| First Author | Recazens E | Year | 2022 |
| Journal | JCI Insight | Volume | 7 |
| Issue | 4 | PubMed ID | 35041621 |
| Mgi Jnum | J:360847 | Mgi Id | MGI:6886956 |
| Doi | 10.1172/jci.insight.153431 | Citation | Recazens E, et al. (2022) ChREBPbeta is dispensable for the control of glucose homeostasis and energy balance. JCI Insight 7(4):e153431 |
| abstractText | Impaired glucose metabolism is observed in obesity and type 2 diabetes. Glucose controls gene expression through the transcription factor ChREBP in liver and adipose tissues. Mlxipl encodes 2 isoforms: ChREBPalpha, the full-length form (translocation into the nucleus is under the control of glucose), and ChREBPbeta, a constitutively nuclear shorter form. ChREBPbeta gene expression in white adipose tissue is strongly associated with insulin sensitivity. Here, we investigated the consequences of ChREBPbeta deficiency on insulin action and energy balance. ChREBPbeta-deficient male and female C57BL6/J and FVB/N mice were produced using CRISPR/Cas9-mediated gene editing. Unlike global ChREBP deficiency, lack of ChREBPbeta showed modest effects on gene expression in adipose tissues and the liver, with variations chiefly observed in brown adipose tissue. In mice fed chow and 2 types of high-fat diets, lack of ChREBPbeta had moderate effects on body composition and insulin sensitivity. At thermoneutrality, ChREBPbeta deficiency did not prevent the whitening of brown adipose tissue previously reported in total ChREBP-KO mice. These findings revealed that ChREBPbeta is dispensable for metabolic adaptations to nutritional and thermic challenges. |
