Submitted on November 6, 2007
Accepted on February 9, 2008
Weight Regain After Sustained Weight Reduction is Accompanied by Suppressed Oxidation of Dietary Fat and Adipocyte Hyperplasia
Matthew R Jackman1, Amy J. Steig1, Janine A Higgins1, Ginger C Johnson1, Brooke K Fleming-Elder1, Daniel H. Bessesen1, and Paul S MacLean1*
1 Center for Human Nutrition, University of Colorado Denver, Denver, Colorado, United States
* To whom correspondence should be addressed. E-mail: paul.maclean{at}uchsc.edu.
A dual-tracer approach (dietary 14C-palmitate and i.p. 3H-H20) was used to assess the trafficking of dietary fat and net retention of carbon in triglyceride depots during the first 24 h of weight regain. Obesity-prone male Wistar rats were matured under obesogenic conditions for 16 weeks. One group was switched to ad libitum feeding of a low fat diet for 10 weeks (Obese). The remaining rats were switched to an energy restricted, low fat diet for 10 weeks that reduced body weight by 14% and were then assessed in energy balance (Reduced), with free access to the low fat diet (Relapse-Day1), or with a provision that induced a minor imbalance (+10kcal) equivalent to that observed in Obese rats (Gap-Matched). Fat oxidation remained at a high, steady rate throughout the day in Obese rats, but was suppressed in Reduced, Gap-Matched, and Relapse-Day1 rats though 9, 18, and 24 h, respectively. The same caloric excess in Obese and Gap-Matched rats led to less fat oxidation over the day and greater trafficking of dietary fat to visceral depots in the latter. In addition to trafficking nutrients to storage, Relapse-Day1 rats had more small, presumably new, adipocytes at the end of 24 h. Dietary fat oxidation at 24 h was related to the phosphorylation of skeletal muscle acetyl-CoA carboxylase and fatty acid availability. These observations provide evidence of adaptations in the oxidation and trafficking of dietary fat that extend beyond the energy imbalance, which facilitate rapid, efficient regain during the relapse to obesity.
