EFFECTS OF GLUCAGON ON ISLET β CELL FUNCTION IN PATIENTS WITH DIABETES MELLITUS

Objective To evaluate islet β cell response to intravenous glucagon （ a non-glucose secretagogue） stimulation in diabetes mellitus. Methods Nineteen patients with type 1 diabetes （T1 D） and 131 patients with type 2 diabetes （T2D） were recruited in this study. T2D patients were divided into two groups according to therapy： 36 cases treated with insulin and 95 cases treated with diet or oral therapy. The serum C-peptide levels were determined at fasting and six minutes after intra- venous injection of 1 mg of ghicagon. Results Both fasting and 6-minute post-ghicagon-stimulated C-peptide levels in T1D patients were significantly lower than those of T2D patients （0. 76±0. 36 ng/mL vs. 1.81±0. 78 ng/mL, P 〈 0.05 ; 0.88±0.42 ng/mL vs. 3.68±0. 98 ng/mL, P 〈 0. 05 ）. In T1D patients, the C-peptide level after injection of ghicagon was similar to the fasting level. In T2D, patients treated with diet or oral drug had a significantly greater fasting and stimulated C-peptide level than those patients received insulin therapy （2.45±0. 93 ng/mL vs. 1.61±0. 68 ng/mL, P 〈 0.05 ; 5.26±1.24 ng/mL vs. 2.15±0.76 ng/mL, P 〈 0.05 ）. The serum C-peptide level after ghicagon stimulation was positively correlated with C-peptide levels at fasting in all three groups （ r = 0.76, P 〈 0.05 ）. Conclusions The 6-minute ghicagon test is valuable in assessing the function of islet β cell in patients with diabetes mellitus. It is helpful for diagnosis and treatment of diabetes mellitus.

The association of depression and perceived stress with beta cell function between African and Haitian Americans with and without type 2 diabetes

Background: Diabetes and diabetes-related complications are major causes of morbidity and mortality in the United States. Depressive symptoms and perceived stress have been identified as possible risk factors for beta cell dysfunction and diabetes. The purpose of this study was to assess associations between depression symptoms and perceived stress with beta cell function between African and Haitian Americans with and without type 2 diabetes. Participants and Methods: Informed consent and data were available for 462 participants (231 African Americans and 231 Haitian Americans) for this cross-sectional study. A demographic questionnaire developed by the Primary Investigator was used to collect information regarding age, gender, smoking, and ethnicity. Diabetes status was determined by self-report and confirmed by fasting blood glucose. Anthropometrics (weight, and height and waist circumference) and vital signs (blood pressure) were taken. Blood samples were drawn after 8 10 hours over-night fasting to measure lipid panel, fasting plasma glucose and serum insulin concentrations. The homeostatic model assessment, version 2 (HOMA2) computer model was used to calculate beta cell function. Depression was assessed using the Beck Depression Inventory-II (BDI-II) and stress levels were assessed using the Perceived Stress Scale (PSS). Results: Moderate to severe depressive symptoms were more likely for persons with diabetes (p = 0.030). There were no differences in perceived stress between ethnicity and diabetes status (p = 0.283). General linear models for participants with and without type 2 diabetes using beta cell function as the dependent variable showed no association with depressive symptoms and perceived stress;however, Haitian Americans had significantly lower beta cell function than African Americans both with and without diabetes and adjusting for age, gender, waist circumference and smoking. Further research is needed to compare these risk factors in other race/ethnic groups.

Six-year follow-up of pancreatic β cell function in adults with latent autoimmune diabetes

