Plasma acylation stimulating protein, adipsin and lipids in non‐obese and obese populations

Maslowska, Phelis, Sniderman, Rhode… - European journal of …, 1999 - Wiley Online Library
Maslowska, Phelis, Sniderman, Rhode, Blank, Cianflone
European journal of clinical investigation, 1999Wiley Online Library
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 …
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.
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