I suspect the paper didn't discuss the role of de novo lipogenesis because DNL only really becomes a factor in cases of significant and prolonged overfeeding of CHO. In terms of day to day regulation your body deals with any excess CHO by increasing it's rate of oxidation proportionally and it's this preferential oxidization of CHO that causes dietary fat to be stored rather than be oxidised. (Link
It might seem logical to avoid this problem by cutting carbs and increasing your fat intake but as the paper and this passage from Clinical Sports Nutrition 3rd ed. (Ch. 5.3; p.115) suggests it is likely that your dietary fat intake ultimately determines adiposity not your CHO intake (with the exception of significant overfeeding of course).
Under normal physiological condition CHO, protein and alcohol are not easily converted to bodyfat (Swinburn & Ravussin 1993; Prentice 1998). Thus, increases in the intake of non-fat nutrients stimulate their oxidation rates proportionally. Conversely an increase in dietary fat intake does not immediately stimulate fat oxidation, thus increasing the probability that excess dietary fat will be stored as adipose tissue (Abbott et al. 1988; Westerterp 1993; Prentice 1998; schuts 2004a).
This may well explain why the average Japanese salaryman stays relatively slim eating their traditional high carb low fat diet with rice or noodles at every meal while his western contemporaries gain weight on their traditional mixed diet.