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Objectives Achieving glycated hemoglobin (A1C) and blood pressure targets is an important strategy for preventing chronic vascular complications in diabetes. Our aim in this study was to determine the proportion of type 2 diabetes patients who meet the recommended A1C and arterial blood pressure targets and to identify the determinants of failure to do so. Methods A cross-sectional study was conducted in an outpatient endocrine clinic at a university hospital. The A1C goal was 7% in general and 8% for patients with advanced chronic complications. Regarding blood pressure, the overall expected target was 140/90 mmHg. Results A total of 602 type 2 diabetes patients were analyzed: 62% were female, 14% self-reported as black, mean age was 63±11 years, mean diabetes duration was 17±9 years and median A1C was 8.0% (interquartile range, 7.0% to 9.5%). Macrovascular disease was present in 33% of the patients, diabetic retinopathy in 47%, peripheral neuropathy in 43% and diabetic kidney disease in 56%. Regarding metabolic control, 403 (67%) patients were not at the adjusted target A1C level, and being female, black, young and an insulin user were the main determinants of poor glycemic control. Regarding blood pressure, 348 (58%) patients were not at the recommended targets, and a more advanced age was the main associated factor. Conclusions Because more than half of type 2 diabetes outpatients do not meet the recommended A1C and blood pressure target values, there is a major call to overcome the therapeutic inertia and target treatment of patients on an individual basis.

OBJECTIVE Precocious pubarche (PP) has been linked to higher prevalence of metabolic disturbances and polycystic ovary syndrome (PCOS). The aim of the study was to assess echocardiographic parameters in PP girls and to analyse their relationship with androgens and insulin resistance (IR). DESIGN Case-control study. PATIENTS Thirty-five PP girls and 35 healthy age-matched controls. MEASUREMENTS Clinical, hormonal and metabolic profiles, echocardiography, body composition and oral glucose tolerance test. RESULTS Chronological age (10·04 ± 2·6 years in PP vs 10·13 ± 2·56 years in controls, P = 0·227), and pubertal stage at the time of the study were similar between the groups. PP girls had higher free androgen index (FAI) [1·39 (0·48-3·64) vs 1·06 (0·39-1·7), P = 0·005] and QUICKI (0·58 ± 0·08 vs 0·63 ± 0·12, P = 0·021). However, HOMA-IR was not significantly different between the groups [2·79 (1·84-4·05) vs 2·15 (1·09-3·23), P = 0·085]. After adjusting for total body fat, left ventricular mass (LVM) was higher in the PP group (97·31 ± 33·37 vs 81·25 ± 19·06 g, P = 0·017) as well as A' wave (5·66 ± 1·34 vs 5·09 ± 0·98 cm/s, P = 0·025), a measurement of diastolic function. FAI and total body fat were independent predictors of higher LVM and together with HOMA-IR contributed 72% of LVM variability in the PP group. CONCLUSION In this study with PP girls, greater LVM, associated with higher androgen levels, IR and total body fat, occurred early in pubertal development.

Polycystic ovary syndrome (PCOS), a complex condition that affects women of reproductive age, is characterized by ovulatory dysfunction and androgen excess. Women with PCOS present higher prevalence of obesity, central adiposity, and dyslipidemia, and face increased risk of type 2 diabetes. PCOS is closely linked to functional derangements in adipose tissue. Adipocytes seem to be prone to hypertrophy when exposed to androgen excess, as experienced by women with PCOS, and both adipose tissue hypertrophy and hyperandrogenism are related to insulin resistance. Hypertrophic adipocytes are more susceptible to inflammation, apoptosis, fibrosis, and release of free fatty acids. Disturbed secretion of adipokines may also impact the pathophysiology of PCOS through their influence on metabolism and on sex steroid secretion. Chronic low-grade inflammation in PCOS is also related to hyperandrogenism and to the hypertrophy of adipocytes, causing compression phenomena in the stromal vessels, leading to adipose tissue hypoperfusion and altered secretion of cytokines. Lifestyle changes are the first-line intervention for reducing metabolic risks in PCOS and the addition of an insulin-sensitizing drug might be required. Nevertheless, there is not sufficient evidence in favor of any specific pharmacologic therapies to directly oppose inflammation. Further studies are warranted to identify an adipokine that could serve as an indirect marker of adipocyte production in PCOS, representing a reliable sign of metabolic alteration in this syndrome.

Alternative methods to assess ventricular diastolic function in the fetus are proposed. Fetal myocardial hypertrophy in maternal diabetes was used as a model of decreased left ventricular compliance (LVC), and fetal respiratory movements as a model of increased LVC. Comparison of three groups of fetuses showed that, in 10 fetuses of diabetic mothers (FDM) with septal hypertrophy (SH), the mean excursion index of the septum primum (EISP) (ratio between the linear excursion of the flap valve and the left atrial diameter) was 0.36 +/- 0.09, in 8 FDM without SH it was 0.51 +/- 0.09 (P=0.001), and in the 8 normal control fetuses (NCF) it was 0.49 +/- 0.12 (P=0.003). In another study, 28 fetuses in apnea had a mean EISP of 0.39 +/- 0.05 which increased to 0.57 +/- 0.07 during respiration (P0.001). These two studies showed that the mobility of the septum primum was reduced when LVC was decreased and was increased when LVC was enhanced. Mean pulmonary vein pulsatility was higher in 14 FDM (1.83 +/- 1.21) than in 26 NCF (1.02 +/- 0.31; P=0.02). In the same fetuses, mean left atrial shortening was decreased (0.40 +/- 0.11) in relation to NCF (0.51 +/- 0.09; P=0.011). These results suggest that FDM may have a higher preload than normal controls, probably as a result of increased myocardial mass and LV hypertrophy. Prenatal assessment of LV diastolic function by fetal echocardiography should include analysis of septum primum mobility, pulmonary vein pulsatility, and left atrial shortening.

