Prevention of insulin resistance in adolescents at risk for type 2 diabetes with depressive symptoms: 1-year follow-up of a randomized trial

Background: Depression is associated with poor insulin sensitivity. We evaluated the long-term effects of a cognitive behavioral therapy (CBT) program for prevention of depression on insulin sensitivity in adolescents at risk for type 2 diabetes (T2D) with depressive symptoms. Methods: One-hundred nineteen adolescent females with overweight/obesity,T2Dfamily history, and mild-to-moderate depressive symptoms were randomized to a 6-week CBT group (n = 61) or 6-week health education (HE) control group (n = 58). At baseline, posttreatment, and 1 year, depressive symptoms were assessed, and whole body insulin sensitivity (WBISI) was estimated from oral glucose tolerance tests.Dual energy X-ray absorptiometry assessed fat mass at baseline and 1 year. Primary outcomes were 1-year changes in depression and insulin sensitivity, adjusting for adiposity and other relevant covariates. Secondary outcomeswere fasting and 2-hr insulin and glucose.We also evaluated the moderating effect of baseline depressive symptom severity. Results: Depressive symptoms decreased in both groups (P \u3c .001). Insulin sensitivity was stable inCBTandHE(ΔWBISI: .1 vs. .3) and did not differ between groups (P=.63).However, among girls with greater (moderate) baseline depressive symptoms (N = 78), those in CBT developed lower 2- hr insulin than those in HE (Δ-16 vs. 16 �IU/mL, P \u3c .05). Additional metabolic benefits of CBT were seen for this subgroup in post hoc analyses of posttreatment to 1-year change. Conclusions: Adolescent females at risk for T2D decreased depressive symptoms and stabilized insulin sensitivity 1 year following brief CBT or HE. Further studies are required to determine if adolescents with moderate depression show metabolic benefits after CBT

Retrospective study of inpatient diabetes management service, length of stay and 30-day readmission rate of patients with diabetes at a community hospital

Background: Hospitalized patients with diabetes are at risk of complications and longer length of stay (LOS). Inpatient Diabetes Management Services (IDMS) are known to be beneficial; however, their impact on patient care measures in community, non-teaching hospitals, is unknown. Objectives: To evaluate whether co-managing patients with diabetes by the IDMS team reduces LOS and 30-day readmission rate (30DR). Methods: This retrospective quality improvement cohort study analyzed LOS and 30DR among patients with diabetes admitted to a community hospital. The IDMS medical team consisted of an endocrinologist, nurse practitioner, and diabetes educator. The comparison group consisted of hospitalized patients with diabetes under standard care of attending physicians (mostly internal medicine-trained hospitalists). The relationship between study groups and outcome variables was assessed using Generalized Estimating Equation models. Results: 4,654 patients with diabetes (70.8 ± 0.2 years old) were admitted between January 2016 and May 2017. The IDMS team co-managed 18.3% of patients, mostly with higher severity of illness scores (p < 0.0001). Mean LOS in patients co-managed by the IDMS team decreased by 27%. Median LOS decreased over time in the IDMS group (p = 0.046), while no significant decrease was seen in the comparison group. Mean 30DR in patients co-managed by the IDMS decreased by 10.71%. Median 30DR decreased among patients co-managed by the IDMS (p = 0.048). Conclusions: In a community hospital setting, LOS and 30DR significantly decreased in patients co-managed by a specialized diabetes team. These changes may be translated into considerable cost savings

Human Obesity Associated with an Intronic SNP in the Brain-Derived Neurotrophic Factor Locus

Brain-derived neurotrophic factor (BDNF) plays a key role in energy balance. In population studies, SNPs of the BDNF locus have been linked to obesity, but the mechanism by which these variants cause weight gain is unknown. Here, we examined human hypothalamic BDNF expression in association with 44 BDNF SNPs. We observed that the minor C allele of rs12291063 is associated with lower human ventromedial hypothalamic BDNF expression (p < 0.001) and greater adiposity in both adult and pediatric cohorts (p values < 0.05). We further demonstrated that the major T allele for rs12291063 possesses a binding capacity for the transcriptional regulator, heterogeneous nuclear ribonucleoprotein D0B, knockdown of which disrupts transactivation by the T allele. Binding and transactivation functions are both disrupted by substituting C for T. These findings provide a rationale for BDNF augmentation as a targeted treatment for obesity in individuals who have the rs12291063 CC genotype

Human obesity associated with an intronic SNP in the brain-derived neurotrophic factor locus

Brain-derived neurotrophic factor (BDNF) plays a key role in energy balance. In population studies, SNPs of the BDNF locus have been linked to obesity, but the mechanism by which these variants cause weight gain is unknown. Here, we examined human hypothalamic BDNF expression in association with 44 BDNF SNPs. We observed that the minor C allele of rs12291063 is associated with lower human ventromedial hypothalamic BDNF expression (p < 0.001) and greater adiposity in both adult and pediatric cohorts (p values < 0.05). We further demonstrated that the major T allele for rs12291063 possesses a binding capacity for the transcriptional regulator, heterogeneous nuclear ribonucleoprotein D0B, knockdown of which disrupts transactivation by the T allele. Binding and transactivation functions are both disrupted by substituting C for T. These findings provide a rationale for BDNF augmentation as a targeted treatment for obesity in individuals who have the rs12291063 CC genotype