Document Detail


Short-chain fatty acid propionate alleviates Akt2 knockout-induced myocardial contractile dysfunction.
MedLine Citation:
PMID:  21960994     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND AIMS. Dysregulation of Akt has been implicated in diseases such as cancer and diabetes, although little is known about the role of Akt deficiency on cardiomyocyte contractile function. This study was designed to examine the effect of Akt2 knockout-induced cardiomyocyte contractile response and the effect of dietary supplementation of short-chain fatty acid propionate on Akt2 knockout-induced cardiac dysfunction, if any. METHODS AND RESULTS. Adult male wild-type (WT) and Akt2 knockout mice were treated with propionate (0.3 g/kg, p.o.) or vehicle for 7 days. Oral glucose tolerance test (OGTT) was performed. Cardiomyocyte contractile function and mitochondrial membrane potential were assessed. Expression of insulin-signaling molecules Akt, PTEN, GSK3β, and eNOS receptors for short-chain fatty acids GPR41, and GPR43 as well as protein phosphatase PP2AA, PP2AB, PP2C were evaluated using Western blot analysis. Our results revealed that Akt2 knockout led to overt glucose intolerance, compromised cardiomyocyte contractile function (reduced peak shortening and maximal velocity of shortening/relengthening as well as prolonged relengthening), loss of mitochondrial membrane potential, decreased GPR41 and elevated GPR43 expression, all of which, with the exception of glucose intolerance and elevated GPR43 level, were significantly attenuated by propionate. Neither Akt2 knockout nor propionate affected the expression of protein phosphatases, eNOS, pan, and phosphorylated PTEN and GSK3β. CONCLUSIONS. Taken together, these data depicted that Akt2 knockout may elicit cardiomyocyte contractile and mitochondrial defects and a beneficial role of propionate or short-chain fatty acids against Akt2 deficiency-induced cardiac anomalies.
Authors:
Linlin Li; Yinan Hua; Jun Ren
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-09-22
Journal Detail:
Title:  Experimental diabetes research     Volume:  2012     ISSN:  1687-5303     ISO Abbreviation:  Exp Diabetes Res     Publication Date:  2012  
Date Detail:
Created Date:  2011-09-30     Completed Date:  2012-01-16     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  101274844     Medline TA:  Exp Diabetes Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  851717     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Xinjiang Medical University, Urumqi, China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Dietary Supplements
Glucose Intolerance / etiology,  genetics,  physiopathology
Glycogen Synthase Kinase 3 / metabolism
Insulin / metabolism
Male
Mice
Mice, Knockout
Mitochondria, Heart / metabolism
Myocardial Contraction / drug effects*,  genetics,  physiology*
Myocytes, Cardiac / drug effects,  physiology
Nitric Oxide Synthase Type III / metabolism
PTEN Phosphohydrolase / metabolism
Propionates / pharmacology*
Proto-Oncogene Proteins c-akt / deficiency*,  genetics,  physiology
Receptors, G-Protein-Coupled / metabolism
Signal Transduction / drug effects
Chemical
Reg. No./Substance:
0/Ffar2 protein, mouse; 0/Gpr41 protein, mouse; 0/Insulin; 0/Propionates; 0/Receptors, G-Protein-Coupled; 79-09-4/propionic acid; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, mouse; EC 2.7.11.1/Akt2 protein, mouse; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.1/glycogen synthase kinase 3 beta; EC 2.7.11.26/Glycogen Synthase Kinase 3; EC 3.1.3.48/Pten protein, mouse; EC 3.1.3.67/PTEN Phosphohydrolase
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