The Effect of Tuberculosis Infection on Pancreatic Beta-Cell Function in Patients with Type 2 Diabetes Mellitus

Objective: The aim of this study is to investigate how individuals with type 2 diabetes mellitus’ pancreatic β-cell function index and insulin resistance index are affected by tuberculosis infection. Methods: The study group consisted of 89 patients with type 2 diabetes mellitus and tuberculosis infection who were admitted to Jingzhou Chest Hospital between March 2019 and March 2021. Gender and duration of diabetes were matching conditions. The control group was made up of 89 patients with type 2 diabetes who were admitted to Jingzhou Central Hospital’s endocrinology department during the same period. The two patient groups provided general information such as gender, age, length of diabetes, and blood biochemical indexes such as glycosylated hemoglobin (HbA1c), fasting glucose (FPG), and fasting C-peptide (FC-P). The HOMA calculator was used to calculate the HOMA-β and the HOMA-IR, and intergroup comparisons and correlation analyses were carried out. Results: Regarding gender, age, disease duration, FC-P, and HbA1c, the differences between the two groups were not statistically significant (P > 0.05). However, BMI, FPG, HOMA-β, and HOMA-IR showed statistically significant differences (P < 0.05). In comparison to the control group, the study group’s HOMA-β was lower and its HOMA-IR was greater. According to Spearman’s correlation analysis, HOMA-β had a negative association (P th FPG, HbA1c, and the length of the disease, and a positive correlation with BMI and FC-P. A positive correlation was found between HOMA-IR and BMI, FPG, and FC-P (P < 0.01), as well as a correlation with the length of the disease (P > 0.05) and HbA1c. Conclusions: In type 2 diabetes mellitus combined with tuberculosis infection, the patients had higher FPG levels and lower FC-P levels, the secretory function of pancreatic β-cells was more severely impaired, and insulin resistance was more obvious.

Pancreatic fat and β-cell function in overweight/obese children with nonalcoholic fatty liver disease

AIM: To analyze the associations of pancreatic fat with other fat depots and β-cell function in pediatric nonalcoholic fatty liver disease(NAFLD).METHODS: We examined 158 overweight/obese children and adolescents, 80 with NAFLD [hepatic fat fraction(HFF) ≥ 5%] and 78 without fatty liver. Visceral adipose tissue(VAT), pancreatic fat fraction(PFF) and HFF were determined by magnetic resonance imaging. Estimates of insulin sensitivity were calculated using the homeostasis model assessment of insulin resistance(HOMA-IR), defined by fasting insulin and fasting glucose and whole-body insulin sensitivity index(WBISI), based on mean values of insulin and glucose obtained from oral glucose tolerance test and the corresponding fasting values. Patients were considered to have prediabetes if they had either:(1) impaired fasting glucose, defined as a fasting glucose level ≥ 100 mg/d L to < 126 mg/d L;(2) impaired glucose tolerance, defined as a 2 h glucose concentration between ≥ 140 mg/d L and < 200 mg/d L; or(3) hemoglobin A1 c value of ≥ 5.7% to < 6.5%.RESULTS: PFF was significantly higher in NAFLD patients compared with subjects without liver involvement. PFF was significantly associated with HFF and VAT, as well as fasting insulin, C peptide, HOMA-IR, and WBISI. The association between PFF and HFF was no longer significant after adjusting for age, gender, Tanner stage, body mass index(BMI)-SD score, and VAT. In multiple regression analysis withWBISI or HOMA-IR as the dependent variables, against the covariates age, gender, Tanner stage, BMI-SD score, VAT, PFF, and HFF, the only variable significantly associated with WBISI(standardized coefficient B,-0.398; P = 0.001) as well as HOMA-IR(0.353; P = 0.003) was HFF. Children with prediabetes had higher PFF and HFF than those without. PFF and HFF were significantly associated with prediabetes after adjustment for clinical variables. When all fat depots where included in the same model, only HFF remained significantly associated with prediabetes(OR = 3.38; 95%CI: 1.10-10.4; P = 0.034).CONCLUSION: In overweight/obese children with NAFLD, pancreatic fat is increased compared with those without liver involvement. However, only liver fat is independently related to prediabetes.

