De novo lipogenesis is a a reaction to stress on the liver; it is one of the results when the ethanol/fructose pathway gets overwhelmed, and if unchecked it leads to fatty liver disease, steatohepatitis, cirrhosis, and eventually, death. It is a separate process, at least as I understand matters, from the turning of carbohydrates into fatty acids for storage in adipose tissue. Those fatty acids get packaged into VLDL (if memory serves) for transport to the adipose, whereas the fat droplets produced by de novo lipogenesis remain trapped in the liver.
The study I read that suggested it was carbohydrate that gets turned into fat and stored, whereas dietary fat gets metabolised, was performed with radio-labeled nutrients, so it was pretty definitive. I will see if I can track down the reference all over again, since I read the paper before losing all my links to a computer accident. (Of course, if I have to watch a bunch of David Diamond and Benjamin Bikman videos to find the link again, I wonāt be complaining!)
Moreover, a caloric surplus is not necessarily stored, because the body is perfectly capable of increasing metabolic expenditure in the face of a caloric excess, just as it is capable of reducing metabolic expenditure in the face of a caloric shortage. (Naturally, there are limits to both these reactions.) You are falling into the trap of considering caloric intake as what Dr. Fung calls a āone-compartmentā problem, when in reality (as the good doctor points out) it is a ātwo-compartmentā problem. The hormonal effects of the foods we eat must be taken into account; calories are not fungible. (In other words, a calorieās worth of high-fructose corn syrup has quite a different effect on the body from that of a calorieās worth of protein.)