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May 10, 2018EndocrinologyOpen Access

HDAC3-Selective Inhibition Activates Brown and Beige Fat Through PRDM16

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Key result

Treatment with the HDAC3-selective inhibitor RGFP966 induced thermogenic gene expression in murine and human fat cultures, an effect that was blunted in the absence of PRDM16.

Population

Murine and human fat cultures

Design

Preclinical

Authors

JLJiling LiaoChinese Academy of Medical Sciences & Peking Union Medical CollegeJJJuan JiangSun Yat-sen UniversityHJHeejin JunUniversity of Nebraska–Lincoln

Discussion

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Implication

Does not support clinical use in obesity; hypothesis-generating for PRDM16-dependent thermogenesis as a therapeutic target.

Structured PICO

P
Population
Murine and human fat cultures
I
Intervention
HDAC3-selective inhibitor RGFP966
O
Outcome
Thermogenic gene expressionsurrogate

HDAC3-selective inhibition activates thermogenic gene expression in brown and beige fat via PRDM16, suggesting a potential therapeutic target for obesity and metabolic disorders.

Cite This Study

Liao et al. (2018) studied obesity and metabolic disorders. HDAC3-selective inhibitor RGFP966 was evaluated on thermogenic gene expression. Treatment with the HDAC3-selective inhibitor RGFP966 induced thermogenic gene expression in murine and human fat cultures, an effect that was blunted in the absence of PRDM16.

synapsesocial.com/papers/6ab4bf31b7f31e39744d1915https://doi.org/10.1210/en.2018-00257
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