Types of voltage-dependent calcium channels involved in high potassium depolarization-induced amylase secretion in the exocrine pancreatic tumour cell line AR4-2J

In the perifused fura-2 loaded exocrine pancreatic acinar cell line AR4-2J pulses of high potassium induced repetitive increases in intracellular calcium. Attached cells when stimulated with high potassium secreted large amount of amylase. High potassium-induced secretion was dependent both on the concentration of potassium and duration of stimulation. High potassium induced increases in intracellular calcium were inhibited by voltage-dependent calcium channel antagonists with an order of potency as follows: nifedipine > ω-agatoxin IVA > ω-conotoxin GVIA. In contrast, the L-type calcium channel antagonist nifedipine almost completely inhibited potassium-induced amylase secretion, whereas the N-type channel antagonist ω-conotoxin GVIA was without effect. The P-type channel antagonist ω-agatoxin IVA had a small inhibitory effect, but this inhibition was not significant at the level of amylase secretion. In conclusion, the AR4-2J cell line possesses different voltage-dependent calcium channels (L, P,N) with the L-type predominantly involved in depolarization induced amylase secretion.

Na^+/HCO_3^- cotransporter is expressed on β and α cells during rat pancreatic development

AIM To determine the expression and localization of the electrogenic Na^+/HCO_3^- cotransporter(NBC1) in rat pancreas during development. METHODS The rat pancreas from postnatal and embryos removed from the uterus of pregnant rats that had been sacrificed by CO2 asphyxiation were used. Rat pancreas from embryonic day(E) 15.5 and E18.5 rat embryos was isolated under a stereomicroscope. Rat pancreas from postnatal(P) days 0, 7, 14, 21 and adult was directly isolated by the unaided eye. The RT-PCR analysis of the NBC1 specific region on rat pancreastissues from different developmental stages. The two antibodies which target the NBC1 common COOHterminal region and NH2-terminal region detected a clear band of about 145 k Da in the Western blot analysis. The localization of NBC1 was examined by immuno-fluorescence detection. RESULTS The results revealed the first peak of NBC1 expression at E18.5 and the second peak at P14. Meanwhile, the low NBC1 expression occurred at P7 and adult stages. Our results demonstrated, for the first time, the presence of NBC1 in the plasma membrane of β and α cells, as well as in the basolateral membrane of acinar cells of the rat pancreas at different stages of development. CONCLUSION The data strongly suggests that NBC1 is diversely expressed in the pancreas at different developmental stages, where it may exert its functions in pancreatic development especially islet cell growth through HCO_3^- transport and pH regulation.

THE CHANGES OF PANCREATIC ACINAR CELL FUNCTION IN ACUTE NECROTIZING PANCREATITIS OF RATS

ObjectiFe To evaluate the changes of pancreatic acinar cell functions in the rats with acutenecrotizing pancreatitis (ANP). methods Seventy SD rats were randomized into two groups: experimental group(n=35) and control group (n=35). To prepare the experimental model, the retrograde injection of 5% sodiumtaurocholate into the pancreatic duct was used for inducing ANP. Radioactive tracing by L -3H-phenylalanineand autoradiography were performed for scoring the differences of changes of amino acid uptake, enzyme-proteinsynthesis and output from acinar cells in rats between both groups. Results No changes were observed in aminoacid uptake and enzyme -protein synthesis in rats with dotted and haemorrhagic necrotizing foci as compared withcontrol group. However, accumulated zymogen granules in the interstitial of acinar cells were seen in theexperimental group. Conclusion It indicates that in experimental ANP rats, the functions of acinar cells in bothamino acid uptake and protein synthesis were essentially normal, but the pathway of enzyme output was affectedinto ectopic secretion through the bottom or lateral cellular membrane of pancreatic acinar cell.

