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The cocaine- and amphetamine-regulated transcript (CART) was first isolated from rat striatum following the acute administration of cocaine or amphetamine. It was quickly determined that CART or CA...

The cocaine- and amphetamine-regulated transcript (CART) was first isolated from rat striatum following the acute administration of cocaine or amphetamine. It was quickly determined that CART or CA...

Osteopenia has been described as a complication of insulin-dependent diabetes mellitus (IDDM). We measured bone modeling indexes during the first year of IDDM. At each time point the values obtained from diabetic children have been compared with those of control subjects. We selected 27 prepubertal children with IDDM (6.35 +/- 2.16 years). We also enrolled 30 healthy prepubertal children of comparable age (5.85 +/- 3.05 years). Height, height standard deviation scores, glycated haemoglobin (HbA(1C)), basal c-peptide concentrations, insulin dose, serum concentrations of procollagen type I C-terminal propeptide (PICP), and collagen type I C-terminal telopeptide (ICTP) were measured at onset of IDDM and at 3, 6 and 12 months. ICTP was in the normal range at onset of IDDM and decreased during the follow-up to reach a significant difference compared to controls after 3, 6 and 12 months of insulin treatment (P < 0.04). PICP concentrations increased significantly at 3 months (P = 0.05) compared to onset. At 3 and 12 months PICP values were significantly higher than those of control children (P = 0.04). Correlations were found be tween PICP concentrations and HbA(1C) and c-peptide at onset of diabetes (r = -0.45 and r = 0.47, respectively). Bone formation at onset of IDDM is not impaired; the introduction of insulin therapy, together with the achievement of a good metabolic control, determines an increase of bone matrix formation coupled with a decrease of bone resorption, that determines a positive balance of bone modeling.

Impairment of calcium metabolism and low bone density have been found in hypothyroid adults. We investigated the effect of thyroid replacement therapy on calcium metabolism and bone mineralization in congenital hypothyroid (CH) infants and children. One hundred and 16 Caucasian CH consecutive patients were studied and were grouped according to their age: 23 patients at diagnosis, 20 at 3 mo, 24 at 6 mo, 25 at 12 mo and 24 at 36 mo. Thyroid replacement therapy was started at an initial dose of 6-8 micrograms/kg/day of L-thyroxine, and then decreased progressively. Calcium, phosphorus, magnesium, alkaline phosphatase (AP), parathyroid hormone (PTH) and osteocalcin (BGP) were measured as calcium metabolism indices. Bone mineral content (BMC) was measured at the mid-portion of the right radius AP, PTH and BGP concentrations were significantly higher in subjects at 3 mo of age (p0.05). This rise coincided with the end of the period of maximum dosage of L-thyroxine. Mild asymptomatic hypercalcemia was observed in 20 patients. All the other indices did not differ between age groups. BMC values and BMC annual increment were not different from those calculated for age-matched controls. We found that L-thyroxine replacement therapy does not alter bone mineralization of CH infants and children. Only a transitory increase of osteoblastic function was observed after the first few months of therapy.

Osteoporosis is a complication of celiac disease in adulthood, but little is known about the influence of the disease on bone mineralization in children. In the present study we evaluated radial bone mineral content (BMC) in celiac children and adolescents at diagnosis and after they consumed a gluten-free diet (GFD). The BMC values of 33 celiac patients at diagnosis were significantly lower than those of 255 control subjects (P < 0.001). There was no difference between diabetic and non-diabetic celiac patients. In 14 patients the BMC increased significantly (P < 0.05, ANCOVA) after 1.28 y of GFD. In these patients the mean annual BMC increment was 0.07 g/cm, significantly greater (P < 0.05) than the increment of normal growing children (0.05 g.cm-1.y-1). Our data indicate that although osteoporosis complicates celiac disease during childhood and adolescence, GFD alone is able to remarkably improve bone mineralization.