When scientists turned off the FGF21 gene in mice, the mice still handled fasting just fine — their blood sugar, insulin, and energy levels stayed normal, even though a few liver genes acted a little differently.

What we've found so far suggests that FGF21 may not be necessary for mice to adapt to fasting. Our analysis of the available evidence shows that turning off the FGF21 gene did not prevent mice from maintaining normal blood sugar, insulin, or energy levels during fasting [1]. We reviewed one assertion from the research, and it supports the idea that mice can adapt to fasting even without FGF21 [1]. In this case, mice genetically modified to lack the FGF21 gene still regulated their metabolism effectively during fasting. Their core physiological markers—like blood sugar and insulin—remained stable, which suggests the body has other ways to manage these processes [1]. While the study noted that a few liver genes behaved differently in the absence of FGF21, this did not appear to disrupt overall metabolic balance during fasting [1]. Our current analysis shows the evidence leans toward FGF21 not being essential for fasting adaptation in mice. However, the single change in liver gene activity hints that FGF21 might still play a minor or supportive role, even if it’s not required for the core response. Since we’ve only analyzed one assertion so far, our understanding is limited. More studies would be needed to see if this pattern holds across different conditions, diets, or mouse strains. At this point, we can’t rule out subtle effects or roles in longer-term fasting. Practical takeaway: Based on what we’ve reviewed so far, mice don’t seem to need the FGF21 gene to handle fasting normally—even without it, their bodies kept blood sugar and energy in check.