Gender- and Age-Specific REE and REE/FFM Distributions in Healthy Chinese Adults.

Basic data on the resting energy expenditure (REE) of healthy populations are currently rare, especially for developing countries. The aims of the present study were to describe gender- and age-specific REE distributions and to evaluate the relationships among glycolipid metabolism, eating behaviors, and REE in healthy Chinese adults. This cross-sectional survey included 540 subjects (343 women and 197 men, 20-79 years old). REE was measured by indirect calorimetry and expressed as kcal/day/kg total body weight. The data were presented as the means and percentiles for REE and the REE to fat-free mass (FFM) ratio; differences were described by gender and age. Partial correlation analysis was used to analyze the correlations between REE, tertiles of REE/FFM, and glycolipid metabolism and eating behaviors. In this study, we confirmed a decline in REE with age in women (p = 0.000) and men (p = 0.000), and we found that men have a higher REE (p = 0.000) and lower REE/FFM (p = 0.021) than women. Furthermore, we observed no associations among glycolipid metabolism, eating behaviors, and REE in healthy Chinese adults. In conclusion, the results presented here may be useful to clinicians and nutritionists for comparing healthy and ill subjects and identifying changes in REE that are related to aging, malnutrition, and chronic diseases.

Curcumin triggers apoptosis via upregulation of Bax/Bcl-2 ratio and caspase activation in SW872 human adipocytes.

Induction of adipocyte apoptosis has been postulated as a novel strategy with which to treat obesity. The effects of curcumin, a polyphenol compound, on the apoptotic signaling pathway in SW872 adipocytes were investigated in the present study. The results showed that cell viability decreased following curcumin treatment in a time- and dose-dependent manner. The results from a single-stranded DNA ELISA assay indicated that curcumin causes the number of apoptotic cells to increase in a concentration-dependent manner. In addition, curcumin treatment resulted in an increased expression of Bax, and a decrease in that of of Bcl-2, with a concomitant upregulation of the Bax/Bcl-2 ratio. Curcumin treatment also led to the release of cytochrome c from mitochondria into the cytosol. Similarly, caspase-dependent poly (ADP) ribose polymerase (PARP) cleavage by curcumin was observed in the current study. In conclusion the results indicate that curcumin is an effective therapeutic agent with which to induce apoptosis in adipocytes. This effect is, in part, mediated through the mitochondrial pathway, which involves upregulation of the Bax/Bcl-2 ratio, cytochrome c release, activation of caspase-3 and the cleavage of PARP.

Curcuminoids Target Decreasing Serum Adipocyte-fatty Acid Binding Protein Levels in Their Glucose-lowering Effect in Patients with Type 2 Diabetes.

Whether supplementation of curcuminoids decreases serum adipocyte-fatty acid binding protein (A-FABP) level and whether this decrease benefits glucose control is unclear. One-hundred participants (n=50 administered curcuminoids, n=50 administered placebo) from our previous report on the effect of curcuminoids on type 2 diabetes in a 3-month intervention were assessed for levels of serum A-FABP, oxidative stress, and inflammatory biomarkers. Curcuminoids supplementation led to significant decreases in serum A-FABP, C-reactive protein (CRP), tumor necrosis factor-α, and interleukin-6 levels. Curcuminoids supplementation also significantly increased serum superoxide dismutase (SOD) activity. The change in serum A-FABP levels showed positive correlations with changes in levels of glucose, free fatty acids (FFAs), and CRP in subjects supplemented with curcuminoids. Further stepwise regression analysis showed that A-FABP was an independent predictor for levels of FFAs, SOD, and CRP. These results suggest that curcuminoids may exert anti-diabetic effects, at least in part, by reductions in serum A-FABP level. A-FABP reduction is associated with improved metabolic parameters in human type 2 diabetes.

The calcium-sensing receptor R990G polymorphism is associated with increased risk of hypertriglyceridemia in obese Chinese.

