What question did this study set out to answer?

To determine whether caspase-2 is a central driver in the development of diet-induced obesity, metabolic syndrome, and nonalcoholic fatty liver disease.

February 18, 2016Cell Death and DiseaseOpen Access

Caspase-2 promotes obesity, the metabolic syndrome and nonalcoholic fatty liver disease

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To determine whether caspase-2 is a central driver in the development of diet-induced obesity, metabolic syndrome, and nonalcoholic fatty liver disease.
Fed wild-type and caspase-2-deficient mice a Western diet enriched with saturated fatty acids, 0.2% cholesterol, and sugar-supplemented water for 16 weeks.
Evaluated metabolic and hepatic phenotypes alongside in vitro assessments of adipose proliferation and lipoapoptosis sensitivity.
Caspase-2-deficient mice exhibited protection from Western diet-induced abdominal adiposity, diabetes mellitus, dyslipidemia, and hepatic steatosis.
Deficient adipose tissue showed resistance to hypertrophy and cell death, elevated proliferative capacity, and upregulation of mitochondrial uncoupling proteins indicative of browning.
Livers of deficient mice showed marked protection against steatohepatitis and fibrosis due to lower circulating fatty acids, enhanced hepatic lipid metabolism, and fewer lipotoxic hepatocytes.

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Implication

Animal study demonstrates that caspase-2 deficiency protects against diet-induced obesity and liver disease in mice, highlighting its potential as a therapeutic target.

Cite This Study

Machado et al. (2016) studied this question.

synapsesocial.com/papers/6a97df9d378ea914c1fadf0b https://doi.org/10.1038/cddis.2016.19

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Implication

Animal study demonstrates that caspase-2 deficiency protects against diet-induced obesity and liver disease in mice, highlighting its potential as a therapeutic target.

Caspase-2 promotes obesity, the metabolic syndrome and nonalcoholic fatty liver disease

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Discussion

Implication

Cite This Study

Caspase-2 promotes obesity, the metabolic syndrome and nonalcoholic fatty liver disease

Key Points

Discussion

Implication

Cite This Study

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