Abdominal fat quantity and distribution in women with polycystic ovary syndrome and extent of its relation to insulin resistance.

CONTEXT: Increased abdominal fat has been linked to insulin resistance and increased cardiovascular risk. Because many patients with polycystic ovary syndrome (PCOS) present abdominal obesity, it may be the cause of insulin resistance in this disorder. SETTING: Fat quantity and distribution were evaluated by dual x-ray absorptiometry at the Departments of Clinical Medicine at the University of Palermo and the University of Naples, Italy. PATIENTS: A total of 110 patients with PCOS and 112 weight-matched controls were studied. Anthropometric data, blood glucose, serum insulin, and testosterone were evaluated. Total, trunk, and central abdominal fat quantity were measured by total-body dual x-ray absorptiometry. RESULTS: Compared with weight-matched controls, patients with PCOS had similar quantity of total and trunk fat but higher quantity of central abdominal fat. This difference was not observed when comparing obese PCOS and obese controls but depended on differences between overweight and normoweight patients and controls. All obese subjects, independently of having PCOS or not, had increased central abdominal fat. The same parameter was increased in 71% of overweight PCOS, 50% of overweight controls, and 30% of normoweight PCOS patients. PCOS patients with increased central abdominal fat had significantly higher (P < 0.01) insulin levels and significantly reduced (P < 0.01) insulin sensitivity than controls with similar quantities of central abdominal fat. Overweight PCOS patients with normal abdominal fat had significantly higher (P < 0.05) insulin levels and significantly reduced (P < 0.05) insulin sensitivity than overweight controls with normal abdominal fat. CONCLUSIONS: Most obese subjects, independent of being affected by PCOS, have an abdominal form of obesity. However, abdominal fat excess may not be the only determinant of insulin resistance in PCOS

Calcium and vitamin D intakes in children: a randomized controlled trial.

BACKGROUND:Calcium (Ca(2+)) and vitamin D (VitD) play an important role in child health. We evaluated the daily intake of Ca(2+) and VitD in healthy children. Moreover, we demonstrate the efficacy of Ca(2+) and VitD supplementation. METHODS:Daily Ca(2+) and VitD intake was evaluated in consecutive healthy children through a validated questionnaire. Subjects with <70% of dietary reference intakes (DRIs) of Ca(2+) and VitD were invited to participate in a prospective randomized trial with 2 groups of nutritional intervention: Group 1, dietary counseling aiming to optimize daily Ca(2+) and VitD intake plus administration of a commercially available Ca(2+) and VitD supplementation product; Group 2, dietary counseling alone. At the enrollment (T0) and after 4 months (T1) serum 25(OH) Vitamin D levels were assessed. RESULTS:We evaluated 150 healthy children (male 50%, mean age 10 years); at baseline a low VitD intake was observed in all subjects (median 0.79 μg/die, IQR 1.78; range 0.01-5.02); this condition was associated with Ca(2+) intake <70% of the DRIs in 82 subjects (55%). At baseline serum 25(OH)D levels were low (<30 ng/ml) in all study subjects and after 4 months of nutritional intervention, a normalization of serum 25(OH)D levels (≥30 ng/ml) was observed in all children in Group 1 and in only one subject in Group 2 [Group 1: T1 33.8 ng/ml (IQR 2.5) vs Group 2: T1 24.5 ng/ml (IQR 5.2), p <0.001]. CONCLUSIONS:Adequate Ca(2+) and VitD intakes are difficult to obtain through dietary counseling alone in pediatric subjects. Oral supplementation with of Ca(2+) and VitD is a reliable strategy to prevent this condition. TRIAL REGISTRATION:The study was registered in Clinical Trials Protocol Registration System (ID number: NCT01638494)

Calcium and vitamin D intakes in children: a randomized controlled trial.

BACKGROUND:Calcium (Ca(2+)) and vitamin D (VitD) play an important role in child health. We evaluated the daily intake of Ca(2+) and VitD in healthy children. Moreover, we demonstrate the efficacy of Ca(2+) and VitD supplementation. METHODS:Daily Ca(2+) and VitD intake was evaluated in consecutive healthy children through a validated questionnaire. Subjects with <70% of dietary reference intakes (DRIs) of Ca(2+) and VitD were invited to participate in a prospective randomized trial with 2 groups of nutritional intervention: Group 1, dietary counseling aiming to optimize daily Ca(2+) and VitD intake plus administration of a commercially available Ca(2+) and VitD supplementation product; Group 2, dietary counseling alone. At the enrollment (T0) and after 4 months (T1) serum 25(OH) Vitamin D levels were assessed. RESULTS:We evaluated 150 healthy children (male 50%, mean age 10 years); at baseline a low VitD intake was observed in all subjects (median 0.79 μg/die, IQR 1.78; range 0.01-5.02); this condition was associated with Ca(2+) intake <70% of the DRIs in 82 subjects (55%). At baseline serum 25(OH)D levels were low (<30 ng/ml) in all study subjects and after 4 months of nutritional intervention, a normalization of serum 25(OH)D levels (≥30 ng/ml) was observed in all children in Group 1 and in only one subject in Group 2 [Group 1: T1 33.8 ng/ml (IQR 2.5) vs Group 2: T1 24.5 ng/ml (IQR 5.2), p <0.001]. CONCLUSIONS:Adequate Ca(2+) and VitD intakes are difficult to obtain through dietary counseling alone in pediatric subjects. Oral supplementation with of Ca(2+) and VitD is a reliable strategy to prevent this condition. TRIAL REGISTRATION:The study was registered in Clinical Trials Protocol Registration System (ID number: NCT01638494)

The Lumbar Bone Mineral Density Is Affected by Long-Term Poor Metabolic Control in Adolescents with Type 1 Diabetes mellitus

Aim: To analyze whether bone mineral density (BMD) and bone resorption status are influenced by long-term metabolic control and duration of disease in adolescents with long-standing type 1 diabetes mellitus. Methods: Twenty-seven adolescents (age 13.1 +/- 1.7 years, duration of diabetes 6.9 +/- 3.0 years) were studied. The BMD, expressed as z score, was measured at the lumbar spine (L1-L4) using dual-energy X-ray absorptiometry, while the urinary excretion of total deoxypiridinoline (Dpyd), a marker of bone resorption, was measured by immunoassay and was corrected by creatinine (Cr). Linear and multivariate correlations between lumbar BMD z score or Dpyd/Cr excretion and age and disease variables [short-term (Hb A(1c latest)) or long-term (Hb A(1c whole duration)) metabolic control, duration, 'diabetes impact index' (mean Hb A(1c whole duration) x duration of disease in months)] were sought. Results: In diabetic subjects the mean BMD z score was -0.44 +/- (SD) 1.02 (95% Cl: -0.03; -0.84), and the Dpyd/Cr excretion was not increased. A negative correlation was found between lumbar BMD z score and age (r -0.59; p = 0.001), duration (r -0.39; p = 0.04), and the diabetes impact index (r -0.4; p = 0.04). The Dpyd/Cr ratio correlated negatively with age (r -0.40; p = 0.04) and positively with height velocity (r 0.42; p = 0.04). By using multiple linear regression, age showed a significant inverse correlation with lumbar BMD z score (P = -0.39; p = 0.0005). A negative correlation was found between lumbar BMD z score and Hb A(1c whole duration) (beta = -0.40; p = 0.02) or diabetes impact index (beta = -0.001; p = 0.01). Conclusions: Poor metabolic control may expose adolescents with long-standing type 1 diabetes to the risk of developing osteopenia in adult age. Optimization of metabolic control in growing diabetic children may prevent osteoporosis in later life