Lots of research papers suggest that this is impossible, or quite uncommon.
I'm unaware of any research papers that suggest that de novo lipogenesis is impossible, or that it is uncommon. Quite the contrary. The metabolic pathways exist in every animal species, from bacteria on up. The only question is the rate at which it happens, and whether it is a significant source of fat deposition.
On this, studies are mixed, at least with respect to glucose. There have been a number of studies that suggested that de novo lipogenesis is not a major pathway for most people. Which may be true.
The more important question, in my mind, is whether it becomes a major pathway for those with metabolic syndrome. And they suggest that for that population, DNL is a significant source of fat:
http://ajcn.nutrition.org/content/77/1/43.full
Until recently, DNL was believed to be an insignificant pathway in humans who eat a Western, high-fat diet. In addition, very little was known about the effect of the often recommended alternative diet, which is a low-fat, high-carbohydrate diet, on hepatic metabolism. However, with the development of new methodologies for measuring hepatic DNL, it was shown that hepatic DNL varies greatly depending on the health of the subjects (12, 13, 15) and the types of diets they consume (4, 5, 7, 9–11, 18, 19). The present study sought to answer 3 questions. First, do hyperinsulinemic obese subjects fed a Western, high-fat diet have higher fractional hepatic DNL than do normoinsulinemic lean or obese subjects fed the same diet? Second, is hepatic DNL increased when simple carbohydrate represents 54% of a low-fat, high-carbohydrate diet? And third, what is the relation of increased hepatic DNL to VLDL-triacylglycerol concentrations?
[...]
With the high-fat, low-carbohydrate diet, DNL was minimal and did not differ significantly between the lean and obese subjects with normal fasting insulin concentrations. In contrast, hyperinsulinemic obese subjects had a significantly higher DNL compared with both lean and obese normoinsulinemic subjects (Figure 1⇓; P < 0.05). Interestingly, although DNL did not differ significantly between the lean normoinsulinemic and the obese hyperinsulinemic subjects who consumed the low-fat, high-carbohydrate diet (Figure 1⇓), DNL was significantly higher (P < 0.05) with the low-fat, high-carbohydrate diet for both groups when compared with the normoinsulinemic subjects who consumed a high-fat, low-carbohydrate diet for 5 d (Figure 1⇓; P < 0.05).
(And one thing to note - this study's "low carb diet" was 45% of calories from carbs - which is anything but low carb the way the low carb community would define it. Atkins induction is less than 5% of calories from carbs, and I'd be willing to guess that at that level, DNL would be minimal even for those who were hyper-insulinemic.)