Biomedical subjects

Huiling Lu

Publications and source records attributed to Huiling Lu.

4 recordsLinked to original sources

PubMed2006

Thyroid status influence on adiponectin, acylation stimulating protein (ASP) and complement C3 in hyperthyroid and hypothyroid subjects.

BACKGROUND: Thyroid abnormalities (hyperthyroid and hypothyroid) are accompanied by changes in intermediary metabolism including alterations in body weight, insulin resistance and lipid profile. The aims of this study were to examine plasma ASP, its precursor C3 and adiponectin in hyperthyroid and hypothyroid subjects as compared to controls. METHODS: A total of 99 subjects were recruited from endocrinology/out-patient clinics: 46 hyperthyroid subjects, 23 hypothyroid subjects and 30 control subjects. Subjects were evaluated for FT4, FT3, TSH, glucose, insulin, complete lipid profile and the adipokines: adiponectin, acylation stimulating protein (ASP) and complement C3. RESULTS: Hyperthyroidism was associated with a 95% increase in adiponectin (p = 0.0002), a 47% decrease in C3 (p < 0.0001), no change in ASP and increased ASP/C3 ratio (p = 0.0012). Hypothyroidism was associated with a 31% increase in ASP (p = 0.008). Adiponectin and C3 correlated with FT3 (r = 0.383, p = 0.004 and r = -0.277, p = 0.007, respectively) and FT4 (r = 0.464, p = 0.003 and r = -0.225, p = 0.03, respectively). ASP correlated with TSH (r = 0.202, p = 0.04). Adiponectin did not correlate with either ASP or C3, only ASP and C3 correlated (r = -0.197, p = 0.05). Adiponectin was negatively correlated with BMI, total cholesterol and plasma triglyceride, while C3 was positively correlated with BMI and total cholesterol. Surprisingly, adiponectin was positively correlated with insulin (r = 0.293, p = 0.02) and HOMA-IR (r = 0.373, p = 0.003) while C3 was negatively correlated with glucose (r = -0.242, p = 0.022, insulin (r = -0.184, p = 0.05) and HOMA-IR. CONCLUSION: These changes suggest that thyroid disease may be accompanied by changes in adipokines, which may contribute to the phenotype expressed.

Journal Article↗

PubMed2005

Peroxisome proliferator activated receptor-gamma ligands induced cell growth inhibition and its influence on matrix metalloproteinase activity in human myeloid leukemia cells.

Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is one of the best characterized nuclear hormone receptors (NHRs) in the superfamily of ligand-activated transcriptional factors. PPAR-gamma ligands have recently been demonstrated to affect proliferation, differentiation and apoptosis of different cell types. The present study was undertaken to investigate PPAR-gamma ligands induced cell growth inhibition and its influence on matrix metalloproteinase MMP-9 and MMP-2 activities on leukemia K562 and HL-60 cells in vitro. The results revealed that PPAR-gamma expression was detectable in the two kinds of leukemia cells; Both 15-deoxy-delta(12,14)-prostaglandin J2(15d-PGJ2) and troglitazone (TGZ) have significant growth inhibition effects on these two kinds of leukemia cells. These two PPAR-gamma ligands could inhibit the leukemic cell adhesion to the extracellular matrix (ECM) proteins and the invasion through matrigel matrix. The expressions of MMP-9 and MMP-2 as well as their gelatinolytic activities in both HL-60 and K562 cells were inhibited by 15d-PGJ2 and TGZ significantly. We therefore conclude that PPAR-gamma ligands 15d-PGJ2 and TGZ have significant growth inhibition effects on myeloid leukemia cells in vitro, and that PPAR-gamma ligands can inhibit K562 and HL-60 cell adhesion to and invasion through ECM as well as downregulate MMP-9 and MMP-2 expressions. The data suggest that PPAR-gamma ligands may serve as potential anti-leukemia reagents.

Antineoplastic Agents↗

PubMed2005

Adiponectin, acylation stimulating protein and complement C3 are altered in obesity in very young children.

