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| IJCEM Copyright © 2008-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711 |
Int J Clin Exp Med 2010;3(4):303-307
Original Article
Differential fatty acid profile in adipose and non-adipose tissues in obese mice
Mengting Li, Weisi Fu, Xiang-An Li
Department of Pediatrics, University of Kentucky Medical School, Lexington, Kentucky 40536, USA
Received August 23, 2010; accepted September 18, 2010; available online September 27, 2010
Abstract: Obesity is a metabolic disease characterized by chronic inflammation. Early studies indicated that adipose tissue from
obese mice contains more saturated fatty acids and that the saturated fatty acids activate TLR4- mediated inflammatory signaling,
which contributes to inflammation in adipose tissue. In this study, we determined fatty acid profile in non-adipose tissues from obese
(db/db) mice and compared with that from lean mice. Unexpectedly, in contrast to a significant increase in saturated and decrease in
unsaturated fatty acid in adipose tissue from obese mice, the non-adipose tissues from obese mice exhibited a significant decrease in
saturated and increase in unsaturated fatty acid compared with that from lean mice. The liver from obese mice had a 15% and 32%
decrease in palmitic acid and stearic acid, and a 20% increase in linoleic acid; the spleen had a 32% and 60% decrease in
palmitic acid and stearic acid, and a 70% and 50% increase in oleic acid and linoleic acid; and the pancreas had a 50% and 75%
decrease in palmitic acid and stearic acid, and a 130% and 113% increase in oleic acid and linoleic acid. These data suggest that,
different from adipose tissue where elevated saturated fatty acids contributes to inflammation, fatty acids per se in non-adipose tissues
such as liver, spleen and pancreas may not contribute to inflammatory responses in obese mice.s.(IJCEM1008003).
Keywords: Fatty acid, adipose tissue, non-adipose tissue, TLR4, NF-κB, inflammation, obesity
Full text PDF
Address all correspondence to:
Xiang-An Li, PhD
MDS 401B, 725 Rose Street
Lexington, KY 40536, USA.
Tel: 859-257-5113, Fax: 859-257-2120
E-mail: xli2@email.uky.edu
Original Article
Differential fatty acid profile in adipose and non-adipose tissues in obese mice
Mengting Li, Weisi Fu, Xiang-An Li
Department of Pediatrics, University of Kentucky Medical School, Lexington, Kentucky 40536, USA
Received August 23, 2010; accepted September 18, 2010; available online September 27, 2010
Abstract: Obesity is a metabolic disease characterized by chronic inflammation. Early studies indicated that adipose tissue from
obese mice contains more saturated fatty acids and that the saturated fatty acids activate TLR4- mediated inflammatory signaling,
which contributes to inflammation in adipose tissue. In this study, we determined fatty acid profile in non-adipose tissues from obese
(db/db) mice and compared with that from lean mice. Unexpectedly, in contrast to a significant increase in saturated and decrease in
unsaturated fatty acid in adipose tissue from obese mice, the non-adipose tissues from obese mice exhibited a significant decrease in
saturated and increase in unsaturated fatty acid compared with that from lean mice. The liver from obese mice had a 15% and 32%
decrease in palmitic acid and stearic acid, and a 20% increase in linoleic acid; the spleen had a 32% and 60% decrease in
palmitic acid and stearic acid, and a 70% and 50% increase in oleic acid and linoleic acid; and the pancreas had a 50% and 75%
decrease in palmitic acid and stearic acid, and a 130% and 113% increase in oleic acid and linoleic acid. These data suggest that,
different from adipose tissue where elevated saturated fatty acids contributes to inflammation, fatty acids per se in non-adipose tissues
such as liver, spleen and pancreas may not contribute to inflammatory responses in obese mice.s.(IJCEM1008003).
Keywords: Fatty acid, adipose tissue, non-adipose tissue, TLR4, NF-κB, inflammation, obesity
Full text PDF
Address all correspondence to:
Xiang-An Li, PhD
MDS 401B, 725 Rose Street
Lexington, KY 40536, USA.
Tel: 859-257-5113, Fax: 859-257-2120
E-mail: xli2@email.uky.edu
