OBJECTIVETo assess the relationship of the variation of exon 20 of leptin receptor (LEPR) gene to the lipid metabolism and fat distribution of the children with obesity.

METHODSPolymerase chain reaction-restriction fragment length polymorphism(RFLP) and polyacrylamide gel electrophoresis were used to analyze the variation of exon 20 of the LEPR gene of the obesity group(72 obesity children) and the control group(60 healthy children). At the same time, all childrens' serum triglyceride(TG),total cholesterol(TC),high density lipoprotein cholesterol(HDL-C), low density lipoprotein cholesterol(LDL-C), height and weight were measured, and their body mass index(BMI) and fat percent(%fat) were calculated.

RESULTSThree genotypes of exon 20 of LEPR gene were detected in this study. Compared with the control, the frequency of gene variation at 3057 nucleotide G-->A transversion was higher(P<0.05). The concentration of serum TG and the BMI and %fat of the A/A genotype obesity children were higher than those of the G/G genotype ones(P<0.01) but the level of serum HDL of the A/A children were lower than that of the G/G children (P<0.01). As to the G/A genotype children, only their serum TG level was higher than that of the G/G genotype ones(P<0.05).

CONCLUSIONThe above findings indicated there were polymorphisms in the children with obesity, and those polymorphisms might remarkably affect their lipid metabolism and fat distribution.

Adipose Tissue ; metabolism ; Adolescent ; Base Sequence ; Child ; Exons ; Female ; Humans ; Lipid Metabolism ; Male ; Molecular Sequence Data ; Obesity ; genetics ; metabolism ; Polymorphism, Genetic ; Receptors, Cell Surface ; genetics ; Receptors, Leptin ; Sequence Analysis, DNA

The effect of porcine SIRT5 on replication of foot and mouth disease virus type O(FMDV-O)and the underlying regulatory mechanism were investigated.Western blot and RT-qPCR analyses were employed to monitor expression of endoge-nous SIRT5 in PK-15 cells infected with FMDV-O.Three pairs of SIRT5-specific siRNAs were synthesized.Changes to SIRT5 and FMDV-O protein and transcript levels,in addition to virus copy numbers,were measured by western blot and RT-qPCR analyses.PK-15 cells were transfected with a eukaryotic SIRT5 expression plasmid.Western blot and RT-qPCR analyses were used to explore the impact of SIRT5 overexpression on FMDV-O replication.Meanwhile,RT-qPCR analysis was used to detect the effect of SIRT5 overexpression on the mRNA expression levels of type I interferon-stimulated genes induced by SeV and FMDV-O.The results showed that expression of SIRT5 was up-regulated in PK-15 cells infected with FMDV-O and siRNA interfered with SIRT5 to inhibit FMDV-O replication.SIRT5 overexpression promoted FMDV-O replication.SIRT5 over-expression decreased mRNA expression levels of interferon-stimulated genes induced by SeV and FMDV-O.These results suggest that FMDV-O infection stimulated expression of SIRT5 in PK-15 cells,while SIRT5 promoted FMDV-O rep-lication by inhibiting production of type I interferon-stimula-ted genes.These findings provide a reference to further ex-plore the mechanism underlying the ability of porcine SIRT5 to promote FMDV-O replication.