Microalbuminuria and retinopathy in adolescents and young adults with type 1 and type 2 diabetes.

AIM: To estimate the occurrence of complications related to early-onset type 2 diabetes compared with type 1 diabetes. METHODS: All individuals registered in the Swedish Pediatric Quality Diabetes Register and the Swedish National Diabetes Register with type 2 diabetes diagnosis at 10 to 25 years of age between 1996 and 2014 (n = 1413) were included. As controls, individuals with type 1 diabetes were randomly selected from the same registers and were matched for age, sex, and year-of-onset (n = 3748). RESULTS: Of the adolescents with type 2 diabetes in the pediatric register, 7.7% had microalbuminuria and 24.6% had signs of retinopathy 5 years after diagnosis, whereas the adolescents with type 1 diabetes 3.8% had microalbuminuria and 19.2% had retinopathy. Among the young adults with type 2 diabetes from the adult diabetes register 10 years after diagnosis 15.2% had microalbuminuria and 39.7% retinopathy, whereas the young adults with type 1 diabetes 4.8% had microalbuminuria and 43.8% retinopathy. After adjustment for established risk factors measured over time in the whole combined cohort, individuals with type 2 diabetes had significantly higher risk of microalbuminuria with a hazard ratio (HR) of 3.32 (95% confidence interval, CI 2.86-3.85, P < .001), and retinopathy with a HR of 1.17 (95% CI 1.06-1.30, P 0.04). CONCLUSIONS: The prevalence of complications and comorbidities was higher among those with type 2 diabetes compared with type 1 diabetes, although prevalent in both groups. Early monitoring and more active treatment of type 2 diabetes in young individuals is required.

The effect of weight loss and weight gain on blood pressure in children and adolescents with obesity.

OBJECTIVE: Obesity in childhood is a profound risk factor for hypertension, and weight loss has positive effects on blood pressure (BP). However, the expected effect size on BP from weight reduction in children with obesity is insufficiently described. Therefore, the aim was to investigate the association between changes of degree of obesity and BP levels. SUBJECTS: This prospective cohort study examined subjects receiving behavioral lifestyle modification treatment who were registered in the Swedish national registry for treatment of childhood obesity (BORIS). A total of 5279 obese subjects (51.3% boys) had repeated BP measurements. The average follow-up time was 32 months. Degree of obesity was expressed as BMI standard deviation score (SDS) and BP as BP SDS. RESULTS: The mean age at treatment initiation was 10.3 years. The prevalence of hypertensive BP was 15.3% for systolic and 5.5% for diastolic pressure. Both systolic and diastolic BP SDS decreased when a lower BMI SDS was achieved; systolic BP SDS decreased 0.41 [0.33-0.49] and diastolic BP SDS decreased 0.26 [0.20-0.32] per BMI SDS unit reduction. The impact of BMI SDS reduction on BP SDS was greater in subjects with hypertensive levels at treatment initiation, but behavioral modification was an insufficient treatment for 27% of them. Obesity treatment failure increased the risk of developing hypertensive levels; HR = 1.81 [1.38-2.37] (systolic BP) HR = 3.82 [2.34-6.24] (diastolic BP), per unit increase in BMI SDS. CONCLUSIONS: Weight loss is a key factor for hypertension prevention and treatment in children with obesity. However, its limited effect suggests that additional pharmacological antihypertensive treatment more readily should be considered.

Oral intake of mesoporous silica is safe and well tolerated in male humans.

BACKGROUND: Precisely engineered mesoporous silica has been shown to induce weight loss in mice, but whether it is safe to use in humans have not investigated. OBJECTIVE: The aim was to determine whether oral dosing, up to 9 grams/day, of precisely engineered mesoporous silica as a food additive can be used safely in male humans. DESIGN: This single blinded safety study consisted of two study arms including 10 males each (18-35 years). One arm consisted of participants with normal weight and one with obesity. After a placebo run-in period, all subjects were given porous silica three times daily, with increasing dose up to 9 grams/day (Phase 1). Subjects with obesity continued the study with highest dose for additional 10 weeks (Phase 2). RESULTS: All participants completed Phase 1 and 90% completed Phase 2, with approximately 1% missed doses. Participants reported no abdominal discomfort, and changes in bowel habits were minor and inconsistent. The side effects observed were mild and tolerable, biomarkers did not give any safety concern, and no severe adverse events occurred. CONCLUSION: Mesoporous silica intake of up to 9 grams/day can be consumed by males without any major adverse events or safety concerns.

Initial low-dose oral levothyroxine in a child with Down syndrome, myxedema, and cardiogenic shock.

Myxedema is extremely rare in children, and guidelines are lacking. We treated a 12-year-old girl with myxedema and cardiogenic shock with initial low dose (0.3-2.5 µg/kg body weight/day) of oral levothyroxine and intensive care. Oral administration may safely revert children's myxedema in a dosage resembling that for hypothyroidism.

Meal timing, fasting and glucocorticoids interplay in serum leptin concentrations and diurnal profile.

BACKGROUND: In a previous study, we reported a 4-fold increase in serum leptin following total parenteral nutrition given after surgery. We hypothesised that the perioperative fasting and stress contributed to this, possibly mediated by increased serum insulin and cortisol. OBJECTIVE: To test the hypothesis that fasting, in combination with glucocorticoids, sensitises the leptin response to subsequent energy intake. DESIGN: Healthy volunteers were randomised into two groups, one group received dexamethasone (DEX), 0.1 mg twice daily for 3 days, while the other group served as a control. Each group was then subdivided into two feeding protocols. Protocol 1, where a standard meal was given at 0, 24, 36 and 48 h and protocol 2 where the same meal was given at 0 and 48 h. Blood samples were drawn before, as well as every other hour during the study period for determination of serum leptin, insulin, glucose and cortisol concentrations. RESULTS: In all groups serum leptin increased significantly following each meal (P<0.01). The rise in serum leptin in response to the standard meal was higher when the meal was taken in the evening (P<0.001) or following longer duration of fasting (P<0.02). In those fasting for 48 h, leptin decreased by 60% and showed no diurnal variation. DEX intake increased leptin concentrations in those fasting for short periods (P<0.02) but not for 48 h. CONCLUSIONS: Long durations of fasting sensitise the response of leptin to subsequent energy intake and abolish the DEX-induced upregulation of leptin. Meal timing is an important factor determining the leptin diurnal rhythm, but other factors must contribute since the leptin response to a standard meal taken in the evening was greater than to the same meal taken in the morning.