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Journal of Obesity
Volume 2012 (2012), Article ID 319172, 7 pages
doi:10.1155/2012/319172
Choline Deficiency Attenuates Body Weight Gain and Improves Glucose Tolerance in ob/ob Mice
1Group on the Molecular and Cell Biology of Lipids and Department of Biochemistry, University of Alberta, Edmonton, AB, T6G 2S2, Canada
2Cardiovascular Research Group, University of Alberta, Edmonton, AB, T6G 2S2, Canada
3Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, AB, T6G 2S2, Canada
Received 1 November 2011; Revised 2 February 2012; Accepted 16 February 2012
Academic Editor: Bernhard Breier
Copyright © 2012 Gengshu Wu et al. This 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.
Abstract
Previous studies demonstrated that choline supply is directly linked to high-fat-diet-induced obesity and insulin resistance in mice. The aim of this study was to evaluate if choline supply could also modulate obesity and insulin resistance caused by a genetic defect. Eight-week-old male ob/ob mice were fed for two months with either choline-deficient or choline-supplemented diet. Tissue weight including fat mass and lean mass was assessed. Intracellular signaling, plasma glucagon and insulin, and glucose and insulin tolerance tests were also investigated. The choline-deficient diet slowed body weight gain and decreased fat mass. Choline deficiency also decreased plasma glucose level and improved glucose and insulin tolerance although fatty liver was exacerbated. Increased adipose lipolytic activity, decreased plasma glucagon and reduced expression of hepatic glucagon receptor were also observed with the choline-deficient diet. Our results demonstrate that a choline-deficient diet can decrease fat mass and improve glucose tolerance in obese and diabetic mice caused by a genetic defect.