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Pediatric Endocrinology |
Bone and Mineral Metabolism Laboratory, Departments of Physical Medicine, Medicine, and Nutrition, Ohio State University, Columbus, Ohio 43210
Address all correspondence and requests for reprints to: Dr. V. Matkovic, Bone and Mineral Metabolism Laboratory, Davis Medical Research Center, Ohio State University, 480 West 9th Avenue, Columbus, Ohio 43210.
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; ß = -0.450; SE of ß = 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.
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