ASP acts as a paracrine and autocrine signal to increase triglyceride synthesis in adipocytes. ASP administration results in more rapid postprandial lipid clearance. This present work consists of a series of experiments on complement C3 knockout mice (therefore ASP deficient mice) in vivo. The aim of this work is to understand the role of Acylation stimulating protein (ASP) in energy regulation. / Compared to wild type mice, ASP deficient mice have delayed triglyceride and fatty acid clearance, decreased fat mass and body weight with concurrent increases in food intake. Both male and female ASP deficient mice have increased oxygen consumption, an indication of increased energy expenditure. This effect was not dependent on the presence of leptin. On the other hand, the mechanism of increased energy expenditure was different in male and female ASP deficient mice. Female ASP deficient mice have increased movement while the male ASP deficient mice were found to have increased uncoupling protein-3 expression in muscle. Fat load tests in the male mice demonstrate ASP deficiency redirects absorbed energy from storage in adipose tissues towards utilization in liver and muscle. Acute administration of ASP normalizes this process. / The results from these studies suggest that ASP is a key hormone regulating lipid storage in adipocytes. Deficiency of ASP leads to energy repartition, decreased energy storage and increased energy expenditure. In short, ASP deficiency results in obesity resistance.
Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.85106 |
Date | January 2002 |
Creators | Xia, Zhunan |
Publisher | McGill University |
Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
Language | English |
Detected Language | English |
Type | Electronic Thesis or Dissertation |
Format | application/pdf |
Coverage | Doctor of Philosophy (Division of Experimental Medicine.) |
Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
Relation | alephsysno: 002166415, proquestno: AAINR06353, Theses scanned by UMI/ProQuest. |
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