The existence of the phenomenon of diet-induced thermogenesis—and its possible mediation by UCP1 in brown adipose tissue—has long been, and is presently, an important metabolic controversy. Particularly, several recent studies have failed to observe the hallmark of the phenomenon: augmentation of diet-induced obesity (i.e., fat mass) in UCP1-ablated mice, thus further casting doubt on the possible importance of this thermogenesis, for example in human metabolic control. However, scrutiny of the experimental details revealed important procedural differences between experiments that did not show or did show this augmentation of diet-induced obesity. Particularly, there were notable differences between the commercial diets used (Research Diets or Ssniff). We, therefore, tested to what degree these differences would suffice to explain the absence of a UCP1 effect. Wild-type mice fed Research Diets high-fat diet became obese, but UCP1-ablated mice became even more obese, as expected if UCP1-dependent diet-induced thermogenesis exists. Mice fed the Ssniff high-fat diet became less obese than those on the Research Diets food—and, importantly, no effect of UCP1 ablation was seen. The result with the Research Diets diet was fully due to differences in total fat mass and not explainable by differences in food intake. The two diets are different in carbohydrate (sucrose) and lipid (lard vs. palm oil) composition and in texture and taste. Probably some of these factors explain the difference, but the important conclusion is that when an appropriate diet was offered, the body weight manifestation of the phenomenon of UCP1-dependent diet-induced thermogenesis was a reproducible phenomenon, the existence of which may have significance also for human metabolic control.