Plasma acylation stimulating protein (ASP) as a predictor of impaired cellular biological response to ASP in patients with hyperapoB

Xj, Zhang; Cianflone, Katherine; Genest, Jacques; Ad, Sniderman

doi:10.1046/j.1365-2362.1998.00359.x

Cited by 36 publications

(28 citation statements)

References 35 publications

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“…Thus, cells from subjects with high ASP levels were shown to have a reduced specific binding and response to ASP. 31,32 In addition, ASP levels are increased in obese diabetic subjects, and it has been suggested by Koistinen et al 12 that the metabolic disturbances in diabetes may overcome the regulatory role of ASP on lipid and glucose metabolism, again suggesting that high ASP levels indicate ASP resistance. 12 In a study of postprandial lipemia with a range of responses, higher fasting ASP predicted delayed TG clearance in both men and women.…”

Section: Discussionmentioning

confidence: 98%

Acylation-stimulating protein: effect of acute exercise and endurance training

et al. 2005

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INTRODUCTION: Acylation-stimulating protein (ASP) is an adipocyte-derived protein that contributes to fatty acid clearance. Regular exercise training improves fatty acid handling. OBJECTIVE: To examine the effect of acute exercise and short-term endurance training on ASP levels. SUBJECTS: Eight untrained men (age: 23.573.4 y; maximal power output (W max ): 3.770.6 W/kg body weight). DESIGN: Subjects were trained for 2 weeks. Before and after training, blood was sampled during a 3-h exercise test, and insulin sensitivity was assessed by an insulin tolerance test. RESULTS: Before training, ASP levels decreased during exercise (from 17.972.9 to 15.573.7 nmol/l at t ¼ 0 vs 180, Po0.05). Endurance training decreased fasting ASP levels significantly (17.972.9 vs 13.472.3 nmol/l pre-and post-training, Po0.001). Interestingly, after 2 weeks of endurance training, ASP levels tended to increase during exercise (from 13.472.3 to 17.274.5 nmol/l at t ¼ 0 vs 180, P ¼ 0.09). Baseline ASP levels correlated negatively with insulin sensitivity both before (r ¼ À0.86, Po0.01) and after training (r ¼ À0.82, Po0.05). CONCLUSION: Short-term endurance training reduces baseline ASP levels. These data fit with the hypothesis that reduced ASP levels indicate improved ASP sensitivity.

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Section: Discussionmentioning

confidence: 98%

Acylation-stimulating protein: effect of acute exercise and endurance training

et al. 2005

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“…7 In patients with cardiovascular disease, we have demonstrated that subjects with increased plasma Apo B (HyperapoB) and increased ASP are characterized by cellular resistance to the action of ASP as measured by decreased ASP cellular binding and decreased stimulation of both triglyceride synthesis (fatty acid esterification) and glucose transport. 68 Further, subcutaneous and omental adipocyte membranes from obese subjects (especially male subjects) demonstrate reduced ASP binding and affinity. 16 Thus, a high plasma ASP might be a marker for ASP resistance.…”

Section: Discussionmentioning

confidence: 99%

Relationships among acylation stimulating protein, adiponectin and complement C3 in lean vs obese type 2 diabetes

et al. 2005

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Objective: The purpose of this study was to determine the relationships between adipocyte hormones acylation stimulating protein (ASP), adiponectin, complement C3 (C3) (ASP precursor) and insulin, C-reactive protein (CRP), lipid profiles and insulin resistance in lean vs obese type 2 diabetes subjects. Subjects: Lean type 2 diabetes subjects (DL n ¼ 27) vs obese type 2 diabetes subjects (DO n ¼ 55) were compared to agematched nondiabetic groups (Obese, OB n ¼ 55 and control, CTL n ¼ 50).Results: The DO group demonstrated significant increases in plasma ASP and C3 with decreases in plasma adiponectin as compared to CTL. Interestingly, these increases in ASP and C3 were as high, or greater, in the DL group in spite of normal weight. By contrast adiponectin in the DL group was comparable to CTL, in spite of marked insulin resistance. C3 correlated with insulin, glucose and homeostasis model assessment of insulin resistance (HOMA-IR); ASP correlated with body mass index (BMI), glucose, insulin and plasma lipid parameters (non-esterified fatty acids (NEFA), triglyceride, cholesterol and apolipoprotein B). Adiponectin correlated with BMI, glucose, NEFA, triglyceride, high-density lipoprotein cholesterol and apolipoprotein A1 but not HOMA-IR, ASP or C3. CRP correlated only with HOMA-IR. Conclusion: Increased ASP and C3 are both associated with diabetes and related lipid factors but are not regulated coordinately. Adiponectin appears to be more closely related to body size (decreased in obese subjects) than insulin resistance in these subjects.

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“…15 It has been shown that ASPmediated FFA uptake in vitro is impaired in peripheral cells of FCHL patients, suggesting a receptor defect rather than decreased ASP production. 22 Different studies, aimed at investigating the relationship between C3 and lipids, showed that fasting C3 concentrations were correlated strongly not only with lipid parameters but also with several features of the insulin resistance syndrome. 23,32 Ylitalo et al 24 also found a correlation between fasting lipids and insulin concentration with plasma ASP levels.…”

Section: Discussionmentioning

confidence: 99%

Delayed and Exaggerated Postprandial Complement Component 3 Response in Familial Combined Hyperlipidemia

Meijssen

Dijk

Verseyden

et al. 2002

ATVB

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Plasma acylation stimulating protein (ASP) as a predictor of impaired cellular biological response to ASP in patients with hyperapoB

Abstract: A decrease in the ASP cell-surface receptor concentration is responsible for decreased ASP stimulation of TGS, and GT and may contribute to the inefficient postprandial triglyceride (TG) clearance in HASP-HB subjects.

Cited by 36 publications

References 35 publications

Acylation-stimulating protein: effect of acute exercise and endurance training

Acylation-stimulating protein: effect of acute exercise and endurance training

Relationships among acylation stimulating protein, adiponectin and complement C3 in lean vs obese type 2 diabetes

Delayed and Exaggerated Postprandial Complement Component 3 Response in Familial Combined Hyperlipidemia

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