The main mechanisms involved in the obesity-related hypovitaminosis D include decreased bioavailability of vitamin D due to its fat solubility and sequestration in abdominal fat, reduced intestinal absorption, impaired metabolism, decreased liver 25(OH)D synthesis as a result of hepatic steatosis, and the influence of leptin and interleukin-6 (IL-6) on hepatic vitamin D receptors (VDRs) (2, 3, 5–10). Here, IL6 is linked to rickets.