Serum leptin and urine cortisol to cortisone ratio are correlated in familiar partial lipodystrophy type I (Kobberling Syndrome)

Author(s):  
Tommaso Daffara ◽  
Valentina Mancioppi ◽  
Marina Caputo ◽  
Ilaria Leone ◽  
Alice Ferrero ◽  
...  
2014 ◽  
Vol 41 (12) ◽  
pp. 2474-2481 ◽  
Author(s):  
Kati P. Markula-Patjas ◽  
Kaisa K. Ivaska ◽  
Minna Pekkinen ◽  
Sture Andersson ◽  
Eeva Moilanen ◽  
...  

Objective.To evaluate interactions between skeleton and adipose tissue, and association of adipokines and bone turnover markers with disease-related factors in patients with severe juvenile idiopathic arthritis (JIA).Methods.Forty-nine patients (median age 14.8 yrs, median disease duration 10.2 yrs) with refractory polyarticular JIA and 89 sex-matched and age-matched healthy controls participated in the study. Study subjects underwent clinical examination, body composition assessment with dual-energy X-ray absorptiometry, and analyses for leptin, adiponectin, and bone turnover markers.Results.Patients with JIA were shorter and more often overweight (p = 0.001) or obese (p < 0.001) than controls. They had significantly higher serum leptin, even when adjusted for fat mass (p < 0.001), than did controls. Adiponectin did not differ between the groups. Concentration of carboxyterminal telopeptide of type I collagen was higher (p = 0.006) in patients. The inverse association between leptin and bone turnover markers disappeared in controls but was strengthened in patients when adjusted for fat mass. Leptin, adiponectin, or bone markers did not associate with variables of disease activity.Conclusion.Patients with severe JIA had high adiposity accompanied by increased bone resorption. Their serum leptin was higher, even independently of fat mass. Leptin tended to associate inversely with bone turnover markers but did not associate with variables of disease activity.


1997 ◽  
Vol 48 (3) ◽  
pp. 103-107 ◽  
Author(s):  
T. Danne ◽  
A. Gr&uuml;ters ◽  
A. Wladimirova ◽  
B. Weber ◽  
R. Horn ◽  
...  

2006 ◽  
Vol 154 (5) ◽  
pp. 707-714 ◽  
Author(s):  
Patricia Crabbe ◽  
Stefan Goemaere ◽  
Hans Zmierczak ◽  
Inge Van Pottelbergh ◽  
Dirk De Bacquer ◽  
...  

Objective: Across studies it has been suggested that leptin intervenes as a regulator of bone metabolism. This study assesses the contribution in elderly men of leptin and the Gln223Arg leptin receptor gene (LEPR) polymorphism to the variation in bone homeostasis, in relation to body composition and free estradiol as major confounders. Design: We performed cross-sectional (n = 270) and longitudinal (mean follow-up 3.4 years, n = 214) evaluations in elderly men. Methods: Serum leptin, LEPR genotype, baseline bone mineral density (BMD), longitudinal BMD changes at the hip and forearm, and biochemical markers of bone turnover were determined. Results: In cross-sectional analyses absolute fat mass was the index of body composition most strongly associated with leptin (r = 0.74; P < 0.001). LEPR genotypes and serum leptin were not associated. Serum bone-specific alkaline phosphatase (S-BAP) was associated with LEPR genotypes (P = 0.05) and urinary C-terminal telopeptides of type I collagen (U-CTX) were associated with leptin levels (P = 0.03), independently from age, fat mass and free estradiol. Baseline BMD at the hip and forearm was neither associated with leptin nor with LEPR genotypes. Prospectively assessed BMD loss was not associated with serum leptin at the hip, whereas BMD loss was positively associated with leptin at the forearm (P = 0.01), independently from age, fat mass and free estradiol. Longitudinal changes in hip or forearm BMD were not associated with LEPR genotypes. Conclusion: The findings suggest a possible role for leptin as determinant of bone homeostasis in elderly men, but with only modest impact independently from body composition and free estradiol.