Pancreatic stellate cell: Pandora's box for pancreatic disease biology

Pancreatic stellate cells(PSCs) were identified in the early 1980 s, but received much attention after 1998 when the methods to isolate and culture them from murine and human sources were developed. PSCs contribute to a small proportion of all pancreatic cells under physiological condition, but are essential for maintaining the normal pancreatic architecture. Quiescent PSCs are characterized by the presence of vitamin A laden lipid droplets. Upon PSC activation, these perinuclear lipid droplets disappear from the cytosol, attain a myofibroblast like phenotype and expresses the activation marker, alpha smooth muscle actin. PSCs maintain their activated phenotype via an autocrine loop involving different cytokines and contribute to progressive fibrosis in chronic pancreatitis(CP) and pancreatic ductal adenocarcinoma(PDAC). Several pathways(e.g., JAK-STAT, Smad, Wnt signaling, Hedgehog etc.), transcription factors and mi RNAs have been implicated in the inflammatory and profibrogenic function of PSCs. The role of PSCs goes much beyond fibrosis/desmoplasia in PDAC. It is now shown that PSCs are involved in significant crosstalk between the pancreatic cancer cells and the cancer stroma. These interactions result in tumour progression, metastasis, tumour hypoxia, immune evasion and drug resistance. This is the rationale for therapeutic preclinical and clinical trials that have targeted PSCs and the cancer stroma.

Role of bone marrow-derived mesenchymal stem cells in a rat model of severe acute pancreatitis

AIM:To investigate the role and potential mechanisms of bone marrow mesenchymal stem cells(MSCs) in severe acute peritonitis(SAP).METHODS:Pancreatic acinar cells from Sprague Dawley rats were randomly divided into three groups:nonsodium deoxycholate(SDOC) group(non-SODC group),SDOC group,and a MSCs intervention group(i.e.,a co-culture system of MSCs and pancreatic acinar cells + SDOC).The cell survival rate,the concentration of malonaldehyde(MDA),the density of superoxide dismutase(SOD),serum amylase(AMS) secretion rate and lactate dehydrogenase(LDH) leakage rate were detected at various time points.In a separate study,Sprague Dawley rats were randomly divided into either an SAP group or an SAP + MSCs group.Serum AMS,MDA and SOD,interleukin(IL)-6,IL-10,and tumor necrosis factor(TNF)-α levels,intestinal mucosa injury scores and proliferating cells of small intestinal mucosa were measured at various time points after injecting either MSCs or saline into rats.In both studies,the protective effect of MSCs was evaluated.RESULTS:In vitro,The cell survival rate of pancreatic acinar cells and the density of SOD were significantly reduced,and the concentration of MDA,AMS secretion rate and LDH leakage rate were significantly increased in the SDOC group compared with the MSCs intervention group and the Non-SDOC group at each time point.In vivo,Serum AMS,IL-6,TNF-α and MAD level in the SAP + MSCs group were lower than the SAP group;however serum IL-10 level was higher than the SAP group.Serum SOD level was higher than the SAP group at each time point,whereas a significant betweengroup difference in SOD level was only noted after 24 h.Intestinal mucosa injury scores was significantly reduced and the proliferating cells of small intestinal mucosa became obvious after injecting MSCs.CONCLUSION:MSCs can effectively relieve injury to pancreatic acinar cells and small intestinal epithelium,promote the proliferation of enteric epithelium and repair of the mucosa,attenuate systemic inflammation in rats with SAP.

Effect of TCM Combined with Chemotherapy on Immune Function and Quality of Life of Patients with Non-small Cell Lung Cancer inStage Ⅲ-Ⅳ

Objective: To observe and compare the effect of traditional Chinese medicine (TCM) combined with chemotherapy (CT) on immune function and quality of life (QOL)of patients with non-small cell lung cancer (NSCLC) in stage Ⅲ-Ⅳ. Methods: One hundred cases with stage Ⅲ-Ⅳ NSCLC were randomly divided into two groups. The treated group (n=50) received CT combined with TCM, and the control group received CT alone. The percentage of T lymphocyte subset in peripheral blood and the change of natural killer (NK) cell count were observed after treatment. The QOL and tolerance of CT were also compared between the two groups after treatment. Results: In the treated group, CD3 cell count, CD4 cell count, CD4/ CDg ratio and NK cell activity were higher than those in control group, while CD8 cell count in the treated group was lower than that in the control group (P<0.05), and QOL and tolerance of CT in the treated group were also better (P<0.05). Conclusion: TCM combined with CT could raise the patients' ability in tolerating CT in stage Ⅲ-ⅣNSCLC.

