A patient with chronic adipose wasting (lipodystrophy) is noted to develop vitamin D deficiency more quickly than peers. Which mechanism best explains this observation?

Lipodystrophy increases renal conversion of 25‑OH D to calcitriol causing rapid depletion of circulating 25‑OH D and resulting deficiency regardless of the storage pool.

Reduced adipose mass lowers the reservoir of stored vitamin D, decreasing capacity to maintain serum 25‑OH D during periods of low intake or sun exposure and precipitating deficiency earlier.

Adipose tissue is the primary site of vitamin K storage; lack of fat specifically lowers K levels which are mismeasured as low vitamin D by common assays.

Lipodystrophy causes sequestration of vitamin D in muscle tissue making it biologically inactive but detectable at high serum levels, paradoxically creating functional deficiency while assays read normal.