Incorporation of conjugated linoleic acid into brain lipids is not necessary for conjugated linoleic acid–induced reductions in feed intake or body fat in mice

Abstract

Dietary conjugated linoleic acid (CLA) causes reduced feed intake (FI) and body fat (BF). It is unknown, though, if CLA incorporation into tissues, alterations in serum hormones, and/or appetite-regulating neuropeptides are involved. We hypothesized that CLA incorporation into brain lipids would be correlated with changes in appetite-regulating neuropeptide expression and reductions in FI and BF. Male mice (n = 150; 9 weeks old, ICR) received the control diet ad libitum (CON), 2% CLA diet ad libitum (CLA), or control diet pair-fed to the intake of CLA-fed mice for 1, 2, 3, 5, or 7 days. Both FI and body weight were measured daily, and a BF index was calculated. Liver, adipose, and brain fatty acids; serum insulin, leptin, and peptide YY; and arcuate nucleus neuropeptide Y, agouti-related protein, and α-melanocyte–stimulating hormone protein were determined. Mice fed CLA ate less (P < .05) than did the CON on days 1, 2, 3, and 7 but were leaner (P < .05) only on day 7. Mice that received the control diet pair-fed to the intake of CLA-fed mice did not differ in BF from the CON. By days 1 and 2, CLA isomers were incorporated into the liver and adipose but not in the brain. Insulin was increased in CLA-fed mice on days 5 and 7, and leptin was decreased on day 7. Peptide YY and the neuropeptides did not differ. Tissue CLA was not correlated with FI, body weight, or BF but was positively correlated with insulin and negatively correlated with leptin. The reduction in FI is not sufficient to cause the reduction in BF, and tissue CLA accumulation does not appear to be required.