环状RNA-ZNF532表达水平与2型糖尿病患者胰岛细胞功能及微血管并发症的相关性

目的探讨环状RNA-ZNF532(cZNF532)表达水平与2型糖尿病(T2DM)患者胰岛细胞功能及微血管并发症的相关性。方法选择2018年6月至2022年6月南阳市中心医院内分泌科收治的198例T2DM患者为研究对象(观察组),另选择同期于医院进行体检的50例健康志愿者为对照组。采用实时荧光定量聚合酶链式反应检测受试者外周血单核细胞中cZNF532表达水平,采用全自动生化分析仪检测受试者空腹血糖(FPG)、胰岛素(FINS)、糖化血红蛋白(HbA1c)水平及稳态模型评估的胰岛素抵抗指数(HOMA-IR)、稳态模型评估的胰岛β细胞分泌功能指数(HOMA-β),Pearson相关性分析法分析T2DM患者cZNF532表达水平与胰岛细胞功能的相关性。收集T2DM患者临床资料,根据治疗期间是否发生微血管并发症将T2DM患者分为微血管并发症组(n=120)和无微血管并发症组(n=78)。采用多因素logistic回归分析明确T2DM患者发生微血管并发症的危险因素,Spearman相关性分析法分析cZNF532表达水平与T2DM患者微血管并发症的相关性。结果观察组患者cZNF532表达水平及FINS、HbA1c、HOMA-IR水平显著高于对照组,HOMA-β显著低于对照组(P<0.05)。Pearson相关性分析结果显示,T2DM患者cZNF532表达水平与FINS、HbA1c、HOMA-IR呈正相关(r=0.324、0.357、0.410,P<0.05),与HOMA-β呈负相关(r=-0.389,P<0.05)。微血管并发症组与无微血管并发症组患者的性别、年龄、病程、合并高血压例数及高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)、三酰甘油(TG)水平比较差异无统计学意义(P>0.05);微血管并发症患者的LDL-C、FPG、cZNF532表达水平显著高于无微血管并发症组(P<0.05)。多因素logistic回归分析结果显示,LDL-C、FPG、cZNF532是T2DM患者发生微血管并发症的独立危险因素(P<0.05)。Spearman相关性分析结果显示,cZNF532表达水平与T2DM患者微血管并发症发生呈正相关(r=0.681,P<0.05)。结论cZNF532在T2DM患者中呈过表达,cZNF532过表达与T2DM患者胰岛细胞功能、微血管并发症的发生相关。

Pancreatic fat in type 2 diabetes:Causal or coincidental?

Type 2 diabetes(T2D)is a multifactorial metabolic disorder affecting more than 450 million people across the globe.With the increasing prevalence of T2D and obesity,the role of fat accumulation at sites other than subcutaneous adipose tissue has received significant attention in the pathophysiology of T2D.Over the past decade and a half,a pressing concern has emerged on investigating the association of pancreatic fat accumulation or pancreatic steatosis with the development of disease.While a few reports have suggested a possible association between pancreatic fat and T2D and/or impaired glucose metabolism,a few reports suggest a lack of such association.Pancreatic fat has also been linked with genetic risk of developing T2D,prediabetes,reduced insulin secretion,and beta cell dysfunction albeit some confounding factors such as age and ethnicity may affect the outcome.With the technological advancements in clinical imaging and progress in assessment of pancreatic beta cell function,our understanding of the role of pancreatic fat in causing insulin resistance and development of various etiologies of T2D has significantly improved.This review summarizes various findings on the possible association of pancreatic fat accumulation with the pathophysiology of T2D.

