Protection by beta-Hydroxybutyric acid against insulin glycation, lipid peroxidation and microglial cell apoptosis
Background Diabetes mellitus is characterized jointly by hyperglycemia and hyperinsulinemia that make insulin more prone to be glycated and evolve insulin advanced glycation end products (Insulin- AGE). Here, we report the effect of beta-hydroxy butyrate (BHB) (the predominant ketone body) on the fo...
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| Veröffentlicht in: | Daru 2015-08, Vol.23 (1), p.42-42, Article 42 |
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| creator | Sabokdast, Manijheh Habibi-Rezaei, Mehran Moosavi-Movahedi, Ali Akbar Ferdousi, Maryam Azimzadeh-Irani, Effat Poursasan, Najmeh |
| description | Background
Diabetes mellitus is characterized jointly by hyperglycemia and hyperinsulinemia that make insulin more prone to be glycated and evolve insulin advanced glycation end products (Insulin- AGE). Here, we report the effect of beta-hydroxy butyrate (BHB) (the predominant ketone body) on the formation of insulin-AGE, insulin glycation derived liposomal lipid peroxidation and insulin-AGE toxicity in microglial cells.
Methods
The inhibitory effect of BHB was monitored as a result of insulin incubation in the presence of glucose or fructose using AGE-dependent fluorescence, Tyr fluorescence as well as anilinonaphthalenesulfonate (ANS) andthioflavin T (ThT) binding, and circular dichroism (CD) investigations. To study lipid peroxidation induced by insulin glycation, thiobarbituric acid (TBA) assay and thiobarbituric acid reactive substance (TBARS) monitoring were used. The effect of insulin–AGE on microglial viability was investigated by 3-(4, 5 dimethylthiazol-2-yl)—2, 5-diphenyltetrazoliumbromide (MTT) cell assay and Annexin V/propidium iodide (PI) staining.
Results
Here we are reporting the inhibitory effect of BHB on insulin glycation and generation of insulin-AGE as a possible explanation for insulin resistance. Moreover, the protective effect of BHB on consequential glycation derived liposomal lipid peroxidation as a causative event in microglial apoptosis is reported.
Conclusion
The reduced insulin fibril formation, structural inertia to glycation involved conformational changes, anti-lipid peroxidation effect, and increasing microglia viability indicated the protective effect of BHB that disclose insight on the possible preventive effect of BHB on Alzheimer’s disease. |
| doi_str_mv | 10.1186/s40199-015-0126-5 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4551523</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A541669076</galeid><sourcerecordid>A541669076</sourcerecordid><originalsourceid>FETCH-LOGICAL-c568t-cb6b681bf30e60c64ab0c29e4bea0d846d1809410115630073ee7e5ef1d634e3</originalsourceid><addsrcrecordid>eNp1kk2L1TAYhYsozjj6A9xIQBAXdsxHk7YbYRjUEQZ0MfuQpm97M-QmNUnF_ntTex3uFaX0g-Q5p5w3pyheEnxJSCPexwqTti0x4fmmouSPinOKcVNSysjjo--z4lmM9xizphL0aXFGBSNE0Pq8CN-CT6CT8Q51C-ogqfJm6YP_uXRzWoLRSGnTIzUq42JC-TFb49BoF61W1TtkzZSBCbLG9L_XkHI92hsd_GiNskiDtUhNfko-mvi8eDIoG-HF4X1R3H36eHd9U95-_fzl-uq21Fw0qdSd6ERDuoFhEFiLSnVY0xaqDhTuc5CeNLitCCaEC4ZxzQBq4DCQXrAK2EXxYbOd5m4PvQaXgrJyCmavwiK9MvJ0x5mdHP0PWXFOOGXZ4O3BIPjvM8Qk9yauUZQDP0dJatw0LROYZ_T1X-i9n4PL6TJVU9w2m-GBGpUFadzg83_1aiqveEWEaHEtMnX5DypfPeSRegeDyesngjdHgh0om3bR23k9iXgKkg3MBxNjgOFhGATLtVByK5TMhZJroeSa7NXxFB8UfxqUAboBMW-5EcJR9P-6_gIA3tZV</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1772098523</pqid></control><display><type>article</type><title>Protection by beta-Hydroxybutyric acid against insulin glycation, lipid peroxidation and microglial cell apoptosis</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><creator>Sabokdast, Manijheh ; Habibi-Rezaei, Mehran ; Moosavi-Movahedi, Ali Akbar ; Ferdousi, Maryam ; Azimzadeh-Irani, Effat ; Poursasan, Najmeh</creator><creatorcontrib>Sabokdast, Manijheh ; Habibi-Rezaei, Mehran ; Moosavi-Movahedi, Ali Akbar ; Ferdousi, Maryam ; Azimzadeh-Irani, Effat ; Poursasan, Najmeh</creatorcontrib><description>Background
Diabetes mellitus is characterized jointly by hyperglycemia and hyperinsulinemia that make insulin more prone to be glycated and evolve insulin advanced glycation end products (Insulin- AGE). Here, we report the effect of beta-hydroxy butyrate (BHB) (the predominant ketone body) on the formation of insulin-AGE, insulin glycation derived liposomal lipid peroxidation and insulin-AGE toxicity in microglial cells.