OBJECTIVE: Childhood obesity is increasing worldwide. This, in turn, is associated with chronic disease risk factors including hyperlipidaemia. The aim of the present study was to examine adiponectin, acylation-stimulating protein (ASP) and its precursor, complement C3, in very young obese and nonobese children and the corresponding associations with plasma lipid and lipoproteins. All three adipose tissue secreted factors are involved in fat metabolism, and little is known of the levels in very young children. DESIGN AND METHODS: A total of 124 healthy children from 2 to 6 years old were evaluated for weight, height, plasma lipids and adipokines. Based on percentage ideal body weight (%IBW), 60 children were nonobese and 64 were overweight/obese. RESULTS: ASP and C3 were significantly increased (P = 0.0002 and P < 0.0001, respectively) in obese vs. nonobese, and this pattern held true when separated in three age groups: toddler (2-3 years), preschool (4-5 years) and primary school (6 years). By contrast, adiponectin was significantly decreased (P = 0.04). When separated based on a positive family history of obesity, ASP was increased (P = 0.005). Other than a small (23.4%) increase in plasma triglyceride, all other lipids [cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol and nonesterified fatty acids] were normal. ASP, C3 and adiponectin were strongly correlated with %IBW (r = 0.515, P < 0.0001; r = 0.383, P < 0.0001; r = -0.211, P = 0.03, respectively). CONCLUSIONS: Changes in plasma adipokines are seen in very young obese children in the absence of lipid changes. These changes in ASP, C3 and adiponectin in very young obese children may predispose towards enhanced fat storage (ASP) and decreased fat oxidation (adiponectin) further driving the obesity profile.

Adiponectin↗

PubMed2003

Role of adrenomedullin in congenital heart disease associated with pulmonary hypertension.

The changes of adrenomedullin (ADM), endothelin-1 (ET-1) and nitric oxide (NO) levels before and after operation in congenital heart disease (CHD) associated with pulmonary hypertension (PH) were observed in order to investigate their role in CHD with PH and their clinical significance. The CHD patients were divided into 3 groups according to pulmonary artery systolic pressure (PASP): Non-PH group: PASP < or = 30 mmHg (n = 11); mild-PH group: PASP 31-49 mmHg (n = 10); moderate or severe-PH group: PASP > or = 50 mmHg (n = 12). The control group consisted of 15 health children. Plasma ADM, ET-1 and NO levels were determined by radioimmunoassay and colorimetry methods. The correlation between ADM and ET-1, NO, PASP was analyzed. The changes in plasma ADM, ET-1 and plasma NO on the 7th day after operation among the groups were compared. The results showed that plasma ADM levels in non-PH group were significantly higher than that in control group (P < 0.05), but there was no significant difference in ET-1 and NO levels between the two groups (P > 0.05). ADM and ET-1 levels in mild-PH group were significantly elevated as compared with those in non-PH group (both P < 0.05), but NO levels were decreased (P < 0.05). ADM and ET-1 levels in moderate or severe-PH groups were increased as compared with those in mild-PH group (both P < 0.01), but NO level significantly declined (P < 0.05). On the 7th day after operation, plasma ADM and ET-1 levels in PH group were significantly decreased (P < 0.05, P < 0.01) as compared with those before operation, but there was no significant difference in NO levels (P > 0.05). But NO levels in non-PH group were significantly increased (P < 0.05). Plasma ADM levels in CHD were positively correlated with PASP and ET-1 (r = 0.77, P < 0.01; r = 0.82, P < 0.01), negatively correlated with NO (r = -0.56, P < 0.05). It was concluded that during the progression of PH in the cases of CHD, plasma ADM, ET-1 and NO might play an important role in the development of PH. The increased ADM may represent a compensatory mechanism. It can interact with NO and ET-1 to regulate pulmonary circulation in the pathophysiology of PH with CHD. ADM may be involved in the defence mechanism against further increase of pulmonary arterial pressure. ADM could be used as a reliable indicator of the severity of CHD associated PH.

Adolescent↗