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RELATIONS BETWEEN OBESITY AND RENAL OSTEODYSTROPHY: REGULATION OF BONE METABOLISM BY LEPTIN.
Author(s) -
Janaina S. Martins,
João Henrique Castro,
Barbara Vogt,
Rogério de Oliveira,
Jacqueline Teixeira Caramori
Publication year - 2012
Publication title -
kidney research and clinical practice
Language(s) - English
Resource type - Journals
eISSN - 2211-9140
pISSN - 2211-9132
DOI - 10.1016/j.krcp.2012.04.346
Subject(s) - leptin , medicine , endocrinology , bone remodeling , adipose tissue , obesity , renal osteodystrophy , adipokine , metabolic syndrome , kidney disease
Recently, the bone tissue is now recognized as the protagonist in the complex control mechanism energy because their hormone interactions with the adipose tissue. Leptin is an adipokine and its production is proportional to the amount of adipose tissue. Although leptin is associated with obesity, and this is recognized as the protector of bone tissue, little can be said about the inter-relationship in chronic kidney disease. In cross-sectional study, 32 hemodialysis patients at Botucatu Medical School - State University of Sao Paulo - Brazil, were evaluated anthropometrically regarding the diagnosis of metabolic syndrome (based on the harmonization of criteria IDF, AHA/NHLBI, ATP III), biochemically and bone biopsy. Due to variability of serum leptin was applied also values of the natural logarithm (Ln) of leptin corrected by BMI. In comparisons was used Kruskal-Wallis, Pearson correlations were performed using regression analysis and considered the Ln leptin / BMI as the dependent variable was considered significant with p value less than 5%. Positive correlations of leptin have been shown in females (p=0.006), body fat percentage (p<0.001), serum albumin (p=0.035), and markers of metabolic syndrome, such as total cholesterol (p=0.01) , triglycerides (p=0.02) basal insulin (p=0.05) and BMI (p<0.001). About renal osteodystrophy, the sample has higher prevalence (69%) of high turnover diseases - osteitis fibrosa cystica and mixed bone disease. BMI, percent body fat, leptin and Ln leptin/BMI showed no influence on the bone turnover and osteoporosis. In regression analysis Ln leptin/BMI was independently associated with age (p=0.006) and individuals diagnosed with metabolic syndrome (p=0.002), histological classifications of bone tissue showed no associations. In conclusion, this was a preliminary result which reinforced the strong and independent relationship between leptin and metabolic syndrome in chronic renal failure, however, has not found evidence of the relationship between obesity, leptin and bone metabolism. Therefore, we suggest that interferes with uremia anabolic effect of leptin on the bone, irrespective of the very high serum levels, possibly acting on the signals in the leptin receptor osteoblasts. Interpreting the expression of these receptors would understand something more about bone metabolism of chronic renal failure

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