Influence of ultraviolet B radiation on vitamin D₃ metabolism in vitamin D₃‐resistant New World primates

We investigated the occurrence of rickets in adolescent tamarins ( Saguinus imperator ) residing at the Los Angeles Zoo. Compared to tamarins in the same colony without clinical evidence of bone disease (N = 6), rachitic platyrrhines (N = 3) had a decrease in their serum calcium concentration ( P < .05). The affected tamarins also had lower serum 1,25‐dihydroxyvitamin D 3 (1,25‐(OH) 2 D 3 ) levels than did nonaffected colony mates, but 2–10‐fold higher concentrations than in Old World primates of a comparable developmental stage. New World primates in many different genera are known to exhibit target organ resistance to the active vitamin D 3 metabolite, 1,25‐(OH) 2 D 3 , compensated by maintenance of high circulating concentrations of 1,25‐(OH) 2 D 3 . The relatively low serum 1,25‐(OH) 2 D 3 concentration in rachitic tamarins and ultraviolet B radiation deficient environment of these primates suggested that bone disease may be linked to a deficiency in substrate for 1,25‐(OH) 2 D 3 , 25 hydroxyvtamin D 3 (25‐OHD 3 ). Chronic exposure of platyrrhines in three different vitamin D resistant genera to an artificial UVB source resulted in 1) a significant increase in the mean serum 25‐OHD 3 ( P < .001) and 1,25‐(OH) 2 D 3 ( P < .02) level over that encountered in platyrrhines not exposed to UVB; and 2) prevention of rachitic bone disease in irradiated individuals. These data further show that the serum 25‐OHD 3 and 1,25‐OH 2 D 3 levels are positively correlated in vitamin D‐resistant platyrrhines (r = 0.64; P = .0014) and suggest that a compromise in cutaneous vitamin D 3 production by means of UVB deprivation may limit necessary 1,25‐(OH) 2 D 3 production.