Effect of dietary fatty acids on body energy partitioning through the regulation of peroxisome proliferator-activated receptors

Purportedly, dietary fat level and type influence body energy homeostasis. To examine if changes in body weight and body composition were associated with alterations in peroxisome proliferator-activated receptor (PPAR) gene expression, forty-four 3-week-old weanling male Sprague-Dawley rats were fed ad libitum for 5 weeks with either a low fat (15% energy) or high fat (45% energy) diet providing four types of fats, i.e. coconut oil (MCT-SFA), safflower-HOSO oil (MUFA), safflower-HP oil (n-6 PUFA), or flaxseed oil (n-3 PUFA). Our results showed that feeding rats with a high fat diet reduced feed intake regardless of the types of fats. Only in the SFA group did feeding with a high fat diet result in increased weight gain, percent epididymal fat pad, serum and liver TG levels, and liver total lipid concentrations when compared to feeding with low fat (p < .05). This was accompanied with higher gene expression of epididymal adipose tissue PPARgamma and lower expression of liver PPARalpha (p < 0.05). The expression of a downstream gene of PPARgamma in adipose tissue, lipoprotein lipase (LPL), was also increased, confirming the enhanced expression of PPARgamma. However, expression of liver acyl-CoA oxidase (ACO) was increased on the high fat diet regardless of types of dietary fats. Rats fed high fat SFA, high fat MUFA, and low fat n-3 PUFA partitioned more food energy into body fat than their corresponding fatty acid groups (p < 0.05). The consumption of n-3 PUFA suppressed serum cholesterol, liver total lipid and TG concentrations. The fatty acid composition of the liver TG and total lipid reflected dietary lipid manipulation. No difference in serum leptin levels was observed.; This study suggested that during early development when positive energy balance usually occurs, it was the caloric content rather than the amount of food that was under control. Although long-term intake of low MCT diet had the potential for dietary prevention of obesity by suppressing total energy intake, consumption of this readily metabolized fat at a high level may not protect rapidly growing rats against excess fat accumulation, which may be attributed to an increased adipose tissue LPL gene expression through the activation of PPARgamma that enhanced circulating TG removal and hence promoted adipose tissue fat deposition.