OBJETIVO: Testar a hipótese de que a fração de encurtamento atrial esquerda seja menor nos fetos de mães diabéticas do que em fetos de mães sem doenças sistêmicas. MÉTODOS: Foram examinados, por ecocardiografia, 42 fetos de mães com diabetes prévio ou gestacional e 39 fetos normais de mães sem doença sistêmica (controles), com idades gestacionais a partir da 25ª semana até o termo. A fração de encurtamento atrial esquerda foi obtida pelo quociente diâmetro máximo do átrio esquerdo (AE) - diâmetro mínimo AE/diâmetro máximo AE. Os dados foram comparados pelo teste t de Student, com um alfa crítico de 0,05. RESULTADOS: Os filhos de mães diabéticas apresentaram fração de encurtamento atrial esquerda média de 0,39 ± 0,15 e os fetos do grupo controle de 0,51 ± 0,11. Esta diferença foi significativa, com p < 0,001. CONCLUSÃO: A dinâmica atrial esquerda, com diminuição do seu encurtamento global, está acentuada nos filhos de mães diabéticas. Especulamos que este parâmetro possa ser útil na avaliação da função diastólica ventricular esquerda fetal. OBJECTIVE: To test the hypothesis that left atrial shortening fraction is lower in fetuses of diabetic mothers than in fetuses of mothers with no systemic disease. METHODS: Forty-two fetuses of mothers with previous diabetes or gestational diabetes and 39 healthy fetuses of mothers with no systemic disease (controls) underwent echocardiographic examination. Their gestational ages ranged from 25 weeks to term. The left atrial shortening fraction was obtained with the following formula: (left atrial maximum diameter - left atrial minimum diameter)/left atrial maximum diameter. Data were compared using the Student t test, with an alpha level of 0.05. RESULTS: Mean left atrial shortening fractions in fetuses of diabetic mothers and in those in the control group were 0.39±0.15 and 0.51±0.11, respectively. This difference was significant with P < 0.001. CONCLUSION: Left atrial dynamics, with a reduction in global left atrial shortening, is increased in fetuses of diabetic mothers. We speculate that this parameter may be useful in assessing fetal left ventricular diastolic function.

OBJECTIVE: To verify the hypothesis that the pulmonary vein pulsatility index is higher in fetuses of diabetic mothers than it is in normal fetuses of nondiabetic mothers. METHODS: Twenty-four fetuses of mothers with either gestational or previous diabetes (cases), and 25 normal fetuses of mothers without systemic disease (control) were examined. Fetuses were examined through prenatal Doppler and color flow mapping. The pulmonary vein pulsatility index was obtained by placing the pulsed Doppler sample volume over the right superior pulmonary vein and applying the formula (systolic velocity - presystolic velocity)/mean velocity. RESULTS: The mean gestational age of the study fetuses was 30.3±2.7 weeks, and gestational age of the controls was 29±3.3 weeks, with no significant difference in gestational age between groups (p=0.14). Fetuses of diabetic mothers had a mean pulmonary vein pulsatility index of 1.6±1, and those of the control group had an index of 0.86±0.27. CONCLUSION: Fetuses of diabetic mothers had pulmonary vein pulsatility indexes (parameter easily obtained through Doppler echocardiography that may be related to fetal diastolic function) higher than those in fetuses of mothers with normal glycemia.

Background Vitamin D deficiency has been associated with a multitude of disorders including diabetes, defective insulin secretion as well as rickets and poor bone health. Vitamin D is also a concern during childhood and adolescence and has been reported in girls from South Brazil. We determined the prevalence of vitamin D deficiency in girls from South Brazil and investigated whether the genotypic distribution of the BsmI, ApaI and TaqI polymorphisms of the VDR gene and their haplotypes were associated with vitamin D levels. Methods Cross-sectional study including 234 apparently healthy girls aged 7 to 18 years. Height and weight were measured for calculation of body mass index (BMI) percentiles for age. Plasma levels of 25-hydroxyvitamin D [25(OH)D] were assessed. Participants were genotyped for ApaI (rs7975232), TaqI (rs731236), and BsmI (rs1544410) SNPs. Results The median and interquartile range (25-75%) of BMI percentile was 62.0 (33.3 – 84.9). The frequency of overweight/obesity was 24.9%. Circulating levels of 25(OH)D (≥ 30 ng/mL) were adequate in 9.4%; insufficient in 54.3% (20–29 ng/mL); and deficient in 36.3% (< 20 ng/mL). Genotype frequencies were GG = 47.0%, GA = 41.5%, and AA = 11.5% for BsmI; GG = 16.7%, GT = 52.6%, and TT = 30.8% for ApaI; TT = 46.2%, TC = 44.9% and CC = 9.0% for TaqI. Genotypes with no gene variance (ancestral wild genotype) of BsmI (GG vs. GA + AA, two-tailed Student’s t-test p vs. GT + TT, two-tailed Student’s t-test p = 0.031) and TaqI (TT vs. TC + CC, two-tailed Student’s t-test p = 0.005) SNPs and the GGT haplotype (two-tailed Student’s t-test p = 0.036) were significantly associated with lower 25(OH)D levels. Conclusions 25-hydroxyvitamin D deficiency and insufficiency were highly prevalent in this sample. The BsmI, ApaI and TaqI wild variants of the VDR gene, as well as the GGT haplotype, were associated with lower vitamin D levels, suggesting that VDR gene polymorphisms could be linked to higher susceptibility to vitamin D deficiency in a sub-population of children and adolescents.