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To the Editor,

We thank Landrier and colleagues for their thoughtful comments regarding our recent publication regarding the role of decreased expression of CYP2R1 as a basis for reduced circulating levels of 25(OH)D in obese mice.(1)

First, Landrier and colleagues point out one of the weaknesses that we ourselves had noted in our article, specifically that the cholecalciferol content of the two diets was not identical. They further assert that when diet composition is adjusted for vitamin D intake, obese mice show no differences from lean mice in serum 25(OH)D3 concentrations. We agree that the effect of obesity on circulating levels of 25(OH)D is less clear in mice than it is in humans, which is why we extended our observations to conditions in which we altered intake of cholecalciferol. Here we think the situation is at least more consistent if not entirely clear. Similar to Seldeen and colleagues(2) and Park and colleagues,(3) we also found no differences in baseline levels of 25(OH)D of lean and obese mice. And, in agreement with Seldeen, we found that obese mice receiving high but not low intakes of cholecalciferol had lower serum levels of 25(OH)D3 at multiple time points between 4 and 24 weeks of supplementation. These results suggested that under conditions of high cholecalciferol intake, obese mice were less capable of 25‐hydroxylating cholecalciferol than lean mice. And in agreement with Park and colleagues,(3) we found that mRNA levels of the principal hepatic 25‐hydroxylase, Cyp2r1, were significantly lower in the obese group than in the lean group.

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