Abstract | AIMS/HYPOTHESIS: METHODS: To inhibit NF-kappaB activity, db/db mice were infected with adenovirus expressing the IkappaBalpha super-repressor. RESULTS: CONCLUSIONS/INTERPRETATION: Our results indicate that moderate inhibition of NF-kappaB improved glucose tolerance through decreased gluconeogenesis associated with reduced PGC-1alpha gene expression in db/db mice, and suggest that inhibition of NF-kappaB activity in liver is a potentially suitable strategy for the normalisation of blood glucose concentration in type 2 diabetes.
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Authors | Y Tamura, T Ogihara, T Uchida, F Ikeda, N Kumashiro, T Nomiyama, F Sato, T Hirose, Y Tanaka, H Mochizuki, R Kawamori, H Watada |
Journal | Diabetologia
(Diabetologia)
Vol. 50
Issue 1
Pg. 131-41
(Jan 2007)
ISSN: 0012-186X [Print] Germany |
PMID | 17093946
(Publication Type: Journal Article)
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Chemical References |
- Creb1 protein, mouse
- Cyclic AMP Response Element-Binding Protein
- I kappa B beta protein
- I-kappa B Proteins
- Multienzyme Complexes
- NF-kappa B
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
- Ppargc1a protein, mouse
- STAT3 Transcription Factor
- Stat3 protein, mouse
- Trans-Activators
- Transcription Factors
- Triglycerides
- Glycogen
- Protein Serine-Threonine Kinases
- AMP-Activated Protein Kinases
- Glucose
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Topics |
- AMP-Activated Protein Kinases
- Adenoviridae
(genetics)
- Animals
- Cyclic AMP Response Element-Binding Protein
(metabolism)
- Diabetes Mellitus
(metabolism, physiopathology)
- Disease Models, Animal
- Female
- Glucose
(metabolism)
- Glycogen
(metabolism)
- I-kappa B Proteins
(genetics, metabolism)
- Insulin Resistance
(physiology)
- Liver
(metabolism)
- Mice
- Mice, Inbred C57BL
- Multienzyme Complexes
(metabolism)
- NF-kappa B
(antagonists & inhibitors, metabolism)
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
- Protein Serine-Threonine Kinases
(metabolism)
- STAT3 Transcription Factor
(metabolism)
- Trans-Activators
(physiology)
- Transcription Factors
- Triglycerides
(metabolism)
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