Methods
The inhibitory effect of BHB was monitored as a result of insulin incubation in the presence of glucose or fructose using AGE-dependent fluorescence, Tyr fluorescence as well as anilinonaphthalenesulfonate (ANS) andthioflavin T (ThT) binding, and circular dichroism (CD) investigations. To study lipid peroxidation induced by insulin glycation, thiobarbituric acid (TBA) assay and thiobarbituric acid reactive substance (TBARS) monitoring were used. The effect of insulin–AGE on microglial viability was investigated by 3-(4, 5 dimethylthiazol-2-yl)—2, 5-diphenyltetrazoliumbromide (MTT) cell assay and Annexin V/propidium iodide (PI) staining.
Results
Here we are reporting the inhibitory effect of BHB on insulin glycation and generation of insulin-AGE as a possible explanation for insulin resistance. Moreover, the protective effect of BHB on consequential glycation derived liposomal lipid peroxidation as a causative event in microglial apoptosis is reported.
Conclusion
The reduced insulin fibril formation, structural inertia to glycation involved conformational changes, anti-lipid peroxidation effect, and increasing microglia viability indicated the protective effect of BHB that disclose insight on the possible preventive effect of BHB on Alzheimer’s disease.</description><identifier>ISSN: 2008-2231</identifier><identifier>ISSN: 1560-8115</identifier><identifier>EISSN: 2008-2231</identifier><identifier>DOI: 10.1186/s40199-015-0126-5</identifier><identifier>PMID: 26311627</identifier><language>eng</language><publisher>London: BioMed Central</publisher><subject>3-Hydroxybutyric Acid - pharmacology ; Animals ; Apoptosis ; Apoptosis - drug effects ; Biomedical and Life Sciences ; Biomedicine ; Circular Dichroism ; Development and progression ; Dextrose ; Esters ; Fluorescence ; Fructose ; Genetic aspects ; Glucose ; Glycosylation ; Health aspects ; Hyperglycemia ; Insulin ; Insulin - metabolism ; Insulin resistance ; Lipid peroxidation ; Lipid Peroxidation - drug effects ; Liposomes ; Medicinal Chemistry ; Microglia - drug effects ; Pharmaceutical Sciences/Technology ; Pharmacology/Toxicology ; Rats, Wistar ; Research Article ; Type 2 diabetes</subject><ispartof>Daru, 2015-08, Vol.23 (1), p.42-42, Article 42</ispartof><rights>Sabokdast et al. 2015</rights><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Copyright BioMed Central Aug 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c568t-cb6b681bf30e60c64ab0c29e4bea0d846d1809410115630073ee7e5ef1d634e3</citedby><cites>FETCH-LOGICAL-c568t-cb6b681bf30e60c64ab0c29e4bea0d846d1809410115630073ee7e5ef1d634e3</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/PMC4551523/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4551523/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26311627$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sabokdast, Manijheh</creatorcontrib><creatorcontrib>Habibi-Rezaei, Mehran</creatorcontrib><creatorcontrib>Moosavi-Movahedi, Ali Akbar</creatorcontrib><creatorcontrib>Ferdousi, Maryam</creatorcontrib><creatorcontrib>Azimzadeh-Irani, Effat</creatorcontrib><creatorcontrib>Poursasan, Najmeh</creatorcontrib><title>Protection by beta-Hydroxybutyric acid against insulin glycation, lipid peroxidation and microglial cell apoptosis</title><title>Daru</title><addtitle>DARU J Pharm Sci</addtitle><addtitle>Daru</addtitle><description>Background
Diabetes mellitus is characterized jointly by hyperglycemia and hyperinsulinemia that make insulin more prone to be glycated and evolve insulin advanced glycation end products (Insulin- AGE). Here, we report the effect of beta-hydroxy butyrate (BHB) (the predominant ketone body) on the formation of insulin-AGE, insulin glycation derived liposomal lipid peroxidation and insulin-AGE toxicity in microglial cells.
