PLX102740

GSE157270: Crtc1 deficiency aggravates fat accumulation in the white adipose tissue

• Organsim mouse
• Type RNASEQ
• Target gene
• Project ARCHS4

Obesity is described as excessive fat accumulation that drives the development of glucose and lipid metabolism disorders, which is linked to multiple diseases. Crtc1, known as a transducer to regulate Creb activity, plays an important role in several basic physiological functions. Previous studies have shown visible hyperappetite and obesity in Crtc1 knockout (Crtc1-/-) mice. To investigate the effect of Crtc1 on fat accumulation in different organs, we generated Crtc1-/- mice by CRISPR/Cas9 system and regarded Crtc1+/+ as control under the normal feeding conditions. Compared with Crtc1+/+ mice, Crtc1-/- mice exhibited increase of bodyweight which was resulted from the abnormal expansion of white adipocyte. In addition, Crtc1-/- mice were more prone to hyperglycemia and dyslipidemia, supported by the levels of plasma glucose and FABP4. The results of RNA-seq and qRT-PCR in liver and epididymal white adipose tissue (eWAT) showed that the fat accumulation caused by Crtc1 deletion was mainly related to the lipid metabolism of adipose tissue, not liver. Moreover, the up-regulation of lipid metabolism in eWAT induced by Crtc1 deficiency was closely related to the up-regulation of Ppar signaling pathway. Our findings suggested that endogenous Crtc1 had a protective role in obesity development and Crtc1 deficiency aggravates the progression of fat accumulation and related co-morbidities, which introduced a new insight for treatment of obesity. SOURCE: Zhihua Wang (zhihuawang@whu.edu.cn) - Renmin Hospital of Wuhan University