Type 2 diabetes in youth.

The rise in type 2 diabetes in children and adolescents is occurring at a rapid rate. Screening for at risk individuals beginning at or around age 10 and treatment in the phase of insulin resistance is recommended as a prevention measure. For those with overt type 2 diabetes, attention to overall glucose control, prevention of micro- and macro-vascular complications, and assessment of lipids and blood pressure are necessary, along with close monitoring of medication side effects, especially of medications not traditionally used in pediatrics.

Pubertal alterations in growth and body composition: IX. Altered spontaneous secretion and metabolic clearance of growth hormone in overweight youth.

Deconvolution analysis was used to determine 12-hour spontaneous nocturnal growth hormone (GH) secretion and GH half-life in lean (body mass index, <85th percentile; n = 39) and overweight (body mass index, > or =85th percentile; n = 18) youth. The integrated GH concentration, GH burst mass, and half-life were lower (P < .05) in overweight than in lean youth.

Relationship of leptin to bone mineralization in children and adolescents.

Serum leptin concentrations and bone mass are concordant in several respects. Obesity is associated with increased serum leptin concentrations and bone mineral, whereas undernutrition reduces serum leptin concentrations and bone mineral. Furthermore, both bone mineral and serum leptin concentrations increase at the initiation of puberty.

Growth at puberty.

Somatic growth and maturation are influenced by a number of factors that act independently or in concert to modify an individual's genetic potential. The secular trend in height and adolescent development is further evidence for the significant influence of environmental factors on an individual's genetic potential for linear growth. Nutrition, including energy and specific nutrient intake, is a major determinant of growth.

A novel mutation in helix 12 of the vitamin D receptor impairs coactivator interaction and causes hereditary 1,25-dihydroxyvitamin D-resistant rickets without alopecia.

Hereditary vitamin D-resistant rickets (HVDRR) is a genetic disorder most often caused by mutations in the vitamin D receptor (VDR). The patient in this study exhibited the typical clinical features of HVDRR with early onset rickets, hypocalcemia, secondary hyperparathyroidism, and elevated serum concentrations of alkaline phosphatase and 1,25-dihydroxyvitamin D [1,25-(OH)(2)D(3)]. The patient did not have alopecia.