Methods
The inhibitory effect of BHB was monitored as a result of insulin incubation in the presence of glucose or fructose using AGE-dependent fluorescence, Tyr fluorescence as well as anilinonaphthalenesulfonate (ANS) andthioflavin T (ThT) binding, and circular dichroism (CD) investigations. To study lipid peroxidation induced by insulin glycation, thiobarbituric acid (TBA) assay and thiobarbituric acid reactive substance (TBARS) monitoring were used. The effect of insulin–AGE on microglial viability was investigated by 3-(4, 5 dimethylthiazol-2-yl)—2, 5-diphenyltetrazoliumbromide (MTT) cell assay and Annexin V/propidium iodide (PI) staining.
Results
Here we are reporting the inhibitory effect of BHB on insulin glycation and generation of insulin-AGE as a possible explanation for insulin resistance. Moreover, the protective effect of BHB on consequential glycation derived liposomal lipid peroxidation as a causative event in microglial apoptosis is reported.
Conclusion
The reduced insulin fibril formation, structural inertia to glycation involved conformational changes, anti-lipid peroxidation effect, and increasing microglia viability indicated the protective effect of BHB that disclose insight on the possible preventive effect of BHB on Alzheimer’s disease.</description><subject>3-Hydroxybutyric Acid - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Circular Dichroism</subject><subject>Development and progression</subject><subject>Dextrose</subject><subject>Esters</subject><subject>Fluorescence</subject><subject>Fructose</subject><subject>Genetic aspects</subject><subject>Glucose</subject><subject>Glycosylation</subject><subject>Health aspects</subject><subject>Hyperglycemia</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin resistance</subject><subject>Lipid peroxidation</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Liposomes</subject><subject>Medicinal Chemistry</subject><subject>Microglia - drug effects</subject><subject>Pharmaceutical Sciences/Technology</subject><subject>Pharmacology/Toxicology</subject><subject>Rats, Wistar</subject><subject>Research Article</subject><subject>Type 2 diabetes</subject><issn>2008-2231</issn><issn>1560-8115</issn><issn>2008-2231</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kk2L1TAYhYsozjj6A9xIQBAXdsxHk7YbYRjUEQZ0MfuQpm97M-QmNUnF_ntTex3uFaX0g-Q5p5w3pyheEnxJSCPexwqTti0x4fmmouSPinOKcVNSysjjo--z4lmM9xizphL0aXFGBSNE0Pq8CN-CT6CT8Q51C-ogqfJm6YP_uXRzWoLRSGnTIzUq42JC-TFb49BoF61W1TtkzZSBCbLG9L_XkHI92hsd_GiNskiDtUhNfko-mvi8eDIoG-HF4X1R3H36eHd9U95-_fzl-uq21Fw0qdSd6ERDuoFhEFiLSnVY0xaqDhTuc5CeNLitCCaEC4ZxzQBq4DCQXrAK2EXxYbOd5m4PvQaXgrJyCmavwiK9MvJ0x5mdHP0PWXFOOGXZ4O3BIPjvM8Qk9yauUZQDP0dJatw0LROYZ_T1X-i9n4PL6TJVU9w2m-GBGpUFadzg83_1aiqveEWEaHEtMnX5DypfPeSRegeDyesngjdHgh0om3bR23k9iXgKkg3MBxNjgOFhGATLtVByK5TMhZJroeSa7NXxFB8UfxqUAboBMW-5EcJR9P-6_gIA3tZV</recordid><startdate>20150827</startdate><enddate>20150827</enddate><creator>Sabokdast, Manijheh</creator><creator>Habibi-Rezaei, Mehran</creator><creator>Moosavi-Movahedi, Ali Akbar</creator><creator>Ferdousi, Maryam</creator><creator>Azimzadeh-Irani, Effat</creator><creator>Poursasan, Najmeh</creator><general>BioMed Central</general><general>BioMed Central Ltd</general><general>Springer Nature B.V</general><scope>C6C</scope><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PADUT</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150827</creationdate><title>Protection by beta-Hydroxybutyric acid against insulin glycation, lipid peroxidation and microglial cell apoptosis</title><author>Sabokdast, Manijheh ; Habibi-Rezaei, Mehran ; Moosavi-Movahedi, Ali Akbar ; Ferdousi, Maryam ; Azimzadeh-Irani, Effat ; Poursasan, Najmeh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c568t-cb6b681bf30e60c64ab0c29e4bea0d846d1809410115630073ee7e5ef1d634e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>3-Hydroxybutyric Acid - pharmacology</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Circular Dichroism</topic><topic>Development and progression</topic><topic>Dextrose</topic><topic>Esters</topic><topic>Fluorescence</topic><topic>Fructose</topic><topic>Genetic aspects</topic><topic>Glucose</topic><topic>Glycosylation</topic><topic>Health