AIM: To investigate the characteristics of the progression of islet β cell function in Chinese latent autoimmune diabetes in adult (LADA) patients with glutamic acid decarboxylase antibody (GAD-Ab) positivity, and to explore the prognostic factors for β cell function. METHODS: Forty-five LADA patients with GAD-Ab positivity screened from phenotypic type 2 diabetic (T2DM) patients and 45 T2DM patients without GAD-Ab matched as controls were followed-up every 6 mo. Sixteen patients in LADA1 and T2DM1 groups respectively have been followed-up for 6 years, while 29 patients in LADA2 and T2DM2 groups respectively for only 1.5 years. GAD-Ab was determined by radioligand assay, and C-peptides (CP) by radioimmune assay.RESULTS: The percentage of patients whose fasting CP(FCP) decreased more than 50% compared with thebaseline reached to 25.0% at 1.5th year in LADA1 group, and FCP level decreased (395.8±71.5 vs 572.8±72.3 pmol/L, P＜0.05) at 2.5th year and continuously went down to the end of follow-up. No significant changes of the above parameters were found in T2DM1 group. The average decreased percentages of FCP per year in LADA and T2DM patients were 15.8% (4.0-91.0%) and 5.2% (-3.5 to 35.5%, P= 0.000) respectively. The index of GAD-Ab was negatively correlated with the FCP in LADA patients (rs= -0.483, P = 0.000). The decreased percentage of FCP per year in LADA patients were correlated with GAD-Ab index, body mass index (BMI) and age at onset (rs = 0.408, -0.301 and -0.523 respectively, P＜0.05). Moreover, GAD-Ab wasthe only risk factor for predicting βcell failure in LADA patients (B = 1.455, EXP (B) = 4.283, P = 0.023). CONCLUSION: The decreasing rate of islet β cell function in LADA, being highly heterogeneous, is three times that of T2DM patients. The titer of GAD-Ab is an important predictor for the progression of islet β cell function, and age at onset and BMI could also act as the predictors.

Adult neural stem cell dysfunction in the subventricular zone of the lateral ventricle leads to diabetic olfactory defects

Sensitive smell discrimination is based on structural plasticity of the olfactory bulb,which depends on migration and integration of newborn neurons from the subventricular zone.In this study,we examined the relationship between neural stem cell status in the subventricular zone and olfactory function in rats with diabetes mellitus.Streptozotocin was injected through the femoral vein to induce type 1 diabetes mellitus in Sprague-Dawley rats.Two months after injection,olfactory sensitivity was decreased in diabetic rats.Meanwhile,the number of Brd U-positive and Brd U＋/DCX＋double-labeled cells was lower in the subventricular zone of diabetic rats compared with agematched normal rats.Western blot results revealed downregulated expression of insulin receptorβ,phosphorylated glycogen synthase kinase 3β,and β-catenin in the subventricular zone of diabetic rats.Altogether,these results indicate that diabetes mellitus causes insulin deficiency,which negatively regulates glycogen synthase kinase 3β and enhances β-catenin degradation,with these changes inhibiting neural stem cell proliferation.Further,these signaling pathways affect proliferation and differentiation of neural stem cells in the subventricular zone.Dysfunction of subventricular zone neural stem cells causes a decline in olfactory bulb structural plasticity and impairs olfactory sensitivity in diabetic rats.

Prevention of beta cell death in chronic pancreatitis

Chronic pancreatitis is best described as a relentless, continuous inflammatory destruction of the pancreas parenchyma, characterized by irreversible destruction of the exocrine tissues, fibrosis, and at the late stage, the destruction of endocrine cells. Current therapies for chronic pancreatitis patients focus on pain relief by medical and minimally invasive endoscopic treatment as well as surgical management with resection of diseased parenchyma and drainage of obstructed ducts. Radical treatment of chronic pancreatitis has been successful with total pancreatictomy and islet autotransplantation (TP-IAT) that may prevent maladaptive intractable pain pathways and also avoid pancreatogenic diabetes in the well-selected patient. Distinct loss of pancreatic islet cells occurs in about 30%-50% of patients during the progression of chronic pancreatitis when severe fibrosis develops at the late stage of the disease. Profound β cell apoptosis induced by stresses encountered during islet isolation and transplantation further compromises β cell survival and function after TP-IAT. The molecular mechanisms that lead to β cell dysfunction in chronic pancreatitis remain largely undelineated. In this review, we summarize factors that may contribute β cell apoptosis during the disease progress and after TP-IAT and discuss potential interventional approaches that may prevent islet cell death during these processes. Such information is critical to the development of therapeutic protocols that can preserve the viability and function of β cell in patients with chronic pancreatitis.

