DPP-4 Inhibitor and PPARγ Agonist Restore the Loss of CA1 Dendritic Spines in Obese Insulin-resistant Rats

© 2014 IMSS. Background and Aims: Obesity induced by high-fat diet (HFD) impaired brain insulin receptor function, caused cognitive decline as well as reduced dendritic spine density. Previous studies suggested that dipeptidyl peptidase IV (DPP-4) inhibitor and peroxisome proliferator-activated rece...

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Main Authors: Sripetchwandee,J., Pipatpiboon,N., Pratchayasakul,W., Chattipakorn,N., Chattipakorn,S.C.
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Published: Elsevier Inc. 2015
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spelling th-cmuir.6653943832-383462015-06-16T07:47:02Z DPP-4 Inhibitor and PPARγ Agonist Restore the Loss of CA1 Dendritic Spines in Obese Insulin-resistant Rats Sripetchwandee,J. Pipatpiboon,N. Pratchayasakul,W. Chattipakorn,N. Chattipakorn,S.C. Medicine (all) © 2014 IMSS. Background and Aims: Obesity induced by high-fat diet (HFD) impaired brain insulin receptor function, caused cognitive decline as well as reduced dendritic spine density. Previous studies suggested that dipeptidyl peptidase IV (DPP-4) inhibitor and peroxisome proliferator-activated receptor-gamma (PPARγ) agonist exerted the neuroprotective effects in obese insulin-resistant rats. However, the effects of these drugs on dendritic spines in obese insulin-resistant rats have not yet been investigated. In the present study, we determined the effects of DPP-4 inhibitor and PPARγ agonist on dendritic spines density of obese insulin-resistant rats caused by HFD. Methods: Male Wistar Rats were divided into two groups. Animals in each group were fed with normal diet (ND) or HFD for 12weeks. After then, rats in each group were subdivided into three subgroups to receive either vehicle or vildagliptin (3mg/kg/day) or pioglitazone (10mg/kg/day) for 3-4weeks. At the end of the experiment, the metabolic parameters and density of dendritic spines in CA1 hippocampus were determined. Results: We found that HFD-fed rats caused peripheral insulin resistance as well as the reduction of the density of dendritic spines in CA1 hippocampus. Treatment with both DPP-4 inhibitor and PPARγ agonist in HFD-fed rats improved insulin sensitivity as well as increased the number of dendritic spines in CA1 hippocampus. Moreover, both drugs have equally improved this deterioration. Conclusion: Our findings indicate that DPP-4 inhibitor and PPARγ agonist restored the reduction of dendritic spines caused by HFD, suggesting the beneficial roles of DPP-4 inhibitors and PPARγ agonists in neurodegenerative disorders. 2015-06-16T07:47:02Z 2015-06-16T07:47:02Z 2014-01-01 Article 01884409 2-s2.0-84915816950 10.1016/j.arcmed.2014.09.002 http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84915816950&origin=inward http://cmuir.cmu.ac.th/handle/6653943832/38346 Elsevier Inc.
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
collection CMU Intellectual Repository
topic Medicine (all)
spellingShingle Medicine (all)
Sripetchwandee,J.
Pipatpiboon,N.
Pratchayasakul,W.
Chattipakorn,N.
Chattipakorn,S.C.
DPP-4 Inhibitor and PPARγ Agonist Restore the Loss of CA1 Dendritic Spines in Obese Insulin-resistant Rats
description © 2014 IMSS. Background and Aims: Obesity induced by high-fat diet (HFD) impaired brain insulin receptor function, caused cognitive decline as well as reduced dendritic spine density. Previous studies suggested that dipeptidyl peptidase IV (DPP-4) inhibitor and peroxisome proliferator-activated receptor-gamma (PPARγ) agonist exerted the neuroprotective effects in obese insulin-resistant rats. However, the effects of these drugs on dendritic spines in obese insulin-resistant rats have not yet been investigated. In the present study, we determined the effects of DPP-4 inhibitor and PPARγ agonist on dendritic spines density of obese insulin-resistant rats caused by HFD. Methods: Male Wistar Rats were divided into two groups. Animals in each group were fed with normal diet (ND) or HFD for 12weeks. After then, rats in each group were subdivided into three subgroups to receive either vehicle or vildagliptin (3mg/kg/day) or pioglitazone (10mg/kg/day) for 3-4weeks. At the end of the experiment, the metabolic parameters and density of dendritic spines in CA1 hippocampus were determined. Results: We found that HFD-fed rats caused peripheral insulin resistance as well as the reduction of the density of dendritic spines in CA1 hippocampus. Treatment with both DPP-4 inhibitor and PPARγ agonist in HFD-fed rats improved insulin sensitivity as well as increased the number of dendritic spines in CA1 hippocampus. Moreover, both drugs have equally improved this deterioration. Conclusion: Our findings indicate that DPP-4 inhibitor and PPARγ agonist restored the reduction of dendritic spines caused by HFD, suggesting the beneficial roles of DPP-4 inhibitors and PPARγ agonists in neurodegenerative disorders.
format Article
author Sripetchwandee,J.
Pipatpiboon,N.
Pratchayasakul,W.
Chattipakorn,N.
Chattipakorn,S.C.
author_facet Sripetchwandee,J.
Pipatpiboon,N.
Pratchayasakul,W.
Chattipakorn,N.
Chattipakorn,S.C.
author_sort Sripetchwandee,J.
title DPP-4 Inhibitor and PPARγ Agonist Restore the Loss of CA1 Dendritic Spines in Obese Insulin-resistant Rats
title_short DPP-4 Inhibitor and PPARγ Agonist Restore the Loss of CA1 Dendritic Spines in Obese Insulin-resistant Rats
title_full DPP-4 Inhibitor and PPARγ Agonist Restore the Loss of CA1 Dendritic Spines in Obese Insulin-resistant Rats
title_fullStr DPP-4 Inhibitor and PPARγ Agonist Restore the Loss of CA1 Dendritic Spines in Obese Insulin-resistant Rats
title_full_unstemmed DPP-4 Inhibitor and PPARγ Agonist Restore the Loss of CA1 Dendritic Spines in Obese Insulin-resistant Rats
title_sort dpp-4 inhibitor and pparγ agonist restore the loss of ca1 dendritic spines in obese insulin-resistant rats
publisher Elsevier Inc.
publishDate 2015
url http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84915816950&origin=inward
http://cmuir.cmu.ac.th/handle/6653943832/38346
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