Abstract | AIMS/HYPOTHESIS: METHODS: Metabolic studies were performed in Chop ( -/- ) and wild-type C57Bl/6 mice, and included euglycaemic-hyperinsulinaemic clamps and indirect calorimetry. The inflammatory state of liver and adipose tissue was determined by quantitative RT-PCR, immunohistology and macrophage cultures. Viability and absence of ER stress in islets of Langerhans was determined by electron microscopy, islet culture and quantitative RT-PCR. RESULTS: Systemic deletion of Chop induced abdominal obesity and hepatic steatosis. Despite marked obesity, Chop ( -/- ) mice had preserved normal glucose tolerance and insulin sensitivity. This discrepancy was accompanied by lower levels of pro-inflammatory cytokines and less infiltration of immune cells into fat and liver. CONCLUSIONS/INTERPRETATION:
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Authors | M Maris, L Overbergh, C Gysemans, A Waget, A K Cardozo, E Verdrengh, J P M Cunha, T Gotoh, M Cnop, D L Eizirik, R Burcelin, C Mathieu |
Journal | Diabetologia
(Diabetologia)
Vol. 55
Issue 4
Pg. 1167-78
(Apr 2012)
ISSN: 1432-0428 [Electronic] Germany |
PMID | 22237685
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Ddit3 protein, mouse
- Insulin
- Transcription Factor CHOP
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Topics |
- Adipose Tissue
(metabolism)
- Animals
- Fatty Liver
(genetics, metabolism)
- Glucose Intolerance
(genetics, metabolism)
- Inflammation
(genetics, metabolism)
- Insulin
(metabolism)
- Insulin Resistance
(physiology)
- Insulin-Secreting Cells
(metabolism)
- Liver
(metabolism)
- Mice
- Mice, Knockout
- Obesity
(genetics, metabolism)
- Transcription Factor CHOP
(genetics, metabolism)
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