BACKGROUND: Acylation stimulating protein (ASP) is a potent stimulator of TG synthesis in human adipocytes. DESIGN: In the present study, we have analysed plasma ASP and adipsin levels and their relationships to plasma lipids in non-obese and obese groups. RESULTS: The results show that the frequency distribution of ASP is skewed but that of adipsin is normal in both groups. In the non-obese population, the mean levels of plasma ASP and adipsin were 20.2 nmol L-1 (median) and 66.6 +/- 19 nmol L-1 (mean) respectively. No difference was observed between men and women for each of the parameters. In the obese population, the median plasma ASP was increased by 246% (69.9 nmol L-1) and adipsin by 31% (87.0 +/- 22.7 nmol L-1) above that of the control group. Although the levels for men and women were not statistically different for adipsin, the median ASP plasma concentration was 1.9-fold higher in obese women than in obese men (71.8 nmol L-1 vs. 37.6 nmol L-1, P < 0.05). Best subset regression analysis provided a model with variables that best predict plasma ASP [r2 = 0.160, P < 0.008 for body mass index (BMI), P < 0.05 for triacylglycerol (TG), P < 0.03 for free fatty acid (FFA)] and plasma adipsin (r2 = 0.057, P < 0.017 for BMI) in a non-obese population. In obese subjects, the model was different for plasma ASP (P = NS for any of the variables) and plasma adipsin (r2 = 0.356, P < 0.008 for FFA, P < 0.0002 for BMI, P < 0.02 for age). There was no correlation between ASP and adipsin in either the non-obese or the obese group. CONCLUSION: The present data suggest involvement of the ASP/adipsin pathway in the pathogenesis of obesity.
BACKGROUND: Acylation stimulating protein (ASP) is a potent stimulator of TG synthesis in human adipocytes. DESIGN: In the present study, we have analysed plasma ASP and adipsin levels and their relationships to plasma lipids in non-obese and obese groups. RESULTS: The results show that the frequency distribution of ASP is skewed but that of adipsin is normal in both groups. In the non-obese population, the mean levels of plasma ASP and adipsin were 20.2 nmol L-1 (median) and 66.6 +/- 19 nmol L-1 (mean) respectively. No difference was observed between men and women for each of the parameters. In the obese population, the median plasma ASP was increased by 246% (69.9 nmol L-1) and adipsin by 31% (87.0 +/- 22.7 nmol L-1) above that of the control group. Although the levels for men and women were not statistically different for adipsin, the median ASP plasma concentration was 1.9-fold higher in obesewomen than in obesemen (71.8 nmol L-1 vs. 37.6 nmol L-1, P < 0.05). Best subset regression analysis provided a model with variables that best predict plasma ASP [r2 = 0.160, P < 0.008 for body mass index (BMI), P < 0.05 for triacylglycerol (TG), P < 0.03 for free fatty acid (FFA)] and plasma adipsin (r2 = 0.057, P < 0.017 for BMI) in a non-obese population. In obese subjects, the model was different for plasma ASP (P = NS for any of the variables) and plasma adipsin (r2 = 0.356, P < 0.008 for FFA, P < 0.0002 for BMI, P < 0.02 for age). There was no correlation between ASP and adipsin in either the non-obese or the obese group. CONCLUSION: The present data suggest involvement of the ASP/adipsin pathway in the pathogenesis of obesity.
Authors: K Sivakumar; M F Bari; A Adaikalakoteswari; S Guller; M O Weickert; H S Randeva; D K Grammatopoulos; C C Bastie; M Vatish Journal: J Clin Endocrinol Metab Date: 2013-08-16 Impact factor: 5.958
Authors: D H Biesma; A J Hannema; H van Velzen-Blad; L Mulder; R van Zwieten; I Kluijt; D Roos Journal: J Clin Invest Date: 2001-07 Impact factor: 14.808
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Authors: Tina E Brinkley; Noriaki Kume; Hirokazu Mitsuoka; Dana A Phares; James M Hagberg Journal: Obesity (Silver Spring) Date: 2008-04-03 Impact factor: 5.002