It's from here if anyone wants to peek at the methods. Two sets of animals on the same chow. It's 9F 5020, 21% of calories from fat (7% of calories from PUFA) and 55% from carbohydrate.
At all time points the SC-VIS mice have an higher RQ, ie are oxidising more glucose, than the SHAM mice. But they are all fed the same chow, which should average out at the same overall RQ.
Clearly you can increase the RQ, even above 1.0, during de novo lipogenesis, especially when hungry mice suddenly eat carbohydrate. But there is either a payback during the sleep phase where RQ falls below the food derived RQ while that carbohydrate-derived fat is oxidised or there can be no fall in that fasting RQ if the DNL generated fat is "lost" in to adipocytes and stays there, ie under weight gain. Of course simply sequestering dietary fat in to adipocytes will generate an RQ more typical of glucose oxidation because less fat is being oxidised, full stop, during weight gain.
During on-going fat loss the extra low RQ from adipose derived fat oxidation does not have to be payed back either. "Food" of very low RQ, has been supplied from adipocytes. It's gone out of the body as CO2 and water.
But the black square mice are weight stable or actually losing adipose weight (ie should have an extra low RQ) at the time these RQs were measured, while the open diamond mice are actively gaining weight (including adipose tissue), so should have that higher RQ.
Food intakes are describes as "no significant difference" between the groups, despite the differential weight shifts.
To me this is inexplicable and should have been discussed in the paper. My feeling is the CLAMS equipment is generating a totally illogical result.
Unless I've totally missed something. I would really like to know whether I have totally missed something.
Just on general principles of substrate oxidation, never mind what they have done to the mice.......
Peter