急性胰腺炎继发器官功能衰竭患者凝血功能及外周血TIM-3 TAT ACE2水平变化分析

目的:本研究旨在探究急性胰腺炎继发器官功能衰竭患者凝血功能的变化,并分析外周血中T细胞免疫球蛋白黏蛋白分子3(TIM-3)、凝血酶-抗凝血酶复合物(TAT)以及血管紧张素转换酶2(ACE2)水平的变化。方法:本研究开展时间为2020年8月至2022年8月,研究对象为在我院接受诊疗的118例急性胰腺炎患者,根据亚特兰大分级标准对患者的病情严重程度进行评价,并据此进行分组:轻度组(n=72)和重度组(n=46),对两组患者间的凝血功能指标及外周血TIM-3、TAT、ACE2水平进行比较,并探究患者继发器官功能衰竭与各指标的联系。结果:重度组患者的凝血功能指标(PT、INR、APTT和FIB)和外周血中TIM-3和TAT水平均高于轻度组,ACE2水平低于轻度组(P<0.05);继发组患者的凝血功能指标(PT、INR、APTT和FIB)和外周血中TIM-3和TAT水平均高于未继发组,ACE2水平低于未继发组(P<0.05);经多因素分析可知,PT、INR、APTT、FIB、TIM-3、TAT、ACE2均会影响患者继发器官功能衰竭,其预测患者继发器官功能衰竭的AUC值分别为0.846、0.926、0.819、0.862、0.751、0.847、0.858。结论:在急性胰腺炎患者中,凝血功能异常以及外周血中TIM-3、TAT的升高和ACE2的降低与疾病的严重程度密切相关,对急性胰腺炎继发器官功能衰竭风险有潜在的预测价值。

老年2型糖尿病患者血清25-羟维生素D_3水平与胰岛功能、胰岛素抵抗的相关性研究

目的研究老年2型糖尿病(type 2 diabetes mellitus,T2DM)患者体内血清25(OH)D_3水平与胰岛β细胞功能、胰岛素抵抗之间的关系。方法详细收集60例老年T2DM患者和60例健康对照者的临床资料。测定老年T2DM患者及同期健康体检者的空腹血清25-羟维生素D_3水平;老年T2DM患者空腹血糖(FPG)、空腹胰岛素(FINS)水平。使用Pearson相关分析评价血清25-羟维生素D_3水平与胰岛素抵抗、胰岛β细胞功能的相关性。采用多元逐步回归分析评价胰岛β细胞功能的影响因素。结果 1老年T2DM患者血清25(OH)D_3水平显著低于对照组[(35.32±15.24)nmol/L vs.(43.17±17.15)nmol/L,P<0.01]。2老年T2DM患者血清25(OH)D_3与HOMA2-IR、HOMA2-%S无显著相关性(r=-0.235,P=0.073;r=0.223,P=0.090),与HOMA2-%B呈显著正相关(r=0.400,P<0.01)。多元逐步回归分析显示HOMA2-%B的重要相关影响因素是25(OH)D_3(β=0.304,P<0.01)和FPG(β=-0.607,P<0.01)。结论老年T2DM患者体内血清25(OH)D_3的水平明显下降,血清25(OH)D_3水平过低可能会加重胰岛β细胞功能衰竭。

糖尿病综合研究10年(1992-2001年)

本文就近10年来作者所在专科在糖尿病流行病学、临床及基础研究方面所进行的主要工作进行了回顾,包括广东省糖尿病流行病学调查、广州地区儿童及青春期糖尿病发病率调查、胰岛素抵抗性及胰岛β细胞功能的临床研究、胰岛素依赖型糖尿病易感性与HLA-DQ、DR位点关系的研究、有关瘦素基因、瘦素及瘦素受体的系列研究、肥胖和2型糖尿病的分子遗传学研究以及糖尿病的干细胞治疗研究等。不少研究颇具特色,有所创新及发现,对今后糖尿病防治研究提供了有价值的流行病学、临床与实验研究资料,具有重要的理论及应用意义。

