Biomedical subjects

Muxun Zhang

Publications and source records attributed to Muxun Zhang.

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↗

PubMed2006

Expression of resistin protein in normal human subcutaneous adipose tissue and pregnant women subcutaneous adipose tissue and placenta.

The expression of resistin protein in normal human abdominal, thigh, pregnant women abdominal, non-pregnant women abdominal subcutaneous adipose tissue and placenta and the relationship between obesity, type 2 diabetes mellitus (T2DM), pregnant physiological insulin resistance (IR) and gestational diabetes mellitus (GDM) was investigated. The expression of resistin protein in normal human abdominal, thigh, pregnant women abdominal, non-pregnant women abdominal subcutaneous adipose tissue and placenta was detected by using Western blotting method. Fasting serum glucose concentration was measured by glucose oxidase assay. Serum cholesterol (CHOL), serum triglycerides (TG), serum HDL cholesterol (HDL-C) and serum LDL cholesterol (LDL-C) were determined by full automatic biochemical instrument. Fasting insulin was measured by enzyme immunoassay to calculate insulin resistance index (IRI). Height, weight, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured to calculate body mass index (BMI) and body fat percentage (BF %). Resistin protein expression in pregnant women placental tissue (67 905 +/- 8441) (arbitrary A values) was much higher than that in subcutaneous adipose tissue in pregnant women abdomen (40 718 +/- 3818, P < 0.01), non-pregnant women abdomen (38 288 +/- 2084, P < 0.01), normal human abdomen (39 421 +/- 6087, P < 0.01) and thigh (14 942 +/- 6706, P < 0.001) respectively. The resistin expression in abdominal subcutaneous adipose tissue showed no significant difference among pregnant, non-pregnant women and normal human, but much higher than that in thigh subcutaneous adipose tissue (P < 0.001). Pearson analysis revealed that resistin protein was correlated with BMI (r = 0.42), fasting insulin concentration (r = 0.38), IRI (r = 0.34), BF % (r = 0.43) and fasting glucose (r = 0.39), but not with blood pressure, CHOL, TG, HDL-C and LDL-C. It was suggested that resistin protein expression in human abdominal subcutaneous adipose tissue was much higher than that in human thigh subcutaneous adipose tissue. Resistin was closely related with central obesity, leading to IR, subsequently obesity and T2DM. Resistin protein expression in placental tissue was much higher than that in subcutaneous adipose tissue in normal human abdomen, pregnant abdomen, non-pregnant women abdomen and thigh. It was indicated that resistin protein could be secreted from human placental tissue. Resistin might be one of the factors that lead to pregnant physiological IR and GDM.

Blood Glucose↗

PubMed2005

Effect of tumor necrosis factor-alpha on resistin expression in 3T3-L1 adipocytes and its mechanism.

In order to investigate the effect of tumor necrosis factor-alpha (TNFalpha) on resistin expression in 3T3-L1 adipocytes, and further explore its mechanisms, the differentiated 3T3-L1 adipocytes were incubated with 0, 1, 10, 100 ng/mL TNFalpha respectively for 24 h, and then the expression of resistin was determined. The differentiated 3T3-L1 adipocytes were incubated with 100 ng/ mL TNFalpha for 3, 6, 24 h respectively, and then the expression of resistin mRNA was analyzed. 3T3-L1 adipocytes were induced to differentiate into mature adipocytes. The cells were randomly divided into 4 groups for culture. In the control group, no drugs were added. Cells of TNFalpha group were treated with 100 ng/mL TNFalpha. In Ro-31-8220 group, 5 micromol/L protein kinase C inhibitor Ro-31-8220 was added. With TNFalpha+Ro-31-8220 group, 100 ng/mL TNFalpha were added 1 h after the addition of 5 micromol/L Ro-31-8220. All adipocytes were cultured for 24 h. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were employed to detect the expression of resistin gene. Our results showed that resistin protein and mRNA in 3T3-L1 adipocytes were inhibited by TNFalpha at different concentrations (P<0.01), and the inhibitory effect increased with the concentration (P<0.01). At the same concentrations, the inhibitory effect increased with time (P <0.01). Ro-31-8220 could inhibit its expression and the inhibitive effect remained unchanged with addition of TNFalpha (P>0.05). It was concluded that TNFalpha could inhibit the expression of resistin in 3T3-L1 adipocytes. The mechanism may be that the expression of resistin is partly controlled by protein kinase C signal conduction pathway.

3T3-L1 Cells↗

PubMed2005

The influence of the Pro12Ala mutation of PPARgamma2 receptor gene on beta-cells restoration and insulin resistance in type 2 diabetes with hypertension.

The aim of this investigation was to determine whether a PPARgamma2 Pro12Ala polymorphism was associated with insulin resistance, beta-cell function and hypertension in Chinese populations. 289 unrelated Chinese subjects first diagnosed Type 2 diabetes (HbAC1 < 6.0) were investigated, including 132 hypertensive diabetic (HTD) subjects, 157 normotensive diabetic (NTD) subjects. Blood pressure and anthropometric measurements were collected from all participants, as well as several venous blood samples during oral glucose tolerance test (OGTT). Biochemical measurements (high-density lipoprotein (HDL) and low-density lipoprotein-cholesterol (LDL), triglycerides) and PPARgamma2 Pro12Ala genotype were also determined. And insulin resistance and beta-cells function was assessed by HOMA-IR and HOMA-beta respectively. The frequency of subjects bearing the Pro12Ala was lower in the hypertension group (3.03%) than in the non-hypertension group (5.7%) (P < 0.05) after adjusted for age, BMI and gender. Hypertensive diabetic Pro12Ala subjects had lower fasting plasma glucose level (P = 0.0127), and better glucose tolerance 60 min after oral glucose (P = 0.0361). Moreover, plasma insulin concentrations at 60 min was lower than those without A variant (P = 0.0275), and both hypertensive Ala/Pro in HOMA-beta (P = 0.0455) and AUC for insulin (P = 0.0473) were higher, and HOMA-IR was lower (P = 0.0375) as compared with hypertensive Pro/Pro subjects. No association was observed between Pro12Ala genotype and BMI, total cholesterol, HDL- cholesterol or triglycerides in either group. Our findings suggested that the Ala 12 allele of the PPARgamma2 gene may improve insulin resistance and ameliorate beta-cell function reserves in T2DM with hypertension, and protect patients from hypertension in T2DM. As an important thrifty gene, environment factors may exerts an effect of PPAR gamma2 on glucose homeostasis and insulin resistance.

Alanine↗