aspects</topic><topic>Hyperglycemia</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Insulin resistance</topic><topic>Lipid peroxidation</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Liposomes</topic><topic>Medicinal Chemistry</topic><topic>Microglia - drug effects</topic><topic>Pharmaceutical Sciences/Technology</topic><topic>Pharmacology/Toxicology</topic><topic>Rats, Wistar</topic><topic>Research Article</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sabokdast, Manijheh</creatorcontrib><creatorcontrib>Habibi-Rezaei, Mehran</creatorcontrib><creatorcontrib>Moosavi-Movahedi, Ali Akbar</creatorcontrib><creatorcontrib>Ferdousi, Maryam</creatorcontrib><creatorcontrib>Azimzadeh-Irani, Effat</creatorcontrib><creatorcontrib>Poursasan, Najmeh</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Middle East & Africa Database</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Research Library China</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Daru</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sabokdast, Manijheh</au><au>Habibi-Rezaei, Mehran</au><au>Moosavi-Movahedi, Ali Akbar</au><au>Ferdousi, Maryam</au><au>Azimzadeh-Irani, Effat</au><au>Poursasan, Najmeh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protection by beta-Hydroxybutyric acid against insulin glycation, lipid peroxidation and microglial cell apoptosis</atitle><jtitle>Daru</jtitle><stitle>DARU J Pharm Sci</stitle><addtitle>Daru</addtitle><date>2015-08-27</date><risdate>2015</risdate><volume>23</volume><issue>1</issue><spage>42</spage><epage>42</epage><pages>42-42</pages><artnum>42</artnum><issn>2008-2231</issn><issn>1560-8115</issn><eissn>2008-2231</eissn><abstract>Background
Diabetes mellitus is characterized jointly by hyperglycemia and hyperinsulinemia that make insulin more prone to be glycated and evolve insulin advanced glycation end products (Insulin- AGE). Here, we report the effect of beta-hydroxy butyrate (BHB) (the predominant ketone body) on the formation of insulin-AGE, insulin glycation derived liposomal lipid peroxidation and insulin-AGE toxicity in microglial cells.
Methods
The inhibitory effect of BHB was monitored as a result of insulin incubation in the presence of glucose or fructose using AGE-dependent fluorescence, Tyr fluorescence as well as anilinonaphthalenesulfonate (ANS) andthioflavin T (ThT) binding, and circular dichroism (CD) investigations. To study lipid peroxidation induced by insulin glycation, thiobarbituric acid (TBA) assay and thiobarbituric acid reactive substance (TBARS) monitoring were used. The effect of insulin–AGE on microglial viability was investigated by 3-(4, 5 dimethylthiazol-2-yl)—2, 5-diphenyltetrazoliumbromide (MTT) cell assay and Annexin V/propidium iodide (PI) staining.
Results
Here we are reporting the inhibitory effect of BHB on insulin glycation and generation of insulin-AGE as a possible explanation for insulin resistance. Moreover, the protective effect of BHB on consequential glycation derived liposomal lipid peroxidation as a causative event in microglial apoptosis is reported.
Conclusion
The reduced insulin fibril formation, structural inertia to glycation involved conformational changes, anti-lipid peroxidation effect, and increasing microglia viability indicated the protective effect of BHB that disclose insight on the possible preventive effect of BHB on Alzheimer’s disease.</abstract><cop>London</cop><pub>BioMed Central</pub><pmid>26311627</pmid><doi>10.1186/s40199-015-0126-5</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3-Hydroxybutyric Acid - pharmacology Animals Apoptosis Apoptosis - drug effects Biomedical and Life Sciences Biomedicine Circular Dichroism Development and progression Dextrose Esters Fluorescence Fructose Genetic aspects Glucose Glycosylation Health aspects Hyperglycemia Insulin Insulin - metabolism Insulin resistance Lipid peroxidation Lipid Peroxidation - drug effects Liposomes Medicinal Chemistry Microglia - drug effects Pharmaceutical Sciences/Technology Pharmacology/Toxicology Rats, Wistar Research Article Type 2 diabetes |
| title | Protection by beta-Hydroxybutyric acid against insulin glycation, lipid peroxidation and microglial cell apoptosis |
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