Comparison of absorptiometric evaluations from total-body and local-regional skeletal scans.

The most common measurement sites for dual-energy absorptiometry (DXA) in clinical practice are posteroanterior (PA) spine and femur. However, other skeletal regions may provide different bone density information. The purpose of this study was to establish the least number of DXA measurements needed to obtain complete information about bone. A total of 262 normal female subjects, 8-50, were measured on a Lunar DPX-L scanner under total body, PA spine, lateral spine, and femur protocol. Forearm measurements were performed with a Lunar SP2 single-photon absorptiometry scanner. The various measurements were compared based on a linear regression model. The correlation coefficients for bone mineral density (BMD) between adjacent vertebrae were 0.92-0.95, and the associated standard errors of the estimate (SEE) were 4.5-5.5%. Total-body BMD can best predict BMD of the trunk, arms, and legs (SEE<4.3%), but least that of the lateral view of the spine (SEE>13.9%). BMD values of the leg from total-body scans predict those from the femoral neck with an error of 9.0%, and those of the trochanteric region with 11.1%. The error between adjacent vertebrae (6%) is considered acceptable, then a total-body measurement combined with a lateral view of the spine and a femur scan are adequate.

Leptin is inversely related to age at menarche in human females.

Over the last century there has been a trend toward an earlier onset of menarche attributed to better nutrition and body fatness. With the discovery of the obesity gene and its product, leptin, we reexamined this hypothesis from a new perspective. As delayed menarche and leanness are considered risk factors for osteoporosis, we also evaluated the relation between leptin and bone mass. Body composition and serum leptin levels were measured, and the timing of menarche was recorded in 343 pubertal females over 4 yr. Body composition was measured by dual x-ray absorptiometry, and leptin by a new RIA. All participants were premenarcheal at baseline (aged 8.3-13.1 yr). Leptin was strongly associated with body fat (r = 0.81; P < 0.0001) and change in body fat (r = 0.58; P < 0.0001). The rise in serum leptin concentration up to the level of 12.2 ng/mL (95% confidence interval, 7.2-16.7) was associated with the decline in age at menarche. An increase of 1 ng/mL in serum leptin lowered the age at menarche by 1 month. A serum leptin level of 12.2 ng/mL corresponded to a relative percent body fat of 29.7%, a body mass index of 22.3, and-body fat of 16.0 kg. A gain in body fat of 1 kg lowered the timing of menarche by 13 days. Leptin was positively related to bone area (r = 0.307; P < 0.0001) and change in bone area (r = 0.274; P < 0.0001). A critical blood leptin level is necessary to trigger reproductive ability in women, suggesting a threshold effect. Leptin is a mediator between adipose tissue and the gonads. Leptin may also mediate the effect of obesity on bone mass by influencing the periosteal envelope. This may have implications for the development of osteoporosis and osteoarthritis.

Gain in body fat is inversely related to the nocturnal rise in serum leptin level in young females.

Both genetic and environmental factors contribute to adolescent obesity. Evidence of a genetic basis for obesity development is substantial, although the exact mechanism of action has yet to be identified. The purpose of this study was to document the circadian rhythmicity of the serum leptin level in young females and to assess the impact of the change in body fat stores during growth on the nocturnal rise in the serum leptin level with implications for obesity traits. There was a significant rise in serum leptin at midnight and 0400 h, suggesting a diurnal variation in serum leptin concentrations (ANOVA F ratio = 6.2; P < 0.0001). There was also a strong association between relative total body fat and the average daytime serum leptin level (r = 0.78; P < 0.0001). The percent increase in the nocturnal leptin concentration was inversely related to the percent gain in total body fat (r = 0.45; P < 0.024). Forward stepwise regression analysis selected the change in total body fat over a 6-month interval as the most powerful determinant of the percent increase in the nocturnal leptin concentration (partial R2 = 0.203; beta = -0.450; SE of beta = 0.186; t = -2.418; P < 0.024). If the lack of a nocturnal rise in serum leptin persists over a longer period of time, it may have implications for the development of obesity, presumably by inadequate suppression of nighttime appetite.