| Objectives Nephrotic syndrome (NS) in children is characterizedby proteinuria, hypoproteinemia, edema, and hyperlipidemia. Consistenthyperlipidemia may cause to the deposition of lipid in kidney, whichresulted in the damage of glomerulus blood vessel endothelial cells andproliferation of mesangium cells. As a result, glomerular capillary wallpermeability will be matrix increased. And in long time following up, thehyperlipidemia may be associated with the pathogenesis ofglomerulosclerosis and is the potential risk factor of atherosclerosis inchildren with NS. Leptin, encoded by obese gene, is mainly synthesised and secretedby adipocytes, which is considered as a key agent in adjusting the lipidmetabolism in humans since it has been cloned successfully in 1994. Inhuman circulation, it is bound to be a high affinity binding protein ofleptin (soluble leptin receptor, sOBR), modulating the effects of leptin.Leptin imposes on linking with membrane receptor on the other cells toexpress its biology activity, sOBR may combine to leptin in circulationand only free leptin is capable of linking with membrane receptor on othercells. Animal experiment in vitro and in vivo have diplaied that leptincould adjust the lipid metabolism, but there have been very few studies onthe effects of leptin on hyperlipidmia in children with NS. Therefore, thisstudy observed whether leptin effects on the abnormal lipid metabolism,the role of sOBR on the bio-function of leptin, and the expression levels ofleptin receptor on the peripheral blood mononuclear cells (PBMC) inchildren with NS. Methods Twenty-three children with untreated NS and 15 age-,sex-, and body mass index-matched healthy controls were enrolled in thestudy. Fasting plasma lipoproteins, total cholesterol (TC), triglyceride(TG), apolipoprotein A (apoA), apoB, leptin, sOBR, and insulin levelswere measured in both groups. Moreover, the titre of leptin and sOBR inurine was also obtained in both groups. Concentration of leptin in serumand urine and the levels of the sOBR in serum and urine were measured byeneyme-linked immuno-sorbent assay (ELISA). Plasma lipid was detectedwith automatic biochemistry analyzer and the level of insulin wasmeasured by radioimmunoassay (RIA). And the expression of leptinreceptor mRNA and its cell membrane protein were detected by reversetranscription polymerase chain reaction (RT-PCR) andimmunocytochemistry. Results 1. Low density lipoproteins, TC, TG, and apoB levels were increasedin the patient group than those of control, plasma high density lipoproteinand apoA levels were similar in two groups, whereas plasma albumin andinsulin levels were lower as compared with those in the control group; 2. Serum sOBR levels, expression of leptin receptor mRNA byPBMC were significantly lower in the patient group compared with thecontrols, whereas fasting serum leptin levels and expression of membraneleptin receptor on PBMC were not significantly different between the twogroups. The ratio of serum leptin levels vs sOBR (free leptin index, FLI)was significantly higher in the NS group. Urinary sOBR excretion wassimilar in both groups, whereas urinary leptin in patient group was higherthan that in control group; 3. Serum leptin levels were correlated with body mass index in bothnephrotic patients and control, but not other parameter. FLI showed nocorrelation with body mass index, TC, TG, apoB in both groups, butplasma albumin, LDL, HDL, apoA and insulin in patient group. Conclusions 1. Fasting serum leptin levels were not different between NS groupand control group, but the expression of sOBR in patient group wasreduced, which enhanced the biologically active form of leptin in childrenwith NS; 2. The decrease of leptin receptor mRNA expression and membraneleptin receptor protein disintegration on cells might be responsible for thereduction of sOBR in srum of children with NS; 3.Serum free leptin is correlated with part of serum lipid parameters, albumin, and insulin, in which the sOBR play a key role; 4. The increased free leptin in serum might be a...
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