Melatonin is induced by light information through the retina and leads to growth factor activation. Thus, we investigated the effects of melatonin by controlling the photoperiod of growing young rats. Male Sprague‐gDawley rats (n=6; 4 weeks old) were divided into two experimental groups: the L/D group (normal photoperiod; light/dark: 12/12 h; lights on at 9:00 a.m.) and the L/L group (light/light: 24 h). Rat body weight and food consumption were measured daily for 8 weeks. After 8 weeks, the rats were anesthetized with a mixture of ketamine (50 mg/kg) and xylazine (10 mg/kg) and sacrificed. Tissue was then collected for RNA isolation (from brain, heart, liver, kidney, adrenal gland, testis, tibia, hind limb muscles). Also, serum was isolated from blood using a centrifugal separation. The L/L group had significantly lower body weight than the L/D group from 4 to 6 weeks (p<0.05). The L/D group had increased tissue mass, compared with the L/L group, but the difference was not statistically significant. The L/D group had a significantly higher melatonin concentration than the L/L group between the hours of midnight and 2:00 a.m (p<0.01). These results indicate that photoperiod length may affect the secretion of melatonin from the pineal gland. Also, the reduction of nocturnal melatonin secretion may retard the development of growing young rats. In future studies, we plan to compare exogenous melatonin administration with endogenous melatonin concentration induced by photoperiod control. Moreover, we will confirm whether the effects seen in pathological animal models can be reversed by controlling the photoperiod.

Our objective of current study was to investigate the development of bone and heart in association with diabetes mellitus (DM). DM was induced by administering an intraperitoneal injection of streptozotocin (STZ; 60 mg/kg) to 4‐gweek‐gold Sprague‐gDawley rats. Body weight and blood glucose were monitored, and rats were sacrificed after 2 or 5 weeks. The left ventricle (LV), including the interventricular septum, was weighed, and body weight and tibial bone length were assessed. Young diabetic rats showed reduced growth in terms of tibial length and body weight compared to controls. Moreover, diabetic males showed more significant growth suppression and reduced LV size than diabetic females. Morphometric analysis of tibiae from diabetic rats revealed suppressed bone growth at 2 and 5 weeks, with no difference between genders. STZ‐ginduced diabetes decreased bone growth and retarded pre‐gpubertal heart development. As a result, diabetes may increase cardiovascular risk factors and lead to eventual heart failure. Therefore, new therapeutic approaches are required for diabetic children exhibiting growth retardation. Heart growth factor, exercise, and cardiopulmonary physical therapy may be required to promote heart development and physiological function.