Rabbits with hereditary postprandial
hypertriglyceridemia exhibit
central obesity and are regarded as a reliable model for
metabolic syndrome. This study was performed to gain insight into the affected process of lipid metabolism and into the causative genes of the postprandial
hypertriglyceridemia rabbits. Eleven genes that play key roles in lipid metabolism were selected, their
mRNA levels were assessed by quantitative PCR, and their expressions were compared among postprandial
hypertriglyceridemia rabbits using Japanese white rabbits as the control. Two genes appeared to be in causal connection with postprandial
hypertriglyceridemia, and these were regarded as likely candidates for the pathogenesis. One was the
fatty acid synthase gene, which had an expression constitutively higher in postprandial
hypertriglyceridemia rabbits than in Japanese white rabbits during the fasting state and reached quite high levels after feeding. The other was the gene for hepatic
triglyceride lipase with an expression that was approximately one order lower than that found in the Japanese white rabbits. The low plasma hepatic
triglyceride lipase activities were consistent with the low levels of the transcript in the livers of the postprandial
hypertriglyceridemia rabbits. Thus, elevated
fatty acid synthesis and defected
lipid hydrolysis together would cause the postprandial
hypertriglyceridemia in postprandial
hypertriglyceridemia rabbits.