Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA399695 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5960222.fastq.gz | Fastqsanger.gz | |||
| SRR5960223.fastq.gz | Fastqsanger.gz | |||
| SRR5960224.fastq.gz | Fastqsanger.gz | |||
| SRR5960225.fastq.gz | Fastqsanger.gz | |||
| SRR5960226.fastq.gz | Fastqsanger.gz |
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Project description:Obesity and insulin resistance are associated with oxidative stress, which may be implicated in their progression. The kinase JNK1 emerged as a promising drug target for the treatment of obesity and type-2 diabetes. However, JNK1 is a key mediator of the oxidative stress response, promoting either cell dead or survival depending on magnitude and context of its activation. Furthermore, JNK inactivation shortens lifespan in drosophila and c. elegans. To learn on the safety and efficacy of long-term JNK inhibition in vertebrates, we investigated mice lacking JNK1 (JNK1-/-) exposed over a long period to an obesogenic high-fat diet (HFD). JNK1-/- mice chronically fed an HFD developed more skin oxidative damage because of reduced catalase expression, but also showed sustained protection from obesity, adipose tissue inflammation, steatosis, and insulin resistance, paralleled by decreased oxidative damage in fat and liver. We conclude that JNK1 is a relatively safe drug target for obesity-related diseases.
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