1998 ◽  
Vol 156 (1) ◽  
pp. 187-194 ◽  
Author(s):  
R Vettor ◽  
C Macor ◽  
F Novo ◽  
C Gottardo ◽  
S Zovato ◽  
...  

Abnormalities of the hypothalamus-pituitary-adrenal axis and hypersensitivity to corticosteroids have been suggested as major determinants of the development of visceral obesity. Since at the cellular level most effects of corticosteroids are mediated by specific receptors, we evaluated the number of type I and type II corticosteroid receptors in mononuclear leucocytes of 26 obese and 13 control subjects. We also studied the relationship between corticosteroid receptors, measured by radioreceptor assay, and abdominal visceral fat, evaluated by computed tomography scan, plasma and urine corticosteroid hormone concentrations and overall glucose metabolism, assessed by euglycaemic-hyperinsulinaemic clamp. We observed a decrease in type II receptors in the obese subjects (1746 +/- 160 vs 2829 +/- 201 per cell; P < 0.0001), with no change in type I receptors. Type II receptors decreased in relation to body mass index (r = -0.53; P < 0.005) and total glucose disposal (r = 0.51; P < 0.01). Abdominal visceral fat did not correlate with type II receptor number, but did correlate with total glucose disposal (r = -0.35; P < 0.05); the rate of glucose disposal was lower in obese subjects (3.3 +/- 0.3 vs 7.4 +/- 0.4 mg/kg per min; P < 0.001). Plasma and urine cortisol did not differ between the two groups. However, a direct correlation between type II receptor number and both plasma (r = 0.43; P < 0.02) and urine cortisol concentrations (r = 0.60; P < 0.05) was observed. In conclusion, the number of type II corticosteroid receptors in mononuclear leucocytes was found to be lower in obese subjects. This abnormality appears to be related to the degree of adiposity and to the main endocrine-metabolic features of the obesity syndrome, further supporting the hypothesis of involvement of hypothalamus-pituitary-adrenal axis hyperactivity in the pathophysiology of obesity.


2009 ◽  
Vol 296 (5) ◽  
pp. E1157-E1163 ◽  
Author(s):  
R. L. Araujo ◽  
B. M. Andrade ◽  
M. L. da Silva ◽  
A. C. F. Ferreira ◽  
D. P. Carvalho

The relationship between thyroid function and leptin has been extensively studied; however, the mechanisms underlying the changes in thyroid hormone economy that occur during caloric deprivation remain elusive. Our goal was to evaluate the thyroid function of rats submitted to 40% food restriction after chronic leptin replacement. Caloric restriction for 25 days led to significantly reduced serum leptin, thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3) and increased serum corticosterone, while liver, kidney, and thyroid type I deiodinase (D1) and brown adipose tissue (BAT) type II deiodinase (D2) activities were decreased and hypothalamic D2 was significantly increased. Interestingly, thyroid iodide uptake was unchanged by caloric restriction, but thyroperoxidase (TPO) activity was significantly reduced. Leptin replacement for the last 10 days of caloric restriction normalized serum leptin and TSH levels, but serum T4 and T3 levels and thyroid D1 and TPO activities were not reestablished. Also, a negative effect of leptin administration on Na+-I− symporter function was detected. Liver and kidney D1 and hypothalamic and BAT D2 were normalized by leptin, while pituitary D2 was significantly decreased. In conclusion, a tissue-specific modulation of deiodinases might be implicated in the normalization of thyroid function during leptin replacement in food-restricted rats. Although leptin restores the hypothalamus-pituitary axis during food restriction, it exerts a direct negative effect on the thyroid gland; thus normalization of serum thyroid hormones might depend on changes in deiodinase activities and the long-term thyroid stimulation by TSH to counterbalance the direct negative effects of leptin on the thyroid gland.


Author(s):  
Anastasia Stavropoulou ◽  
Gina E. Christopoulou ◽  
George Anastassopoulos ◽  
Sofia D. Panteliou ◽  
George P. Lyritis ◽  
...  

