Relationship between plasma leptin levels and the tumor necrosis factor-α system in obese subjects

Corica, Francesco; Allegra, Alessandro; Corsonello, Andrea; Buemi, Michele; Calapai, Gioacchino; Ruello, Antonella; Mauro, Vittorio Nicita; Ceruso, D

doi:10.1038/sj.ijo.0800826

Cited by 109 publications

(91 citation statements)

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“…Indeed, it is well known that plasma leptin concentrations are related to total fat mass, and are not affected by the distribution of fat between peripheral and abdominal stores. [40][41][42] Thus, highest BMI values and leptin concentrations contribute to define the clinical and metabolic profile of the cluster with the lower sensitivity to leptin. On the contrary, highest waist circumference values, as a marker of insulin resistance, 28 contribute to define the clinical profile of responsive patients.…”

Section: Discussionmentioning

confidence: 99%

Relationship between metabolic syndrome and platelet responsiveness to leptin in overweight and obese patients

et al. 2006

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Objective: To verify whether platelet responsiveness to leptin is associated with metabolic syndrome risk factors. Design: Cross-sectional study. Subjects: We studied 169 consecutive patients, mean age ¼ 43.679.9 years, with overweight (N ¼ 57) or obesity (N ¼ 112). Measurements: Cluster analysis was used to generate three clusters based on platelet responsiveness to increasing doses of leptin. Profiles of metabolic syndrome risk factors of the three clusters were compared by discriminant analysis. Results: Platelet responsiveness to leptin was absent in cluster 1, whereas cluster 3 had the greatest platelet aggregation response to leptin pre-incubation. Plasma leptin levels significantly decreased from cluster 1 to cluster 3 in both gender. Patients in cluster 2 had an intermediate profile of leptin responsiveness. Highest body mass index (BMI) values were more frequent in non-responders, whereas the prevalence of high waist circumference, as well as hypertriglyceridemia and hypertension, increased with increasing responsiveness to leptin from cluster 1 to cluster 3. Pattern of metabolic syndrome risk factors qualified as group specific in 69.0% of the cluster 1, 54.9% of the cluster 2 and 55.8% of the cluster 3. Circulating leptin, waist circumference, plasma triglycerides and BMI defined distinctive patterns of metabolic syndrome risk factors in the clusters. Conclusions: In overweight and obese outpatients, metabolic syndrome risk factors parallel to some extent platelet responsiveness to leptin. Such a correlation involves plasma leptin levels, waist circumference, plasma triglycerides and BMI, and may contribute to the excess risk of cardiovascular events in overweight and obese patients.

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Section: Discussionmentioning

confidence: 99%

Relationship between metabolic syndrome and platelet responsiveness to leptin in overweight and obese patients

et al. 2006

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“…18 Plasma concentration of sTNFR2 strongly correlated with BMI in some 13,[22][23][24] but not all studies. 25 Similarly, circulating sTNFR1 levels were not associated with BMI, 13,22,23 although in other studies the relationship was significant. 24,25 The independent contribution of smoking, as a confounding factor, on the relationship between fat mass and TNF system activation, as measured using circulating sTNFR1 and sTNFR2, has not been evaluated, despite the evidences that smoking alters cytokine production.…”

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confidence: 92%

Smoking, fat mass and activation of the tumor necrosis factor-α pathway

et al. 2003

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OBJECTIVE: Obesity may be associated with increased markers of inflammation that could be triggered by metabolic, physical, infectious or environmental processes. As smoking significantly increases cytokine production, we aimed to study how smoking influences the relationship between fat mass and soluble tumor necrosis factor-a (TNF-a) receptors 1 and 2 (sTNFR1 and sTNFR2). DESIGN: Cross-sectional, clinical observational study. SUBJECTS: A total of 133 healthy men (age: 27-53 y, body mass index (BMI): 24-30.2 kg/m 2 ), 80 of whom were never-smokers and 53 smokers, matched for age, BMI and waist-to-hip ratio. MEASUREMENTS: Circulating soluble fractions of the TNF-a receptors sTNFR1 and sTNFR2 were measured to study their relationship with fat mass (bioelectric impedance). RESULTS: Smokers had significantly lower fat mass, lower fasting glucose, insulin and leptin concentrations than nonsmokers. Despite lower fat mass and insulin, smokers showed significantly increased circulating sTNFR2 levels (3.770.8 vs 3.470.7 ng/ ml, P ¼ 0.03). The slopes of the relationships between sTNFR1 and fat mass, and between sTNFR2 and fat mass, were significantly steeper in smokers than in nonsmokers. In a stepwise multiple linear regression analysis, both fat mass (Po0.00001) and smoking (P ¼ 0.025) independently contributed to 13% of sTNFR1 variance and to 4% of sTNFR2 variance (P ¼ 0.03). CONCLUSION: Both fat mass and smoking are related to increased activity of the TNF-a axis.

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“…The homeostasis model assessment of insulin resistance (HOMA IR) was calculated as previously described. 24 Plasma TNFa concentrations were measured by enzymelinked immunoabsorbent assay (Pharmingen, San Diego, CA, USA). The intra-and inter-assay coefficients of variation were < 5.8 and < 13.8%, respectively.…”

Section: Plasma Biochemical Analysismentioning

confidence: 99%

TNFα expression of subcutaneous adipose tissue in obese and morbid obese females: relationship to adipocyte LPL activity and leptin synthesis

et al. 2002

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INTRODUCTION:Tumor necrosis factor (TNFa) has been invoked as an adipostat. Accordingly, the adipose tissue expression of TNFa has been shown to be proportional to the degree of adiposity. The regulatory role of TNFa in obesity may be controlled by several mechanisms. These include the inhibitory effect on LPL activity, the mediation on glucose homeostasis or the effect on leptin. To assess the role of TNFa in obesity we measured adipocyte TNFa expression in 96 females with a wide range of adiposity and with or without type 2 diabetes. We analysed the relationship between TNFa expression, adipocyte LPL activity, insulin resistance and leptin in this population. RESULTS: The TNFa and leptin expression of the adipose tissue in obese and morbid obese patients were significantly higher than in controls. Obese and morbid obese patients had slightly higher levels of LPL activity, but these differences were not significant. We observed a significant relationship between adipose TNFa expression and body mass index (r ¼ 0.35, P < 0.001). TNFa expression was negatively related to LPL activity (r ¼ 7 0.28, P < 0.05) and positively related to leptin expression (r ¼ 0.35, P < 0.001). CONCLUSION: Our results indicate that obese women, even those with morbid obesity, over-express TNFa in subcutaneous adipose tissue in proportion to the magnitude of the fat depot and independently of the presence of type 2 diabetes. The TNFa system may be a homeostatic mechanism that prevents further fat deposition by regulating LPL activity and leptin production.

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Relationship between plasma leptin levels and the tumor necrosis factor-α system in obese subjects

Cited by 109 publications

References 50 publications

Relationship between metabolic syndrome and platelet responsiveness to leptin in overweight and obese patients

Relationship between metabolic syndrome and platelet responsiveness to leptin in overweight and obese patients

Smoking, fat mass and activation of the tumor necrosis factor-α pathway

TNFα expression of subcutaneous adipose tissue in obese and morbid obese females: relationship to adipocyte LPL activity and leptin synthesis

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