Key result
Administration of CREG1 stimulated UCP1 expression, increased adipose tissue browning, and improved diet-induced obesity, glucose tolerance, and fatty liver in mice.
Why the study?
Although CREG1 overexpression promotes adipose browning and inhibits diet-induced obesity, the effects of CREG1 administration remained to be investigated.
Does CREG1 administration improve diet-induced obesity and stimulate adipose browning in mice?
Does CREG1 administration improve diet-induced obesity and stimulate adipose browning in mice?
CREG1 administration stimulates brown and beige adipocyte formation and improves diet-induced obesity, glucose tolerance, and fatty liver in mice, suggesting a potential therapeutic target for metabolic diseases.
Supports CREG1 as a potential metabolic target; leaves open translation from this murine model to humans.
Brown and beige adipocytes, which express thermogenic uncoupling protein-1 (UCP1), stimulate glucose and lipid metabolism, improving obesity and metabolic diseases such as type 2 diabetes and hyperlipidemia. Overexpression of cellular repressor of E1A-stimulated genes 1 (CREG1) promotes adipose tissue browning and inhibits diet-induced obesity (DIO) in mice. In this study, we investigated the effects of CREG1 administration on DIO inhibition and adipose browning. Subcutaneous administration of recombinant CREG1 protein to C57BL/6 mice stimulated UCP1 expression in interscapular brown adipose tissue (IBAT) and improved DIO, glucose tolerance and fatty liver compared with those in phosphate-buffered saline-treated mice. Injection of Creg1-expressing adenovirus into inguinal white adipose tissue (IWAT) significantly increased browning and mRNA expression of beige adipocyte marker genes compared with that in mice injected with control virus. The effect of Creg1 induction on beige adipocyte differentiation was supported in primary culture using preadipocytes isolated from IWAT of Creg1-transgenic mice compared with that of wild-type mice. Our results indicate a therapeutic effect of CREG1 on obesity and its associated pathology and a potential of CREG1 to stimulate brown/beige adipocyte formation.
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Kusudo et al. (2021) studied Diet-induced obesity. Recombinant CREG1 protein and Creg1-expressing adenovirus vs. Phosphate-buffered saline and control virus was evaluated on UCP1 expression, diet-induced obesity, glucose tolerance, fatty liver, and adipose browning. Administration of CREG1 stimulated UCP1 expression, increased adipose tissue browning, and improved diet-induced obesity, glucose tolerance, and fatty liver in mice.
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