c-met及相关基因在大鼠胰腺发育功能完善中的表达

目的：研究原癌基因c-met及其相关基因在大鼠胰腺发育及细胞功能完善过程中的表达。方法：采用高密度寡核苷酸芯片(Affymetrix芯片)对孕12．5(E12．5)、E15．5和E18．5、新生、成年胰腺进行基因转录水平分析,并用RT-PCR验证基因在大鼠胰腺不同发育时期的表达。结果：c-met基因在E15．5、E18．5较成年特异高表达。芯片中c-met转录调控基因和信号传导通路相关基因的表达趋势与c-met高度相似。RT-PCR(所用引物设计区域与芯片相同)验证,c-met表达趋势与芯片结果相符；与芯片c-met探针所用引物不同RT-PCR,结果却在各发育阶段呈现与芯片不同的表达趋势。结论：提示c-met可能在胰腺发育细胞功能完善的关键阶段起调控作用,参与胚胎胰腺发育中晚期细胞功能完善的信号传导过程。并且c-met在胰腺发育中发挥作用有可能存在不同转录本。

初诊2型糖尿病患者血清糖类抗原19-9与胰岛β细胞功能的相关性

目的探讨初诊2型糖尿病(T2DM)患者血清糖类抗原19-9(CA19-9)与胰岛β细胞功能的相关性。方法选择初诊T2DM患者59例,健康对照者(NC)59例,均行口服75 g葡萄糖耐量试验(OGTT)及胰岛素释放试验,分别用稳态模型HOMA-β和HOMA-IR评估胰岛β细胞功能和胰岛素抵抗程度,检测血清CA19-9及其他生化指标。结果 T2DM患者血清CA19-9水平[中位数(第25、75百分位数)]为14.48(12.05,19.30)U/mL,高于NC组[5.03(4.37,7.38)U/mL],P<0.05。糖化血红蛋白A1c(HbA1c)>7.0%T2DM患者组、HbA1c<7.0%T2DM患者组及NC组血清CA19-9水平依次下降(P<0.05)。血清CA19-9水平与总胆固醇(TC)、空腹血糖(FPG)、OGTT 2 h血糖(2hPG)、HbA1c呈正相关(r分别为0.320、0.786、0.756、0.782,P均<0.01),与空腹胰岛素(FINS)、HOMA-β呈负相关(r分别为-0.438、-0.644,P<0.05或0.01)。以血清CA19-9为因变量,行多元逐步回归分析,有FPG、HbA1c、HOMA-β进入最后方程(P<0.01)。结论初诊T2DM患者血清CA19-9水平高于NC组,与FPG、HbA1c和HOMA-β相关,可作为判断T2DM患者胰岛β细胞功能障碍的一种生物学标志物。

短期胰岛素强化治疗对2型糖尿病患者外周血MCP-1和NF-κB表达的影响

目的探讨短期胰岛素强化治疗对2型糖尿病患者外周血单核细胞趋化蛋白-1(MCP-1)和核因子-κB(NF-κB)表达的影响。方法选择2015年8月至2016年6月在我院确诊的86例2型糖尿病患者为研究对象,按照随机数表法分为观察组和对照组,每组43例,观察组患者给予短期胰岛素强化治疗,对照组患者给予盐酸二甲双胍口服治疗,2周后观察患者的血糖达标率和胰岛β细胞功能指标,流式细胞仪检测MCP-1和NF-κB表达。结果治疗两周后,观察组患者的空腹血糖、餐后血糖和餐后2 h血糖分别为(6.27±1.21)mmol/L、(9.17±1.19)mmol/L、(7.07±1.12)mmol/L,均低于对照组的(7.41±1.13)mmol/L、(10.88±0.25)mmol/L、(9.91±0.16)mmol/L,差异均有统计学意义(P<0.01);观察组患者的血糖达标率为83.72%,明显高于对照组的58.14%,差异有统计学意义(χ2=6.824,P=0.009);观察组患者的胰岛素分泌指数(HOMA-β)为(41.37±3.43),明显高于对照组的(35.17±2.78),胰岛素抵抗指数(HOMA-IR)为(3.26±0.86),明显低于对照组的(4.93±1.15),差异均有显著统计学意义(P<0.01);观察组患者的MCP-1和NF-κB分别为(62.28±7.76)ng/L、(6.47±1.96)ng/L,均明显低于对照组的(78.67±10.44)ng/L、(9.78±2.13)ng/L,差异均有统计学意义(P≤0.01)。结论短期胰岛素强化治疗可提高2型糖尿病患者的血糖达标率,改善胰岛β细胞功能,降低MCP-1和NF-κB表达。

