Document Detail


Hepatic insulin gene therapy diminishes liver glycogen despite insulin responsive transcriptional effects in diabetic CD-1 mice.
MedLine Citation:
PMID:  19434628     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Hepatic insulin gene therapy (HIGT) produces near-normal glycemia in diabetic rats. Hepatic insulin production is expected to stimulate glycogen storage. However, the effect of HIGT on hepatic glycogen metabolism in vivo is unknown. METHODS: After administration of an adenoviral vector capable of inducing glucose responsive insulin production from hepatocytes, we evaluated circulating hormones, cytokines, hepatic gene expression and hepatic glycogen content in diabetic CD-1 mice receiving intravenous streptozotocin. Nondiabetic mice and diabetic mice treated with empty adenovirus served as controls. RESULTS: Peripheral concentrations of human insulin in HIGT mice were less than concentrations of mouse insulin among controls. However, expression of insulin responsive genes in HIGT livers indicated a significant intra-hepatic insulin effect, with expression changes reflecting appropriate responses to fed-fasting transitions. Transcription factors (hepatocyte nuclear factor-4alpha and peroxisome proliferator-activated receptor gamma co-activator-1alpha), as well as target genes (phospho-enol-pyruvate carboxykinase, glucose-6-phosphatase and glucokinase) exhibited insulin responsive expression. Despite producing near normal glycemia, HIGT diminished hepatic glycogen content in both fasted and fed mice. Serum cytokine responses revealed both vector-related (monocyte chemoatractant protein-1, interleukin-6) and transgene specific (resistin, tumor necrosis factor alpha) effects. CONCLUSIONS: HIGT produces low circulating concentrations of insulin, but produces significant intra-hepatic effects on gene expression. Despite controlling hyperglycemia, HIGT exerts unexpected insulin effects on hepatic carbohydrate metabolism. Although the precise mechanisms remain to be determined, they may relate to vector-induced cytokine effects.
Authors:
Jin-an Zhang; Dingwu Jia; Darin E Olson; Adam G Campbell; Peter M Thulé
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  The journal of gene medicine     Volume:  11     ISSN:  1521-2254     ISO Abbreviation:  J Gene Med     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-24     Completed Date:  2009-08-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9815764     Medline TA:  J Gene Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  588-97     Citation Subset:  IM    
Copyright Information:
2009 John Wiley & Sons, Ltd.
Affiliation:
Department of Endocrinology, First Affiliated Hospital of Medical College of Xi'an Jiaotong University, China.
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MeSH Terms
Descriptor/Qualifier:
Adipokines / metabolism
Animals
Body Weight
Cytokines / metabolism
Diabetes Mellitus, Experimental* / genetics,  metabolism
Disease Models, Animal
Gene Expression Regulation*
Gene Therapy*
Humans
Insulin* / genetics,  metabolism,  therapeutic use
Liver / physiology
Liver Glycogen / metabolism*
Male
Mice
Rats
Transcription, Genetic*
Grant Support
ID/Acronym/Agency:
DKO 7298//PHS HHS
Chemical
Reg. No./Substance:
0/Adipokines; 0/Cytokines; 0/Liver Glycogen; 11061-68-0/Insulin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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