In vitro differentiation of human umbilical cord Wharton's jelly mesenchymal stromal cells to insulin producing clusters

AIM: To investigate the differentiation of human Wharton's jelly derived mesenchymal stromal cells(WJMSCs) to insulin producing clusters(IPC) this study was conducted. METHODS: The umbilical cords samples were collected from full term caesarian section mothers and the WJ-MSCS were cultured from tissue explants in High glucose-Dulbecco's Modified Eagle Medium(H-DMEM); H-DMEM supplemented with 10% fetal bovine serum(FBS) and antibiotics. The expression of CD90, CD44, CD105, CD34 and CD133 as well as osteogenic and adipogenic differentiation of cells in appropriate medium were also evaluated. The cells were differentiated toward IPC with changing the culture medium and adding the small molecules such as nicotinic acid, epidermal growth factor, and exendin-4 during 3 wk period. The gene expression of PDX1, NGN3, Glut2, insulin was monitored by reveres transcription polymerase chain reaction method. The differentiated clusters were stained with Dithizone(DTZ) which confirms the presence of insulin granules. The insulin challenge test(low and high glucose concentration in Krebs-Ringer HEPES buffer) was also used to evaluate the functional properties of differentiated clusters.RESULTS: WJ-MSCS were positive for mesenchymal surface markers(CD90, CD44, CD105), and negative for CD34 and CD133. The accumulation of lipid vacuoles and deposition of calcium mineral in cells were considered as adipogenic and osteogenic potential of WJ-MSCS. The cells also expressed the transcriptional factors such as Nanog and OCT4. During this three step differentiation, the WJ-MSCS morphology was gradually changed from spindle shaped cells in to epithelioid cells and eventually to three dimensional clusters. The clusters expressed PDX1, NGN3, Glut2, and insulin. The cells became bright red color when stained with DTZ and the insulin secretion was also confirmed. In glucose challenge test a significant increase in insulin secretion from 0.91 ± 0.04 μIu/mL(2.8 mmol/L glucose) to to 8.34 ± 0.45 μIu/mL(16.7 mmol/L glucose) was recorded(P < 0.05). The insulin secretion of undifferentiated WJ-MSCS was not changed in this challenge test.CONCLUSION: WJ-MSCs have the ability to differentiate in to islet-like cells in vitro. However, this process needs further optimization in order to generate efficient and functional IPCs.

Present and future cell therapies for pancreatic beta cell replenishment

If only at a small scale,islet transplantation has successfully addressed what ought to be the primary endpoint of any cell therapy:the functional replenishment of damaged tissue in patients.After years of less-thanoptimal approaches to immunosuppression,recent advances consistently yield long-term graft survival rates comparable to those of whole pancreas transplantation.Limited organ availability is the main hurdle that stands in the way of the widespread clinical utilization of this pioneering intervention.Progress in stem cell research over the past decade,coupled with our decades-long experience with islet transplantation,is shaping the future of cell therapies for the treatment of diabetes.Here we review the most promising avenues of research aimed at generating an inexhaustible supply of insulin-producing cells for islet regeneration,including the differentiation of pluripotent and multipotent stem cells of embryonic and adult origin along the beta cell lineage and the direct reprogramming of non-endocrine tissues into insulin-producing cells.

Association of insulin resistance with serum ferritin and aminotransferases-iron hypothesis

