Biotin deficiency in mice is associated with decreased serum availability of insulin-like growth factor-I

Background  Biotin deficiency leads to decreased weight and nose-rump length in mice. Aim of the study  The mechanisms underlying this impairment in body growth are yet unclear. Biotin restriction, however, could affect the availability of growth hormone (GH) and/or insulin like growth factor-I (IGF-I) since both hormones control body growth. We then conducted a correlative study aimed at establishing whether biotin dietary restriction is associated with decreased GH/IGF-I serum concentrations. Methods  Levels of GH and IGF-I were measured through ELISA in serum samples of male BALB/cAnN mice fed with: 1] standard chow diet (control diet); 2] 30% egg-white biotin-deficient diet; or 3] 30% egg-white diet supplemented with 16.4 μmol biotin per kilogram (biotin sufficient diet). Relative food consumption, as adjusted per gram of body weight, was also determined. GH and IGF-I measurements were taken individually for 20 weeks beginning at the postnatal week 3, when the animals started consuming the corresponding diets. In addition, femur’s weight and longitudinal growth and the organization of its growth plate were all analyzed as indicators of GH/IGF-I function. Results  No differences in relative food consumption were observed among the three groups of mice along the experimental period that was evaluated. IGF-I serum levels, but not GH ones, were decreased in biotin deficient mice. These animals also showed decreased femur’s longitudinal growth, speed of lengthening and weight gain, as well as shorter and disorganized growth plates. Conclusions  This study shows that biotin dietary restriction is indeed associated with decreased availability of IGF-I and diminished long bone growth and elongation. These conditions could explain the impairment of longitudinal body growth previously reported in biotin deficient mice. Although cause-effect studies are still needed, we believe our results support the notion that biotin might modulate the availability of IGF-I. This work was supported by grants from the Dirección General de Asuntos del Personal Académico (DGAPA), Universidad Nacional Autónoma de México (PAPIIT IN230905, IN200205, IN208605) and the Consejo Nacional de Ciencia y Tecnología, México (52746, 42568Q).