BACKGROUND: We have demonstrated that the calcium-sensing receptor (CaSR) is involved in lipid metabolism; however, whether CaSR polymorphisms affect lipid metabolism in obesity is still unclear. The present study aimed to determine the effects of CaSR polymorphisms on HTG risk in obese Chinese. METHODS: A total of 972 subjects with HTG and 1197 with normal triglyceride (NTG) were stratified by body mass index (BMI) into normal weight, overweight or obesity subgroups. After 12-h fasting, CaSR polymorphisms in exon 7 were determined in the blood. Serum lipids and glucose, as well as height, body weight and waist circumference were measured. The anthropometric and metabolic characteristics of the NTG subjects were re-evaluated 3 years later. RESULTS: There were no genotypic or allelic distribution differences for the A986S or Q1011E polymorphisms between the NTG and HTG groups. However, the G/G genotypic and G allelic distributions of the CaSR R990G polymorphism in the HTG group were higher than the NTG group (p<0.001). After stratification, in obese subjects, the homozygous (G/G) distribution of the CaSR R990G polymorphism in the HTG group was significantly higher than in the NTG group (p=0.001), and showed an increased risk of HTG at baseline [OR=2.55, 95% CI=1.65-3.92, p<0.006]. Interaction of the CaSR R990G polymorphism with BMI was associated with increased risk of HTG (ß=0.927, p<0.001). Re-evaluation of the NTG subjects revealed significantly increased serum triglyceride levels in obese homozygous versus wildtype carriers (p<0.05). CONCLUSIONS: These results suggest that the CaSR R990G polymorphism is associated with increased risk of HTG, especially in obese Chinese, and may be a potential genetic predictor of diseases related to HTG.

Curcuminoids exert glucose-lowering effect in type 2 diabetes by decreasing serum free fatty acids: a double-blind, placebo-controlled trial.

SCOPE: We previously found that curcuminoids decreased blood glucose and improved insulin resistance by reducing serum free fatty acids (FFAs) and increasing fatty acid oxidation in skeletal muscle of diabetic rats. This study was to investigate whether curcuminoids have beneficial effects on type 2 diabetic patients, and its possible mechanisms. METHODS AND RESULTS: Overweight/obese type 2 diabetic patients (BMI ≥ 24.0; fasting blood glucose ≥ 7.0 mmol/L or postprandial blood glucose ≥11.1 mmol/L) were randomly assigned to curcuminoids (300 mg/day) or placebo for 3 months. Bodyweight, glycosylated hemoglobin A1c (HbA1c ,% ), serum fasting glucose, FFAs, lipids, and lipoprotein lipase (LPL) were determined. A total of 100 patients (curcuminoids, n = 50; placebo, n = 50) completed the trial. Curcuminoids supplementation significantly decreased fasting blood glucose (p < 0.01), HbA1c (p = 0.031), and insulin resistance index (HOMA-IR) (p < 0.01) in type 2 diabetic patients. Curcuminoids also led to a significant decrease in serum total FFAs (p < 0.01), triglycerides (P = 0.018), an increase in LPL activity (p < 0.01). CONCLUSION: These findings suggest a glucose-lowering effect of curcuminoids in type 2 diabetes, which is partially due to decrease in serum FFAs, which may result from promoting fatty acid oxidation and utilization.

[Study of biological characteristics of the IVpi-189 virus derived from persistent influenza A virus-infected cell line].

To investigate biological characteristics of the IVpi-189 progeny virus derived from the culture of influenza A virus as a live-attenuated vaccine candidate. Persistent infection of a cultured cell line with influenza A virus (MDCK-IVpi) was established by incubating continuously influenza virus-infected cells at a lower temperature. The infectious progeny virus derived from MDCK-IVpi cells at the 189rd subculture was designated as the IVpi-189 strain of influenza virus. The cytopathic effect induced by IVpi-189 virus was observed under different temperature conditions. The production of infectious progeny virus was examined at 38 and 32 degrees C by plaque titration of cell-associated and released virus. IVpi-189 virus showed cytopathic effect as strong as that of IVwt in infected cell line of MDCK at 32 degrees C. However, when culture temperature was raised to 38 degrees C, the cytopathic effect induced by IVpi-189 virus was delayed and less pronounced. Virus growth in IVpi-189 virus-infected cells at 38 degrees C was significantly reduced as compared with that of IVwt virus, although both viruses yielded nearly equivalent high titers of cell-associated and released virus at 32 degrees C. The reasons of the decreased proliferative ability of IVpi-189 virus at high culture temperature were unrelated with virus inactivation or the release of progeny virus, but associated with the decreased replication of infectious progeny virus in the infected cells. IVpi-189 virus derived from MDCK cells infected persistently with influenza A virus showed biological characteristics as a potential live-attenuated vaccine candidate.