妊娠期葡萄糖筛查异常孕妇的PTP-1B与IR相关性的研究

目的探讨蛋白酪氨酸磷酸酶1B（PTP-1B）与胰岛素抵抗（IR）的关系及在妊娠期糖尿病（GDM）发病机制中的作用，以早期预防和干预GDM，减少母儿并发症。方法2011年4～10月在我院产前检查的妊娠期糖尿病孕妇（C组）、葡萄糖负荷试验（GCT）异常而葡萄糖耐量试验（OGTr）正常的孕妇（B组）及葡萄糖负荷试验正常的孕妇（A组）各30例，分别测定空腹PTP-1B、空腹血糖、空腹胰岛素水平，同时计算胰岛素抵抗指数（HOMA—IR）和胰岛B细胞功能指数（HOMA—HBCI），分析比较各组的差异与关系。结果①C组的HOMA—IR明显高于A组、B组，差异有统计学意义（P〈0．01，P〈0．05）。②C组的PTP-1B值明显高于A组、B组，差异有统计学意义（P〈0．01）。③相关性分析：血浆PTP-1B与孕前BMI、空腹血糖、空腹胰岛素、HOMA—IR呈正相关．相关系数分别为：r=0．347，P=0．001；r=0．263，P=0．012；r=0．287，P=0．006；r=0．318，P=0．002。结论GDM存在更严重的IR，PTP-1B与IR有关，可能参与GDM的发生和发展。

血必净对重症急性胰腺炎患者炎症因子、血管内皮功能及单核细胞HLA-DR表达的影响

目的探讨血必净对重症急性胰腺炎患者炎症因子、血管内皮功能及单核细胞HLA-DR表达的影响。方法选取2014年1月～2016年5月在我院接受治疗的重症急性胰腺炎患者112例为研究对象,采用随机数字表法分为观察组和对照组,各56例。对照组给予吸氧、禁食、胃肠减压、抗感染、防休克、纠正水电解质失衡,同时静脉滴注乌司他丁。观察组在对照组相同处理的基础上静脉滴注血必净注射液。观察治疗前后,两组患者血清白细胞介素-6(IL-6)、白细胞介素-8(IL-8)、高敏-C反应蛋白(hs-CRP)及肿瘤坏死因子-α(TNF-a)水平,血浆一氧化氮(NO)、血栓调节蛋白(TM)、血栓素A_2(TXA_2)、血管假性血友病因子(VWF)水平,以及CEC计数和外周血单个核细胞HLA-DR表达。结果治疗后,观察组血清IL-6、IL-8、hs-CRP和TNF-α水平,以及血浆TM、TXA_2和VWF水平下降均较对照组更加显著,差异有统计学意义(P<0.05);而观察组血浆NO水平升高较对照组更加显著,差异有统计学意义(P<0.05)。治疗后,观察组外周血单核细胞HLA-DR抗原表达较对照组升高更明显,差异有统计学意义(P<0.05);而循环血CEC计数较对照组减小更明显,差异有统计学意义(P<0.05)。结论血必净注射液能够有效减轻SAP患者机体炎症反应,改善血管内皮细胞功能和提高免疫能力,这对于防止病情恶化和改善患者预后具有重要意义,值得临床推广应用。