AIM: To investigate the relationship of iron indices with diabetes mellitus(DM) in those without hemochromatosis.METHODS: This cross-sectional study examined data collected during the Third National Health and Nutrition Examination Survey(NHANES III). Only those who fasted properly and were not anemic with transferrin saturation < 45% were included(n = 6849). Insulin sensitivity and beta cell function were calculated from fasting glucose and insulin concentrations. Indices of iron metabolism were examined in the presence or absence of DM. We examined the relationship of insulin sensitivity and beta cell function with serum ferritin concentration. The influence of C-reactive protein and liver enzymes was also investigated.RESULTS: Serum ferritin concentration was significantly higher in diabetic subjects(P = 0.0001 to< 0.000001). The difference remained significant after adjustment for age, body mass index, alcohol consumption, and mineral/iron supplement(P = 0.03 to< 0.000001). In those who did not take insulin, serum ferritin concentration was negatively associated with insulin sensitivity(P = 0.05 to 0.00001), but not with beta cell function. The alanine aminotransferase was correlated with serum ferritin concentration(P = 0.02 to< 0.000001) but not with insulin sensitivity, suggesting the role of the liver in iron-associated insulin resistance.CONCLUSION: As most of diabetes is type 2 diabetes and insulin resistance is a cardinal feature of type 2diabetes, disordered iron metabolism could play a role in the pathogenesis of insulin resistance and type 2diabetes through its effect on liver function.

Gastrointestinal manifestations of endocrine disease

The hormonal interactions among the systems throughout the body are not fully understood; many vague clinical symptoms may in fact be manifestations of underlying endocrine diseases. The aim of the following review is to discuss gastrointestinal manifestations of surgically correctable endocrine diseases, focusing on abnormalities of thyroid function, cancer and finally autoimmune diseases. We also review manifestations of pancreatic endocrine tumors, and multiple endocrine neoplasia.

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.

Intra-islet endothelial cell and β-cell crosstalk: Implication for islet cell transplantation

The intra-islet microvasculature is a critical interface between the blood and islet endocrine cells governing a number of cellular and pathophysiological processes associated with the pancreatic tissue. A growing body of evidence indicates a strong functional and physical interdependency of β-cells with endothelial cells(ECs), the building blocks of islet microvasculature. Intra-islet ECs, actively regulate vascular permeability and appear to play a role in fine-tuning blood glucose sensing and regulation. These cells also tend to behave as "guardians", controlling the expression and movement of a number of important immune mediators, thereby strongly contributing to the physiology of islets. This review will focus on the molecular signalling and crosstalk between the intra-islet ECs and β-cells and how their relationship can be a potential target for intervention strategies in islet pathology and islet transplantation.

西藏门巴族人群胰岛细胞功能、脂质代谢、炎症反应与中医体质的相关性研究

目的探讨西藏门巴族人群胰岛细胞功能、脂质代谢和炎症反应与中医体质的相关性。方法选取2023年1月—2023年6月墨脱村、亚东村、朗杰岗村、巴日村、德吉村、玛迪村6个门巴族乡的门巴族人群进行调查,共计237例。分析人群中医体质分布情况,同时比较前三位中医体质人群的胰岛细胞功能、脂质代谢和炎症因子水平。结果中医体质类型中以痰湿质、湿热质和气虚质为主,分别占32.07%、26.16%和18.57%。痰湿质组、湿热质组和气虚质组性别、年龄、体质量指数比较,差异均无统计学意义(P>0.05)。湿热质组空腹血糖和胰岛素抵抗指数分别为(4.98±0.83)mmol/L和(1.75±0.32),均低于痰湿质组和气虚质组(P<0.05),湿热质组胰岛β细胞功能指数为(94.45±9.11),均高于痰湿质和气虚质组(P<0.05);湿热质组总胆固醇和甘油三酯分别为(3.98±0.99)mmol/L和(1.02±0.29)mmol/L,均低于痰湿质组和气虚质组(P<0.05),湿热质组高密度脂蛋白胆固醇为(1.26±0.20)mmol/L,均高于痰湿质组和气虚质组(P<0.05)。痰湿质、湿热质和气虚质组血清白细胞介素-6、超敏c反应蛋白、肿瘤坏死因子-α比较,差异均无统计学意义(P>0.05)。结论西藏门巴族人群中医体质以痰湿质、湿热质和气虚质为主,其中湿热质人群胰岛细胞功能、脂质代谢优于痰湿质和气虚质人群,炎症因子比较无差异。

Beta-cell dysfunction is the primary contributor to the early postpartum diabetes among Chinese women with history of gestational diabetes mellitus

