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Objectives: This study aims to evaluate the association of orthodontic tooth movement with the concentration of leptin in gingival crevicular fluid (GCF). Materials and Methods: In thirty orthodontic patients, the concentration of leptin was assessed at baseline, 1 h, 24 h, 7 days, and 1 month after application of orthodontic force. Distalized tooth movement was evaluated by measuring the difference on dental casts at baseline and 1 month after force application. Results: Average concentration of leptin in GCF raises from baseline (T0) to 1 h after application of force (T1). There was a significant association of the overall average concentration of leptin with the degree of tooth movement (correlation coefficient = 0.625). Conclusion: There was a biphasic change in GCF leptin concentration and significant association between rates of tooth movement with GCF leptin concentration.

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It is of interest to evaluate the association of orthodontic tooth movement with concentration of leptin in Gingival Crevicular Fluid (GCF).Thirty orthodontic patients of both genders with equal sample size were included for the present study. Concentration of leptin was assessed at baseline (T0), 1 hr after application of force (T1), 24 hours later (T2), 7 days after application of force (T3), and 1 month after application of orthodontic force (T4). Using strips of filter paper, GCF was collected from the gingival sulcus on distal aspect of the right maxillary canine. Distalized tooth movement was evaluated by measuring the difference on dental casts, at baseline and one month after force application. One-way ANOVA with Bonferroni correction and Pearson's correlation test were used to analyze the data. Average concentration of leptin in GCF raises from baseline (T0) to 1 hours after application of force (T1), then increased to peak after 24 hours (T2), and declined to a minimum value after 7 days (T3) and again raises after 1 month (T4), closer to the base line value (T0), and this was statistically significant (P < 0.05). There was significant association of the overall average concentration of leptin to degree of tooth movement (correlation coefficient = 0.625). There was a biphasic change in GCF leptin concentration during one cycle of orthodontic force application, thus, a significant association between rates of tooth movement with GCF leptin concentration is noted.

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Polymorphisms in the LEP (G-2548A and A19G), LEPR (A326G, A668G and G3057A) and RETN (C-420G and G+62A) genes were documented according to their association with alterations in biochemical parameters such as glucose, insulin and lipid profiles, along with serum leptin and resistin concentrations. The aim of the study was to establish any contribution of the G-2548A and A19G polymorphisms of the LEP gene, the A326G, A668G and G3057A polymorphisms of the LEPR gene, and the C-420G and G+62A polymorphisms of the RETN gene to serum leptin and resistin levels in Mexican young adults. Clinical and biochemical variables, serum leptin and resistin levels, and genotype profiles were analysed in 66 Mexican young adults. Seven polymorphisms in the LEP, LEPR and RETN genes were genotyped using polymerase chain reaction-restriction fragment length polymorphisms analysis. Individuals carrying allele 3057A of the G3057A polymorphism in the LEPR gene showed significantly higher leptin concentrations than those bearing the genotype G/G (43.78 ± 39.11 vs 28.20 ± 14.12 ng/mL; p = 0.021). There were no associations of serum leptin or resistin levels according to the genotype of the other six analysed polymorphisms. Our results suggest that the allele 3057A of the LEPR G3057A polymorphism contributes to increased serum leptin levels in Mexican young adults.

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BACKGROUND: Leptin is known to affect bone metabolism both centrally and peripherally. This study was performed to investigate the relationship between leptin and bone mineral density(BMD) in healthy premenopausal and postmenopausal Korean women. METHODS: 140 women were recruited for a routine health check-up. Anthro-pometric and biochemical data were checked as usual. BMDs were measured by dual x-ray absorptiometry of the spine and femur in 67 premenopausal women and 73 postmenopausal women, in addition to their serum leptin levels. RESULTS: Serum leptin level showed no correlation with BMD in premenopausal women, but there was a positive correlation betwen serum leptin and spinal BMD in postmenopausal women(r=0.468, p<0.001). After the correcting for age, body mass index, and duration of menopause, the serum leptin level and BMD still showed a positive correlation(r=0.217, p=0.088) although weak. The women in the lowest quartile of serum leptin level showed significantly lower lumbar and femoral neck BMD. CONCLUSION: Leptin level seems to have a weak relationship with BMD showing different features in premenopausal and postmenopausal women.

