ACTA ENDOCRINOLOGICA (BUC)

Background. Peroxisome proliferator– activated receptors (PPAR) α and γ are ligand-activated transcription factors and members of the nuclear hormone receptor superfamily that regulate the metabolism of glucose and lipids. Aim. This study investigated the effects of PPARα deficiency on body weight in wild type and PPAR-αnull mice. Materials and methods. The study was performed on male wild type (WT) mice and homozygous PPAR-αnull (PPARα-knockout) mice of C57BL/6J genetic background. The mRNA expression was quantitatively analyzed by the real time of polymerase chain reaction (RTPCR). Liver TG content was measured by using a commercially available kit. Serum triglyceride (TG) content was measured using enzymatic methods. Serum insulin was determined using an ELISA kit. Serum glucose was determined by the glucose oxidase method using a glucose analyser. Results. Compared with WT, PPAR-αnull mice had high relative adipose tissue weight. These mice exhibited high adiposity state. PPAR-αnull mice also expressed high adiponectin and leptin mRNA levels compared to wild type animals. The PPAR-αnull mice had significantly higher body weight than WT. Hepatic TG and FFA were higher in PPAR- αnull mice as compared to WT animals. PPAR-αnull mice had a high accumulation of TG and FFA in the plasma. Serum insulin concentrations and its pancreatic mRNA transcripts were downregulated in PPAR-αnull mice, suggesting that PPARα gene deletion contributes to low insulin gene transcription. We have reported that PPARα deficiency leads to hypoglycaemia in mice. Conclusion. It is suggested a role of PPARα in obesity-diabetes in mice by studying PPARα-knockout mice.