Bachelor degree. Can't upload word doc. with results and intervention/set up?
But graphs shows mRNA content in the liver from muscle specific PGC1-a knockout mice (MKO) and littermate lox/lox control mice (LOX/LOX) in the fed (FED) and 24h fasted (FAST) state.
I need suggestings/help with:
1) Upregulating of PEPCK mRNA after fasting
Possibilities?:
- The observed increase in PEPCK mRNA content in both lox/lox and PGC-1a MKO mice after 24h of fasting demonstrates, that PGC-1a is not required for this response.
- The higher PEPCK mRNA content in PGC-1a MKO mice in the fasting study, may indicate that lack of PGC-1a leads to compensatory increase in the expression of PEPCK and this potentially an elevated glucose production.
2) why G6Pase mRNA did not increase more (increased approx. 10-20% in both genotypes (lox/lox) and (MKO).
- Based on the knowledge that the G6Pase enzyme, which is mainly found in the liver and the kidneys, plays an important role of providing exactly glucose during starvation, I would have expected a higher upregulation of G6Pase mRNA in both LOX/LOX and MKO in the fasted state (FAST).
Posibilities?:
- Due to the mice strain used? The 24h fasting does not have any significant impact on the strain
- Could the response to fasting in the liver start earlier and peak before 24h of fasting, and then decline thereafter?
- The finding of 10-20% higher (P<0.05) G6Pase mRNA content in the fasted state (FAST) suggests, that during a prolonged fasting (24h), the upregulation of phosphoenolpyruvate carboxykinase (PEPCK) mRNA is more important than the upregulation of G6Pase mRNA.
^ can someone explain me why?
3) why sXBP is not upregulated after fasting (hard to find papers etc. about sXBP)
Thank you!!! (My English may not be perfect).
