Using the Internet-based upload blood glucose monitoring and therapy management system in patients with type 1 diabetes.

The aim of this study is to assess the impact of the internet-based upload blood glucose monitoring and therapy management system (Carelink(®)) in patients with type 1 diabetes. Diabetic patients treated with pump infusion for ≥3 months were prospectively randomized to use the CareLink(®) with (4 months) and without (4 months) diabetes-team initiated contact (n = 36, intervention group) or to continue standard care for 4 months and then transfer to the CareLink(®) without diabetes-team initiated contact (n = 34, control group). In the first 4 months, treatment was adjusted monthly by the same team in both groups. Main outcome measures were HbA1c level and scores on the Diabetes Treatment Satisfaction and Diabetes Quality of Life Questionnaires. Patients who submitted <3 times during each 4-month segment were considered noncompliant. Mean patient age was 14.02 ± 5.33 years; mean diabetes duration, 6.4 ± 4.7 years; median duration of pump treatment, 2.5 years. After 4 months, mean HbA1c level decreased from 8.75 ± 0.84 to 8.45 ± 0.90% in the intervention group (p = 0.013) and from 8.65 ± 0.57 to 8.37 ± 0.73% in the control group (p = 0.054). Within the intervention group, the difference in the change in HbA1c levels between compliant and noncompliant patients was significant (8.17 ± 0.81 vs. 8.99 ± 0.85%, p = 0.017). Only in the compliant subgroup was the decrease from baseline significant (p = 0.006). Similar findings were noted in the control group at 8 months (p < 0.05 and p = 0.018, respectively). There were no significant changes in questionnaire scores at 4 or 8 months in either group. Use of the CareLink(®) system is associated with significantly improved glycemic control in compliant patients, with no apparent effect on patient satisfaction or quality of life.

The aromatase inhibitor letrozole increases epiphyseal growth plate height and tibial length in peripubertal male mice.

Sex hormones may influence longitudinal growth, either indirectly, by affecting the growth-hormone-insulin-like growth factor I (IGF-I) axis, or directly, by affecting changes within the epiphyseal growth plate (EGP). The aim of the present study was to investigate the effects of letrozole, an aromatase inhibitor, on longitudinal growth and changes in the EGP in vivo. Eighteen peripubertal male mice were divided into three groups. The first group was killed at baseline, the second was injected with letrozole (Femara) s.c., 2 mg/kg body weight/day, for 10 days, and the third was injected with the vehicle alone. Serum testosterone levels were found to be significantly higher in the treated group than in the controls. Letrozole induced a significant increase in body weight, tail length and serum growth hormone level, but had no significant effect on the level of serum IGF-I. On histomorphometric study, there was a significant increase (12%) in EGP height in the treated animals compared with controls. Immunohistochemistry showed a 3.4-fold letrozole-induced increase in the proliferation of the EGP chondrocytes, as estimated by the number of proliferation cell nuclear antigen-stained cells, and a decrease in the differentiation of the EGP chondrocytes, as estimated by type X collagen staining. Letrozole did not interfere with type II collagen levels. The study group also showed a twofold increase in the number of IGF-I receptor-positive cells compared with controls. In conclusion, the aromatase inhibitor, letrozole, appears to increase the linear growth potential of the EGP in mice.

Leptin reverses the inhibitory effect of caloric restriction on longitudinal growth.

Caloric imbalance, particularly in critical periods of growth and development, is often the underlying cause of growth abnormalities. Serum levels of leptin are elevated in obesity and are low in malnutrition and malabsorption. The aim of the present study was to determine whether leptin integrates energy levels and growth in vivo, as shown previously in our ex vivo experiments, even in the presence of caloric restriction. In the first part of the study, mice were divided into three groups. Two groups were fed ad libitum and received leptin or vehicle only, and the third group was pair-fed with the group injected with leptin to dissociate leptin's effect on growth from its effect on food consumption. Mice given leptin had a significantly greater tibial length than untreated pair-fed animals and a similar tibial length as control mice fed ad libitum despite their lower weight. In addition, leptin significantly increased the overall size of the epiphyseal growth plate by 11%. On immunohistochemistry and in situ hybridization studies, leptin stimulated both the proliferation and differentiation of tibial growth plate chondrocytes without affecting the overall organization of the plate. There was also a marked increase in the expression and level of IGF-IR. In the second part of the study, two groups of mice were fed only 60% of their normal chow; one was injected with leptin, and the other was injected with vehicle alone. Caloric deprivation by itself reduced serum levels of IGF-I by 70% and the length of the tibia by 5%. Leptin treatment corrected the fasting-induced growth deficiency, but further reduced the level of serum IGF-I. These results indicate that leptin stimulates growth even in the presence of caloric restriction independently of peripheral IGF-I.