AbstractThe role of leptin during the progression of osteoporosis was investigated in ovariectomized rats by correlation of serum leptin levels with N-telopeptide of collagen type I (NTx) and osteocalcin levels before ovariectomy and 20, 40 and 60days after the operation. Furthermore, peripheral quantitative computed tomography was used to confirm the development of severe osteoporosis in rats on day 60. The levels of NTx and osteocalcin were significantly increased on day 20 [61.9±5.4nM BCE (bone collagen equivalents) and 215.6±53.3ng/mL, respectively] in comparison to those before ovariectomy (41.3±1.7nM BCE and 60.4±10.9ng/mL). Accordingly, leptin was significantly elevated on day 20 (3033±661 vs. 606±346 pg/mL before ovariectomy). Bone markers and leptin levels remained constant up to day 40, while a slight, but not statistically significant, decrease was noted for osteocalcin and leptin on day 60. Although leptin and bone markers did not correlate before ovariectomy (r=0.09 for NTx and r=−0.05 for osteocalcin), strong correlation was observed at all time points after ovariectomy. The data obtained suggest that the alterations in serum leptin levels during the progression of osteoporosis in ovariectomized rats follow the alterations in bone markers.


2004 ◽  
Vol 30 (3) ◽  
pp. 491-498 ◽  
Author(s):  
Mehmet Unal ◽  
Durisehvar Ozer Unal ◽  
Fatih Salman ◽  
Abdulkerim Kasim Baltaci ◽  
Rasim Mogulkoc

2006 ◽  
Vol 154 (3) ◽  
pp. 389-395 ◽  
Author(s):  
S Prouteau ◽  
L Benhamou ◽  
D Courteix

Objective: Despite a preliminary understanding of leptin–skeletal interactions, data in humans are inconsistent and the exact roles of leptin on bone metabolism have not yet been defined. The aim of this study was to examine the possible role of leptin in the regulation of bone metabolism in healthy, physically trained adults. Methods and Design: Body composition and bone mass (dual-energy X-ray absorptiometry), anthropometry, serum leptin, insulin, cortisol, osteocalcin, C-terminal telopeptide of type I collagen (CTx) and total plasma proteins were measured in judoists at normal body weight, after weight reduction and after weight regain. Physical training, weight cycling history, menstrual status and nutritional intake using a 7-day food record were assessed. Results: Precompetitive weight loss averaged 4 ± 0.3% of bodyweight and resulted in a significant decrease in leptin levels of 64% (P < 0.001) and of 31% for insulin (P < 0.0001). CTx and cortisol concentrations rose by 33% (P < 0.0001) and 81% (P < 0.05) respectively. Osteocalcin and total plasma protein remained unaffected by weight loss. A 4 ± 0.5% weight regain induced a 276% increase in leptin levels (P < 0.001) and an 18% increase in insulin (P < 0.001). CTx and cortisol decreased by 23% (P < 0.0001) and 27% (P < 0.05) respectively. Changes in leptin were significantly correlated with changes in bone resorption marker in response to both weight loss (r = 0.56, P < 0.01) and regain (r = 0.44, P < 0.05). Conclusions: These findings suggest that leptin is involved in the regulation of bone metabolism in healthy adults and might play a potential role in the prevention of osteoporosis.


Author(s):  
Ronald S. Weinstein ◽  
N. Scott McNutt

The Type I simple cold block device was described by Bullivant and Ames in 1966 and represented the product of the first successful effort to simplify the equipment required to do sophisticated freeze-cleave techniques. Bullivant, Weinstein and Someda described the Type II device which is a modification of the Type I device and was developed as a collaborative effort at the Massachusetts General Hospital and the University of Auckland, New Zealand. The modifications reduced specimen contamination and provided controlled specimen warming for heat-etching of fracture faces. We have now tested the Mass. General Hospital version of the Type II device (called the “Type II-MGH device”) on a wide variety of biological specimens and have established temperature and pressure curves for routine heat-etching with the device.


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