity of ω-3PUFAs to preserve retinal function in a mouse model of type 2 diabetes mellitus (T2DM). Design: Male leptin-receptor-deficient ( db/db ) mice were maintained for 22 weeks (4 weeks–26 weeks of life) on calorically and compositionally matched diets, except for 2% enrichment in either ω-3 or ω-6PUFAs. Visual function was assessed at 9, 14 and 26 weeks by electroretinography. Retinal capillary and neuronal integrity, as well as glucose challenge responses, were assessed on each diet. Results: The ω-3PUFA diet significantly preserved retinal function in the mouse model of T2DM to levels similar to those observed in nondiabetic control mice on normal chow. Conversely, retinal function gradually deteriorated in db/db mice on a ω-6PUFA-rich diet. There was also an enhanced ability of ω-3PUFA-fed mice to respond to glucose challenge. The protection of visual function appeared to be independent of cytoprotective or anti-inflammatory effects of ω-3PUFAs. Conclusion: This study identifies beneficial effects of dietary ω-3PUFAs on visual function in T2DM. The data are consistent with dyslipidemia negatively impacting retinal function. As ω-3PUFA lipid dietary interventions are readily available, safe and inexpensive, increasing ω-3PUFA intake in diabetic patients may slow the progression of vision loss in T2DM.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>23448719</pmid><doi>10.1038/nutd.2012.10</doi><oa>free_for_read</oa></addata></record>
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subjects 692/699/2743/137/138
692/699/2743/137/773
692/700/139/1449
692/700/459/1994
Clinical Nutrition
Diabetes
Epidemiology
Internal Medicine
Medicine
Medicine & Public Health
Metabolic Diseases
Original
original-article
title Omega-3 polyunsaturated fatty acids preserve retinal function in type 2 diabetic mice
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