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The ob gene product leptin is thought to be an adipostatic hormone through the regulation of food intake and energy expenditure. There are many reports that serum leptin concentration was increased in CRF patients, especially CAPD patients. The causes of elevated serum leptin concentration in CRF are believed to be multifactorial. Increased body fat mass, decreased residual renal function, active inflammation and hyperinsulinemia all are suggested to influence serum leptin concentration in CAPD patients. In this study, in order to investigate the pathogenic mechanism of increased serum leptin level in CAPD patients, we observed the changes of serum leptin concentration, leptin expression in the abdominal subcutaneous fat tissue, body fat composition, residual renal function, serum insulin concentration and CRP. Thirteen patients(7 men and 6 women, mean age 53+/-14 years) were enrolled in this study. Serum leptin concentration was measured by RIA before start of CAPD(baseline data), 5 days and 1, 3 months after start of CAPD. Simultaneously, fat tissues were aspirated from the abdominal subcutaneous fat tissues for analysis of ob gene expression. Ob mRNA expression was measured by semiquantitative RT-PCR method. The changes of serum insulin concentration, C-reactive protein, residual renal function were measured. All studies were done immediately before starting CAPD, 5 days, 1 month and 3 months after starting CAPD. Total body fat was estimated by dual energy X-ray absorptiometry and abdominal visceral and parietal fat area measured by computed tomography were done at 1-3 days(baseline data), 1 month, 3 months after start of CAPD. Serum leptin concentration increased significantly as early as 5 days after start of CAPD and maintained high up to 3 months(4.3+/-2.6->8.2+/-7.6->7.4+/-6.5->10.8+/-13.8ng/mL), while leptin expression in the abdominal subcutaneous fat tissue did not change during the study period(0.24+/-0.06->0.25+/-0.08->0.20+/-0.07->0.34+/-0.21ng/mL). No significant changes of body fat composition, residual renal function and serum insulin concentration were observed during the study period. These results suggest that increase of serum leptin concentration after CAPD may be due to increase of local leptin production, especially from the peritoneum, as has also been suggested by several reports of relatively higher dialysate leptin.

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PURPOSE: Leptin is a highly hydrophilic 16-kDa protein which is produced in the adipose tissue and participates in the regulation of food intake and energy expenditure. The aim of the present study was to examine the relation between umbilical cord blood leptin concentration and intrauterine growth. METHODS: Ninety-seven full-term newborn infants who were born in Yeungnam University Hospital from July to August 1998 were included in the study. They were divided into 3 groups related to birth weight : appropriate for gestational age(AGA) group(n=73), large for gestational age(LGA) group(n=17), small for gestational age(SGA) group(n=7). Birth weight, head circumference, mid-arm circumference, mid-arm circumference to head circumference ratio, Ponderal index, and BMI were measured at birth. Maternal body weight and placental weight were measured. Leptin concentrations of cord blood and maternal serum were measured by a RIA method, and testosterone, estradiol, insulin, c-peptide, glucose, white blood cell, hemoglobin, platelet count of cord blood were also measured. RESULTS: Leptin concentration in cord blood was positively correlated to birth weight and body length. Leptin concentrations(microgram/L) in cord blood were significantly different among groups(10.1+/-1.1 in LGA group, 8.7+/-0.9 in AGA group, 1.7+/-0.1 in SGA group). There was a statistically significant difference in leptin concentration of cord blood between female and male infants(11.6+/-1.9, versus 6.7+/-0.9). There was no significant correlations between leptin concentration of cord blood and placental weights or maternal leptin concentration. Therefore leptin concentration of cord blood can not inflect maternal leptin concentration but intrauterine fetal growth. CONCLUSION: Leptin in cord blood might originate mainly from fetal adipose tissue rather than the placenta, and may be related to fetal growth.

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