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Extreme Obesity (extreme + obesity)

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Life Sciences	50%

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Extreme obesity due to impaired leptin signaling in mice does not cause knee osteoarthritis

ARTHRITIS & RHEUMATISM, Issue 10 2009
Timothy M. Griffin
Objective To test the hypothesis that obesity resulting from deletion of the leptin gene or the leptin receptor gene results in increased knee osteoarthritis (OA), systemic inflammation, and altered subchondral bone morphology. Methods Leptin-deficient (ob/ob) and leptin receptor,deficient (db/db) female mice compared with wild-type mice were studied, to document knee OA via histopathology. The levels of serum proinflammatory and antiinflammatory cytokines were measured using a multiplex bead immunoassay. Cortical and trabecular subchondral bone changes were documented by microfocal computed tomography, and body composition was quantified by dual x-ray absorptiometry. Results Adiposity was increased by ,10-fold in ob/ob and db/db mice compared with controls, but it was not associated with an increased incidence of knee OA. Serum cytokine levels were unchanged in ob/ob and db/db mice relative to controls, except for the level of cytokine-induced neutrophil chemoattractant (keratinocyte chemoattractant; murine analog of interleukin-8), which was elevated. Leptin impairment was associated with reduced subchondral bone thickness and increased relative trabecular bone volume in the tibial epiphysis. Conclusion Extreme obesity due to impaired leptin signaling induced alterations in subchondral bone morphology without increasing the incidence of knee OA. Systemic inflammatory cytokine levels remained largely unchanged in ob/ob and db/db mice. These findings suggest that body fat, in and of itself, may not be a risk factor for joint degeneration, because adiposity in the absence of leptin signaling is insufficient to induce systemic inflammation and knee OA in female C57BL/6J mice. These results imply a pleiotropic role of leptin in the development of OA by regulating both the skeletal and immune systems. [source]

Pulmonary diffusion and aerobic capacity: is there a relation?

ACTA PHYSIOLOGICA, Issue 4 2010
Does obesity matter?
Abstract Aim:, We sought to determine whether pulmonary diffusing capacity for nitric oxide (DLNO), carbon monoxide (DLCO) and pulmonary capillary blood volume (Vc) at rest predict peak aerobic capacity (O2peak), and if so, to discern which measure predicts better. Methods:, Thirty-five individuals with extreme obesity (body mass index or BMI = 50 ± 8 kg m,2) and 26 fit, non-obese subjects (BMI = 23 ± 2 kg m,2) participated. DLNO and DLCO at rest were first measured. Then, subjects performed a graded exercise test on a cycle ergometer to determine O2peak. Multivariate regression was used to assess relations in the data. Results:, Findings indicate that (i) pulmonary diffusion at rest predicts O2peak in the fit and obese when measured with DLNO, but only in the fit when measured with DLCO; (ii) the observed relation between pulmonary diffusion at rest and O2peak is different in the fit and obese; (iii) DLNO explains O2peak better than DLCO or Vc. The findings imply the following reference equations for DLNO: O2peak (mL kg,1 min,1) = 6.81 + 0.27 × DLNO for fit individuals; O2peak (mL kg,1 min,1) = 6.81 + 0.06 × DLNO, for obese individuals (in both groups, adjusted R2 = 0.92; RMSE = 5.58). Conclusion:, Pulmonary diffusion at rest predicts O2peak, although a relation exists for obese subjects only when DLNO is used, and the magnitude of the relation depends on gender when either DLCO or Vc is used. We recommend DLNO as a measure of pulmonary diffusion, both for its ease of collection as well as its tighter relation with O2peak. [source]

Association of the G-2548A polymorphism in the 5, region of the LEP gene with overweight

ANNALS OF HUMAN GENETICS, Issue 5 2000
O. MAMMÈS
Mutations in the translated part of the leptin gene (LEP) have been found in only two families. Nevertheless DNA polymorphisms in the LEP region are linked to extreme obesity. We previously found in the 5, region of LEP a polymorphism, G-2548A, associated with a difference in BMI reduction following a low calorie diet in overweight women. Recently, this polymorphism was associated with extreme obesity in women. In this work, we genotyped a new sample from the general population including 314 normal weight (BMI < 27 kg/m2) and 109 overweight subjects (BMI , 27 kg/m2). The genotype and allele frequencies were significantly different between groups, with the G-2548 allele being more frequent in the overweight subjects (p < 0.01). In men, carriers of this allele had lower leptin concentrations adjusted for fat mass (p= 0.05). Our results indicate that variations at the leptin locus are associated with common obesity phenotypes, and not only with extreme obesity or the rare mendelian obesity syndromes. [source]