DPP4-inhibitor improves neuronal insulin receptor function, Brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption

High-fat diet (HFD) consumption has been demonstrated to cause peripheral and neuronal insulin resistance, and brain mitochondrial dysfunction in rats. Although the dipeptidyl peptidase-4 inhibitor, vildagliptin, is known to improve peripheral insulin sensitivity, its effects on neuronal insulin res...

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Main Authors: Noppamas Pipatpiboon, Hiranya Pintana, Wasana Pratchayasakul, Nipon Chattipakorn, Siriporn C. Chattipakorn
Format: Journal
Published: 2018
Online Access:https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84874525661&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/48067
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spelling th-cmuir.6653943832-480672018-04-25T08:47:21Z DPP4-inhibitor improves neuronal insulin receptor function, Brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption Noppamas Pipatpiboon Hiranya Pintana Wasana Pratchayasakul Nipon Chattipakorn Siriporn C. Chattipakorn High-fat diet (HFD) consumption has been demonstrated to cause peripheral and neuronal insulin resistance, and brain mitochondrial dysfunction in rats. Although the dipeptidyl peptidase-4 inhibitor, vildagliptin, is known to improve peripheral insulin sensitivity, its effects on neuronal insulin resistance and brain mitochondrial dysfunction caused by a HFD are unknown. We tested the hypothesis that vildagliptin prevents neuronal insulin resistance, brain mitochondrial dysfunction, learning and memory deficit caused by HFD. Male rats were divided into two groups to receive either a HFD or normal diet (ND) for 12 weeks, after which rats in each group were fed with either vildagliptin (3 mg/kg/day) or vehicle for 21 days. The cognitive function was tested by the Morris Water Maze prior to brain removal for studying neuronal insulin receptor (IR) and brain mitochondrial function. In HFD rats, neuronal insulin resistance and brain mitochondrial dysfunction were demonstrated, with impaired learning and memory. Vildagliptin prevented neuronal insulin resistance by restoring insulin-induced long-term depression and neuronal IR phosphorylation, IRS-1 phosphorylation and Akt/PKB-ser phosphorylation. It also improved brain mitochondrial dysfunction and cognitive function. Vildagliptin effectively restored neuronal IR function, increased glucagon-like-peptide 1 levels and prevented brain mitochondri al dysfunction, thus attenuating the impaired cognitive function caused by HFD. © 2012 Federation of European Neuroscience Societies and Blackwell Publishing Ltd. 2018-04-25T08:47:21Z 2018-04-25T08:47:21Z 2013-03-01 Journal 14609568 0953816X 2-s2.0-84874525661 10.1111/ejn.12088 https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84874525661&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/48067
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
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description High-fat diet (HFD) consumption has been demonstrated to cause peripheral and neuronal insulin resistance, and brain mitochondrial dysfunction in rats. Although the dipeptidyl peptidase-4 inhibitor, vildagliptin, is known to improve peripheral insulin sensitivity, its effects on neuronal insulin resistance and brain mitochondrial dysfunction caused by a HFD are unknown. We tested the hypothesis that vildagliptin prevents neuronal insulin resistance, brain mitochondrial dysfunction, learning and memory deficit caused by HFD. Male rats were divided into two groups to receive either a HFD or normal diet (ND) for 12 weeks, after which rats in each group were fed with either vildagliptin (3 mg/kg/day) or vehicle for 21 days. The cognitive function was tested by the Morris Water Maze prior to brain removal for studying neuronal insulin receptor (IR) and brain mitochondrial function. In HFD rats, neuronal insulin resistance and brain mitochondrial dysfunction were demonstrated, with impaired learning and memory. Vildagliptin prevented neuronal insulin resistance by restoring insulin-induced long-term depression and neuronal IR phosphorylation, IRS-1 phosphorylation and Akt/PKB-ser phosphorylation. It also improved brain mitochondrial dysfunction and cognitive function. Vildagliptin effectively restored neuronal IR function, increased glucagon-like-peptide 1 levels and prevented brain mitochondri al dysfunction, thus attenuating the impaired cognitive function caused by HFD. © 2012 Federation of European Neuroscience Societies and Blackwell Publishing Ltd.
format Journal
author Noppamas Pipatpiboon
Hiranya Pintana
Wasana Pratchayasakul
Nipon Chattipakorn
Siriporn C. Chattipakorn
spellingShingle Noppamas Pipatpiboon
Hiranya Pintana
Wasana Pratchayasakul
Nipon Chattipakorn
Siriporn C. Chattipakorn
DPP4-inhibitor improves neuronal insulin receptor function, Brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption
author_facet Noppamas Pipatpiboon
Hiranya Pintana
Wasana Pratchayasakul
Nipon Chattipakorn
Siriporn C. Chattipakorn
author_sort Noppamas Pipatpiboon
title DPP4-inhibitor improves neuronal insulin receptor function, Brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption
title_short DPP4-inhibitor improves neuronal insulin receptor function, Brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption
title_full DPP4-inhibitor improves neuronal insulin receptor function, Brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption
title_fullStr DPP4-inhibitor improves neuronal insulin receptor function, Brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption
title_full_unstemmed DPP4-inhibitor improves neuronal insulin receptor function, Brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption
title_sort dpp4-inhibitor improves neuronal insulin receptor function, brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption
publishDate 2018
url https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84874525661&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/48067
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