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Mice lacking acylation stimulating protein (ASP) have delayed postprandial triglyceride clearance
I Murray1, A D Sniderman, K Cianflone
1Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University Health Centre, Montreal, Quebec, Canada H3A 1A1.
Journal of Lipid Research
|September 14, 1999
Summary
Acylation stimulating protein (ASP), derived from C3, is crucial for triglyceride clearance. ASP-deficient mice show delayed fat absorption, highlighting its vital role in lipid metabolism.
Area of Science:
- Biochemistry
- Physiology
- Metabolic Research
Background:
- Acylation stimulating protein (ASP) is a C3-derived peptide that enhances triglyceride synthesis in adipocytes.
- The physiological role of the ASP pathway in vivo, particularly in postprandial fat metabolism, remains incompletely understood.
Purpose of the Study:
- To investigate the in vivo role of the Acylation stimulating protein (ASP) pathway in postprandial triglyceride clearance.
- To determine if C3 deficiency, and consequently ASP deficiency, impacts lipid metabolism in mice.
Main Methods:
- Generation of C3-deficient (C3-/-) and wild-type (C3+/+) mice.
- Oral fat tolerance tests were performed on both genotypes.
- Measurements included postprandial triglyceride and free fatty acid (FFA) levels.
- Intraperitoneal administration of ASP was conducted in C3-/- mice.
Main Results:
- C3-/- mice exhibited significantly delayed postprandial triglyceride clearance compared to C3+/+ mice.
- This delay was more pronounced in males and during the latter half of the postprandial period.
- Fasting and postprandial FFA levels were elevated in C3-/- males.
- ASP administration accelerated triglyceride clearance in C3-/- males.
Conclusions:
- The ASP pathway is a significant physiological determinant of normal postprandial triglyceride clearance.
- ASP plays a critical role in the efficient processing of dietary fats.
- Sex differences exist in the regulation of triglyceride clearance by the ASP pathway.