Date of Graduation


Document Type


Degree Type



Davis College of Agriculture, Natural Resources and Design


Animal and Nutritional Sciences

Committee Chair

Kimberly M. Barnes

Committee Co-Chair

Kenneth P. Blemings

Committee Member

Lisa Salati

Committee Member

Matthew E. Wilson

Committee Member

Jianbo Yao


Obesity is a main health concern and leads to many other health complications. Conjugated linoleic acid (CLA) has been shown to cause a reduction in obesity in several species. CLAinduced body fat loss is enhanced when mice are fed coconut oil (CO). The objectives were to determine if the CLA-induced lipolysis in different oil source-fed mice was time-dependent and to determine the effect of cell signaling inhibitors on CO+CLA-induced lipolysis. Study 1: Male mice (ICR; n=80; 3wk) were fed 7% soybean oil (SO) or CO diets for 6wk and then supplemented with 0 or 0.5% CLA for 3, 7, 10 or 14d. Body fat index (BFI) was calculated as [(epididymal fat pad + retroperitoneal fat pad)/ body weight] and lipolysis was determined by non-esterified fatty acid (NEFA) and glycerol release in 3hr ex vivo cultures. BFI was reduced by CO on d7 (P<0.01) and CLA tended (P=0.09) to decrease BFI in CO-fed mice on d10. BFI was reduced in both CO and SO-fed mice (P<0.05) in response to CLA on d14. NEFA release was increased by CLA in CO-fed mice (P<0.01) but not in SO-fed mice on d7 and 10 but on d14 CLA increased NEFA release in both CO and SO-fed mice (P<0.0001). Glycerol release was also increased by CLA in CO-fed mice but not in SO-fed mice on d3 and d7 (P<0.05). We then determined expression and activation level of proteins involved in lipolysis and lipogenesis. CLA tended to decrease (P=0.06) p-perilipin protein expression in CO-fed mice. There was also a trend for CLA (P=0.06) to decrease adipose triglyceride lipase (ATGL) protein. CO-fed mice had greater fatty acid synthase, stearoyl CoA desaturase 1 mRNA expression and less acetyl CoA carboxylase mRNA expression (P<0.01). Sterol regulatory binding protein 1c and malic enzyme expression was least in CO+CLA-fed mice. Study 2: 3T3-L1 cells were differentiated, exposed to CO or SO for 10d, serum starved overnight, and pre-loaded with 3[H]-oleic acid for 12 hrs. Cells were treated with 50 muM CLA or linoleic acid (LA) with/without cell signaling inhibitors for 12-24 hrs. Lipolysis was measured as the 3-hr release of 3[H]-oleic acid. Without inhibitors, CO+CLA treatment caused more lipolysis (P<0.01) than all other treatments, which did not differ. None of the inhibitors tested reduced lipolysis in CO+CLA treated cells. Cyclooxegenase-2 inhibitor increased lipolysis of SO+CLA treated cells (P=0.05) to the level of CO+CLA. Phospholipase C inhibitor increased lipolysis in all treatments (P<0.0001) except that of CO+CLA. Peroxisome proliferator-activated receptor alpha inhibitor also increased lipolysis of CO+LA (P<0.05) to the level of CO+CLA treated cells and in SO+CLA treated cells. There was no effect of the p42 mitogen-activated protein kinase or protein kinase A inhibitor, compared to absence of inhibitor. Therefore CLA-induced lipolysis occurs more rapidly in CO vs SO-fed mice and the CLA enhanced lipolysis in CO group could involve the PLC pathway.