Abstract | BACKGROUND: OBJECTIVE: DESIGN: The mice were randomly divided into four groups: a normal control group (C57BL/6J), a control group (C57BL/6J-db/db), a CTL 100 group (C57BL/6J-db/db mice fed a dietary supplement of 100 mg/kg of CTL), and a CTL 300 group (C57BL/6J-db/db mice fed a dietary supplement of 300 mg/kg of CTL). After 8 weeks, we performed an oral glucose tolerance test and the mice were sacrificed. RESULTS: The C57BL/6J-db/db mice developed obesity and hyperglycemia, and the ER stress response and inflammation were activated in their livers. Interestingly, there was a marked decrease in the activation of the ER stress response and insulin resistance in the livers of the C57BL/6J-db/db mice treated with CTL due to decreases in the phosphorylation of eIF2α, IRE1α, and IRS-1 serine and decreases in the mRNA expression of ATF4, c-Jun N-terminal kinase, C/EBPα, and C/EBP homologous protein. Dietary supplementation with CTL also induced a statistically significant decrease in the expression of pro-inflammatory cytokines, C-reactive protein (CRP), and NF-κB phosphorylation. CONCLUSIONS:
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Authors | Ok-Kyung Kim, Da-Eun Nam, Woojin Jun, Jeongmin Lee |
Journal | Food & nutrition research
(Food Nutr Res)
Vol. 59
Pg. 29165
( 2015)
ISSN: 1654-661X [Print] Sweden |
PMID | 26507490
(Publication Type: Journal Article)
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