Research Article
Acute Effects of Exogenous Hormone
Administration on Postprandial Acylation Stimulating
Protein Levels in Ovariectomized Rats after a Fat Load
Bashair Al Riyami,
1
Marah El-Tahir,
2
Sultan Al Maskari,
1
Eugene H. Johnson,
3
and Jumana Saleh
1
1
Department of Biochemistry, College of Medicine, Sultan Qaboos University, Al-Khod, 123 Muscat, Oman
2
Department of Microbiology and Immunology, College of Medicine, Sultan Qaboos University, Al-Khod, 123 Muscat, Oman
3
Department of Animal and Veterinary Sciences, College of Agricultural and Marine Sciences, Sultan Qaboos University,
Al-Khod, 123 Muscat, Oman
Correspondence should be addressed to Jumana Saleh; jumanasaleh@hotmail.com
Received 30 June 2014; Accepted 14 November 2014; Published 2 December 2014
Academic Editor: Duo Li
Copyright © 2014 Bashair Al Riyami et al. his is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
Background. ASP, a potent lipogenic factor, was linked to female fat metabolism in association studies. Aim. To investigate acute
efects of sex hormone treatment on postprandial ASP levels in vivo. Methods. 24 female rats were randomly divided into 4 groups
including controls. he rats were ovariectomized and injected with progesterone, estrogen, or testosterone. An hour later, olive oil
was administered orally. Plasma ASP and triglycerides were measured at several postprandial time points. Area under the curve
(TG-AUC) represented TG clearance. Results. Only the progesterone treated group had a signiicant postprandial ASP increase
at two hours compared to basal levels (439.8 ± 62.4 versus 253.4 ± 59.03 g/mL, = 0.04). Interestingly, increased ASP levels
coordinated negatively with corresponding TG levels and TG-AUC postprandially, mostly evident in the opposite efects in the
progesterone and testosterone treated groups. ASP levels increased 3-fold in the progesterone versus testosterone treated groups,
whereas TG-AUC was signiicantly lower. Conclusion. hese indings suggest that progesterone enhances ASP production and TG
clearance simultaneously, supporting the notion of a stimulatory role for progesterone on ASP-mediated TG clearance. his is
the irst functional study demonstrating a cause-efect relationship between hormone treatment and ASP levels in vivo and may
contribute to understanding the mechanism of progesterone function as a female lipogenic hormone.
1. Introduction
Acylation stimulating protein (ASP) is a small basic protein
that consists of 76-amino acids produced from adipocytes.
ASP is produced by the interaction of complement C3, factor
B, and adipsin produced in adipose tissue [1]. Despite numer-
ous identiied adipose tissue derived factors, ASP uniquely
demonstrated a great efect in lipogenesis stimulation. ASP
actively stimulates TG synthesis in human ibroblasts and
to a much greater extent in adipocytes [2]. his occurs
through the enhanced esteriication of fatty acids in adipose
tissue by increasing the activity of diacylglycerol acyltrans-
ferase (DGAT), the rate limiting enzyme in TG synthesis,
and indirectly enhances the activity of lipoprotein lipase
(LPL) in adipocytes by increasing fatty acid trapping within
adipocytes [3]. ASP was also found to inhibit hormone-
sensitive lipase (HSL) [4]. Interestingly, ASP was shown to be
as potent as insulin in its fat storage efects. However, ASP
efects were independent, and additive, to insulin. Dietary
triglyceride rich lipoproteins, chylomicrons (CHYLO) were
the most potent stimulators of ASP production in vitro [5].
In animal studies, using a C3 knockout (ASP deicient) mice
showed delayed postprandial TG clearance and reduced TG
storage capacity ater a fat load [2, 6], which highlighted
the important role of ASP in the postprandial TG clearance.
Such an efect was diminished by the administration of
Hindawi Publishing Corporation
Journal of Nutrition and Metabolism
Volume 2014, Article ID 510916, 7 pages
http://dx.doi.org/10.1155/2014/510916