真皮与血管漫反射光谱的相关性研究

基于真皮与血管漫反射光谱的相关性活体实验研究真皮漫反射光谱法测量血糖浓度的可行性:成功剥离兔子股动脉血管,实现血管光谱的直接测量;在调节兔子的血糖浓度变化的过程中,同时监测兔子的血管漫反射光谱和皮肤漫反射光谱。实验结果表明,血管漫反射光谱与皮肤漫反射光谱之间的相关系数达到0.88以上。分别基于血管漫反射光谱和皮肤漫反射光谱建立校正集模型,并预测得到相应的血糖浓度集G1和G2,两组血糖浓度预测值之间的相关系数为0.90。因此,真皮漫反射光谱信号能够有效地反应血液信息,从而实现血糖浓度的无创检测。     

Degradation Kinetics of Xylose and Glucose in Hydrolysate Containing Dilute Sulfuric Acid

In preparation of fuel alcohol from biomass as feedstock, hydrolysis with dilute acid as catalyst is one way to produce fermentable saccharide, xylose and glucose. However, the acid is also the catalyst in degradation of xylose and glucose and the yield of sacchride is dependent on the kinetic behaviors of saccharide. The degradation kinetics of xylose and glucose in the hydrolysate was investigated under the conventional process conditions of hydrogen ion concentration from 0.05 to 0.2 mol/L and temperature from 150 to 200℃. With a numerical calculation method, the kinetic parameters were estimated, and the activation energy of xylose and glucose in the degradation reaction was obtained. The kinetic equations correlating the effect of hydrogen ion concentration on the rate constants of degradation reaction were established. Comparison between the calculated results from the equations and experimental ones proved that the established kinetic model could satisfactorily predict the degradation behavior of xylose and glucose in the acidic hydrolysate.     

山梨醇用Raney 镍催化剂活化条件的研究

对葡萄糖加氢制山梨醇用Raney镍催化剂的活化条件进行了研究,用丙酮法测定催化剂的加氢活性,考察了活化时NaOH的用量、活化温度及活化时间对Raney 镍催化剂加氢活性的影响.实验结果表明,制备Raney镍催化剂较好的活化条件为:NaOH/Al(物质的量比)为4.5,活化温度50 ℃,活化时间为1.5 h.     

直接法合成十二烷基糖苷反应机理和动力学

由葡萄糖和十二醇直接合成了十二烷基糖苷。研究了该反应的机理,在对反应机理中基元反应分析的基础上建立了反应动力学模型,并计算了相关的动力学参数,确定了反应动力学方程。     

基于多壁碳纳米管修饰的葡萄糖生物传感器

用循环伏安法在玻碳电极表面电沉积了一层稳定的甲苯胺蓝聚合物膜,以此作为电子传递介体,结合多壁碳纳米管、壳聚糖（CHIT）、葡萄糖氧化酶（GOD）混合包埋制备出一种新型葡萄糖生物传感器,实验结果显示,用此法制备的传感器对葡萄特的线性响应范周为5．0×10^-6～2．0×10^-2mol／L,线性相关系数为0．9969。检测限为1×10^-6,响应时间为3．2S,并具有抗尿酸、抗坏血酸等干扰的特点。     

微波辐射下臭氧氧化葡萄糖制备葡萄糖酸

探索一种在微波辐射下通过臭氧氧化葡萄糖制备葡萄糖酸的高效绿色新方法。实验结果表明：在微波辐射下,臭氧在无催化剂条件下可快速催化氧化葡萄糖为葡萄糖酸溶液。对单因素影响实验结果显示,随着葡萄糖溶液浓度的上升,葡萄糖酸产率逐渐下降;微波辐射功率、微波辐射时间、臭氧气体流量增加等因素对葡萄糖酸产率的影响均表现为先上升后下降的变化趋势。通过试验设计,得到本实验的最佳反应条件组合为：葡萄糖溶液浓度400mmol·L-1,气体流量2465mL·min-1,微波辐射功率210W,微波辐射15min时,葡萄糖酸产率为85．6％。     

Endothelial Nox5 Expression Modulates Glucose Uptake and Lipid Accumulation in Mice Fed a High-Fat Diet and 3T3-L1 Adipocytes Treated with Glucose and Palmitic Acid

Obesity is a global health issue associated with insulin resistance and altered lipid homeostasis. It has been described that reactive oxygen species (ROS) derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) activity are involved in the development of these pathologies. The present study describes the role of endothelial NOX5 expression over adipose tissue by using two experimental systems: NOX5 conditional knock-in mice fed with a high-fat diet and 3T3-L1 adipocytes cultured with conditioned media of NOX5-expressing endothelial cells previously treated with glucose and palmitic acid. Animals expressing NOX5 presented lower body weight gain and less mesenteric and epididymal adipose mass compared to control mice fed with the same diet. NOX5-expressing mice also showed significantly lower glycaemia and improved insulin-induced glucose uptake. In addition, Glut4 and Caveolin 1 (Cav1) expression were significantly increased in the adipose tissue of these animals. Likewise, 3T3-L1 adipocytes treated with conditioned media from NOX5-expressing endothelial cells, incubated with high glucose and palmitic acid, presented a reduction in lipid accumulation and an increase in glucose uptake. Moreover, a significant increase in the expression of Glut4 and Cav1 was also detected in these cells. Taken together, all these data support that, in response to a highly caloric diet, NOX5 endothelial activity may regulate glucose sensitivity and lipid homeostasis in the adipose tissue.     

Insulin Resistance Is Not Sustained Following Denervation in Glycolytic Skeletal Muscle

Denervation rapidly induces insulin resistance (i.e., impairments in insulin-stimulated glucose uptake and signaling proteins) in skeletal muscle. Surprisingly, whether this metabolic derangement is long-lasting is presently not clear. The main goal of this study was to determine if insulin resistance is sustained in both oxidative soleus and glycolytic extensor digitorum longus (EDL) muscles following long-term (28 days) denervation. Mouse hindlimb muscles were denervated via unilateral sciatic nerve resection. Both soleus and EDL muscles atrophied ~40%. Strikingly, while denervation impaired submaximal insulin-stimulated [³H]-2-deoxyglucose uptake ~30% in the soleus, it enhanced submaximal (~120%) and maximal (~160%) insulin-stimulated glucose uptake in the EDL. To assess possible mechanism(s), immunoblots were performed. Denervation did not consistently alter insulin signaling (e.g., p-Akt (Thr308):Akt; p-TBC1D1 [phospho-Akt substrate (PAS)]:TBC1D1; or p-TBC1D4 (PAS):TBC1D4) in either muscle. However, denervation decreased glucose transporter 4 (GLUT4) levels ~65% in the soleus but increased them ~90% in the EDL. To assess the contribution of GLUT4 to the enhanced EDL muscle glucose uptake, muscle-specific GLUT4 knockout mice were examined. Loss of GLUT4 prevented the denervation-induced increase in insulin-stimulated glucose uptake. In conclusion, the denervation results sustained insulin resistance in the soleus but enhanced insulin sensitivity in the EDL due to increased GLUT4 protein levels.