Curcumin, a potential inhibitor of up-regulation of TNF-alpha and IL-6 induced by palmitate in 3T3-L1 adipocytes through NF-kappaB and JNK pathway.

OBJECTIVE: To investigate the attenuating effect of curcumin, an anti-inflammatory compound derived from dietary spice turmeric (Curcuma longa) on the pro-inflammatory insulin-resistant state in 3T3-L1 adipocytes. METHODS: Glucose uptake rate was determined with the [3H] 2-deoxyglucose uptake method. Expressions of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were measured by quantitative RT-PCR analysis and ELISA. Nuclear transcription factor kappaB p65 (NF-kappa p65) and mitogen-activated protein kinase (MAPKs) were detected by Western blot assay. RESULTS: The basal glucose uptake was not altered, and curcumin increased the insulin-stimulated glucose uptake in 3T3-L1 cells. Curcumin suppressed the transcription and secretion of TNF-alpha and IL-6 induced by palmitate in a concentration-dependent manner. Palmitate induced nuclear translocation of NF-kappaB. The activities of Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase1/2 (ERK1/2) and p38MAPK decreased in the presence of curcumin. Moreover, pretreatment with SP600125 (inhibitor of JNK) instead of PD98059 or SB203580 (inhibitor of ERK1/2 or p38MAPK, respectively) decreased the up-regulation of TNF-alpha induced by palmitate. CONCLUSION: Curcumin reverses palmitate-induced insulin resistance state in 3T3-L1 adipocytes through the NF-kappaB and JNK pathway.

[DNA damage and changes of antioxidative enzymes in chronic benzene poisoning mice].

OBJECTIVE: To study the damage effect of benzene on DNA and its mechanism and the changes of antioxidative enzymes in vivo. METHODS: DNA break in bone marrow cells and peripheral blood lymphocytes of mice exposed to benzene by 4 h static inhalation per day at different concentrations for two months were analyzed with single cell gel electrophoresis (SCGE). Meanwhile, the activity of SOD, GSH-Px and the level of MDA in liver, spleen and brain were detected. RESULTS: In low and high dosage groups, the rate of DNA migration of bone marrow cells (83.56% +/- 10.28%, 92.54% +/- 15.93%) and peripheral blood lymphocytes (41.27% +/- 6.03%, 65.79% +/- 11.62%) were higher than those in control (4.13% +/- 0.52% and 2.21% +/- 0.31% respectively, P<0.05]. The activity of SOD in liver [(754.33 +/- 116.30), (694.26 +/- 116.30) U/mg pro] and GSH-Px [(22.52 +/- 3.31), (18.56 +/- 4.97) U/mg pro] were lower than those in control [(999.92 +/- 188.24) and (35.31 +/- 6.63) U/mg pro respectively, P<0.05, P<0.01]. But there was no significant difference between the two dosage groups. The activity of GSH-Px in spleen of both groups [(31.38 +/- 2.71), (25.30 +/- 7.44) U/mg pro] were lower than that of control [(37.11 +/- 3.42) U/mg pro, P<0.05] and there was significant difference between the two dosage groups. The activity of GSH-Px in brain of both groups [(5.70 +/- 0.84), (5.24 +/- 1.19) U/mg pro, P<0.05] were lower than that of control [(7.10 +/- 0.46) U/mg pro, P<0.05], but there was no significant difference between the two dosage groups. The level of MDA in brain of high dosage group [(3.99 +/- 1.15) nmol/mg pro] was higher than that of control [(2.58 +/- 0.53) nmol/mg pro, P<0.05]. CONCLUSION: Chronic benzene poisoning may result in DNA break in bone marrow cells and peripheral blood lymphocytes and decrease in the activity of antioxidative enzymes.