Early weight gain after diagnosis may have an impact on remission status in children with new-onset type 1 diabetes mellitus.

BACKGROUND: Residual beta-cell function and improvement in insulin sensitivity by reversal of glucose toxicity are two phenomena thought to be related to partial remission (PR). Body fat mass is the major determinant of insulin sensitivity. The aim of this study is to investigate the relationship between the rate of body weight gain after diagnosis of type 1 diabetes mellitus (T1DM) and other clinical factors for the development and duration of PR. METHODS: Children (2-16 years) with new-onset T1DM (n = 99) were grouped into remitters and non-remitters by using insulin dose-adjusted glycosylated hemoglobin (HbA1c) values. Laboratory and clinical data as well as daily insulin requirement per kilogram of body weight at diagnosis and each visit were recorded, and the duration of PR was determined. Changes in body mass index standard deviation score (BMI-SDS) were calculated by the auxological data collected every 6 months. RESULTS: There were 47 remitters (47.5%) and 52 (52.5%) non-remitters. The mean increase in BMI-SDS at the first 6 months of diagnosis was higher in the non-remitters than in the remitters (p = 0.04). Duration of PR was negatively correlated with the change in BMI-SDS between 6 and 12 months after diagnosis. Male sex, younger age, prepubertal status, and lower HbA1c were predictors of remission, among which male sex had the highest chance by multivariate regression. CONCLUSIONS: Early rapid weight gain after diagnosis of T1DM may play a role in the lack of remission and shorter duration of PR. Interventions to prevent early rapid weight gain can maintain the development and prolongation of remission.

Growth hormone/insulin-like growth factor-1 axis as related to body mass index in patients with idiopathic short stature.

OBJECTIVE: Idiopathic short stature (ISS) is a heterogeneous disorder. An impairment of growth hormone (GH)/insulin-like growth factor 1 (IGF-1)/IGF-1 receptor (IGF-1 R) axis is postulated. To evaluate the somatotropic axis in relation to body mass index (BMI), serum IGF-1, IGF-binding protein-3 (IGFBP-3) and the expression of IGF-1 R genes in patients with ISS. METHODS: Fifty-five ISS patients (24 F/31 M) aged 14.6 ± 5.5 years (range 3.5-28.5 years) and 25 BMI- and pubertal stage-matched peers were enrolled in the study. The ISS patients underwent a four-day standard GH stimulation test to evaluate IGF-1 generation. mRNA expression of the IGF-1 R gene in peripheral blood leukocytes was evaluated. ISS patients and controls were compared with respect to anthropometric and laboratory data. The results were also analyzed after subdividing the two groups into low-normal [BMI standard deviation score (SDS) between -2 to -1)] and normal (BMI SDS between -1 to +1) BMI subgroups. RESULTS: Basal serum IGF-1 concentrations were lower in ISS subjects compared to controls who had similar BMI SDS values (p=0.000). Subgroup analyses revealed that there were no significant differences between low-normal BMI ISS subjects and low-normal BMI controls with respect to serum IGF-1 and IGFBP-3 concentrations. However, in the normal BMI ISS subgroup, basal and stimulated IGF-1 levels were significantly lower than the basal values in their control counterparts (basal: p=0.000; stimulated: p=0.007). mRNA expression of IGF-1 R gene was not found to be significantly different in ISS subjects and controls. CONCLUSIONS: ISS patients were found to have lower IGF-1 concentrations than BMI-matched peers, a finding supporting presence of an impairment in the somatotropic axis. IGF-1 R expression does not seem to be impaired in ISS patients. ISS patients with low-normal BMI SDS also tend to display a relative IGF-1 resistance, whereas those with normal BMI SDS tend to be less GH-sensitive than healthy peers.