胰高血糖素样肽-1类似物利拉鲁肽联合二甲双胍治疗对2型糖尿病胰岛功能及胰岛β细胞的影响分析

目的:分析胰高血糖素样肽-1类似物利拉鲁肽联合二甲双胍对2型糖尿病胰岛功能及胰岛β细胞的临床效果。方法:选取2015年6月-2016年2月本院就诊的48例2型糖尿病患者,在原有二甲双胍治疗的基础上联合应用胰高血糖素样肽-1类似物治疗,比较分析联合用药对2型糖尿病患者胰岛功能及胰岛β细胞的影响。结果:治疗4周后,患者空腹血糖、糖化血红蛋白均低于治疗前(P<0.05);治疗12周后,患者的空腹血糖、餐后2 h血糖、糖化血红蛋白水平均低于治疗前(P<0.05)。治疗前,患者HOMA-B指数为44.01±11.72,治疗4周后患者HOMA-B指数为58.71±11.48,差异无统计学意义(P>0.05);治疗12周后,患者HOMA-B指数为67.88±10.27,高于治疗前的44.01±11.72,差异有统计学意义(P<0.05)。结论:胰高血糖素样肽-1类似物利拉鲁肽联合二甲双胍对2型糖尿病治疗12周后,患者病情有所改善;另外,患者HOMA-B指数也有所提高,胰岛β细胞的分泌能力有所增强。胰高血糖素样肽-1类似物联合二甲双胍治疗2型糖尿病,在临床中具有推广和应用价值。

胰腺纤维化进程中大鼠胰腺GnRH及GnRHR、Bcl-2及Bax、胰岛β细胞功能的变化

目的观察SD大鼠胰腺纤维化进展过程中胰腺促性腺激素释放激素(GnRH)及其受体(GnRHR)、Bcl-2和BaxmRNA水平及胰岛β细胞功能的变化。方法 25只SD雄性大鼠随机均分为5组:正常组及注药1、2、3、6周组。注药组采用反复腹腔内注射二乙基二硫代氨基甲酸盐(DDC)法制作胰腺纤维化大鼠模型,剂量为500mg/kg,每周2次,正常组注射等量生理盐水。所有大鼠灌胃法行口服葡萄糖耐量试验(OGTT)测定血糖、血清胰岛素并计算空腹胰岛素与空腹血糖比值(FINS/FBG)、糖负荷30min时胰岛素与血糖比值[INS/PG(30min)]、糖负荷30min时胰岛素净增量与血糖净增量比值[ΔIRI/ΔBS(30min)]、血糖/胰岛素曲线下面积[GLU/(INS-AUC)]、稳态模型评估胰岛素抵抗(HOMA-IR)评价胰岛β细胞功能;光镜下观察胰腺病理改变;实时定量PCR法检测各组大鼠胰腺GnRH、GnRHR、Bcl-2及BaxmRNA表达水平。结果光镜下观察胰腺切片,注药1、2、3周组可见炎症细胞浸润、空泡变化、小叶间隙增宽,注药6周组可见腺泡细胞呈纤维素样排列。OGTT试验中各组间各时间点血糖无差异(P>0.05);与正常组比较,注药3周组空腹胰岛素(FINS)水平升高,注药2、6周组15min及60min胰岛素、注药2周组30min胰岛素、注药1、2、6周组120min胰岛素水平下降(P<0.05)。与正常组比较,注药3周组FINS/FBG和HOMA-IR明显升高,注药2周组FINS/FBG下降,注药2周组和注药6周组INS/PG(30min)、ΔIRI/ΔBS(30min)和INS-AUC下降(P<0.05)。与正常组比较,注药1、2、3周组胰腺GnRH表达均下降,注药6周组表达上升,注药组胰腺GnRHR表达均降低,胰腺Bcl-2和Bax表达均增加,Bcl-2∶Bax比值升高(P<0.05)。胰腺GnRH与FBG呈负相关(r=-0.443);胰腺GnRHR与糖负荷15min时血清胰岛素呈正相关(r=0.435),与Bcl-2∶Bax呈负相关(r=-0.813)。结论 GnRHR可能参与胰腺纤维化早期阶段的Bcl-2和Bax介导的细胞凋亡,导致早期胰岛β细胞功能下降,减少胰岛素分泌,胰岛素抵抗增加。