Background Women with a history of gestational diabetes mellitus （GDM） are at higher risk of future development of diabetes. This study investigated the risk factors associated with early postpartum abnormal glucose regulation （AGR） among Chinese women with a history of GDM. Methods A total of 186 women with a history of GDM were screened for early postpartum AGR at 6-8 weeks after delivery. Those with AGR were given lifestyle intervention therapy and reevaluated in 6-12 months. The demographic, anthropometric, prenatal and delivery data were recorded. The plasma high-sensitivity C-reactive protein （HsCRP） and lipid concentration were measured, and insulin secretion were analyzed. Insulinogenic index △ins30＇/△BG30＇, the homeostasis model assessment index （HOMA）-B, and HOMA-IR were calculated. Multiple regression analysis was performed to identify the risk factors. Results Of the GDM women 28.0% （52/186） had AGR at 6-8 weeks after delivery; 45.2% （17/40） of these AGR women reminded abnormal after 6-12 month lifestyle intervention. Compared to the women who reverted to normal, women with consistent AGR showed significantly lower fasting insulin concentration, lower △ins30＇/△BG30＇ as well as lower HOMA-B. No significant differences in age, body mass index （BMI）, waist circumference, blood pressure, lipid level HsCRP and HOMA-IR were observed between the two groups. Pre-pregnancy BMI ≥25 kg/m^2, fasting glucose level ≥5.6 mmol/L and/or 75 g oral glucose tolerance test （OGTT） 2 hours glucose level ≥11.1 mmol/L during pregnancy were predictors for the AGR at 6-8 weeks after delivery. △ins30＇/△BG30≤1.05 was a significant risk contributor to the consistent early postpartum AGR. Conclusion There is a high incidence of early postpartum AGR among Chinese woman with prior GDM. Beta-cell dysfunction, rather than insulin resistance or inflammation, is the predominant contributor to the early onset and consistent AGR after delivery.

有氧运动联合抗阻运动对妊娠期糖尿病患者胰岛细胞功能及糖脂代谢的影响

目的:探究有氧运动联合抗阻运动对妊娠期糖尿病患者胰岛细胞功能及糖脂代谢的影响。方法:将2021年5月—2023年6月松滋市人民医院的100例妊娠期糖尿病患者依据随机数字表法分为对照组50例和观察组50例。对照组进行常规妊娠期糖尿病干预,观察组则在对照组的基础上加用有氧运动联合抗阻运动。比较两组的干预总有效率、干预前后的胰岛细胞功能[稳态模型评估胰岛素抵抗指数(HOMA-IR)及稳态模型评估β细胞功能指数(HOMA-β)]、糖代谢指标[空腹血糖(FPG)、餐后2 h血糖(2 h PG)及糖化血红蛋白(HbA1c)]及脂代谢指标[总胆固醇(TC)、三酰甘油(TG)及低密度脂蛋白胆固醇(LDL-C)]。结果:观察组的干预总有效率高于对照组(P<0.05)。干预前两组的胰岛细胞功能、糖代谢指标及脂代谢指标比较,差异均无统计学意义(P>0.05),干预4、8周后,两组的HOMA-β均高于干预前,且观察组均高于对照组,两组的HOMA-IR、糖代谢指标及脂代谢指标均低于干预前,且观察组均低于对照组(P<0.05)。结论:有氧运动联合抗阻运动在妊娠期糖尿病患者中的应用效果较好,且可显著改善患者的胰岛细胞功能及糖脂代谢状态。

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。

大柴胡汤加减结合常规西药治疗2型糖尿病的疗效及对临床症状积分、胰岛β细胞功能指标的影响

目的 探讨大柴胡汤加减结合常规西药治疗2型糖尿病的疗效及对临床症状积分、胰岛β细胞功能指标的影响。方法 选择2022年9月—2023年9月辽阳市中心医院收治的98例2型糖尿病患者为研究对象,以随机数表法分为两组,各49例。对照组用常规西药治疗,观察组用大柴胡汤加减结合常规西药治疗,比较两组的疗效及临床症状积分、胰岛β细胞功能指标。结果 观察组有效率高于对照组,差异有统计学意义(P<0.05);观察组治疗12周的临床症状积分低于对照组,差异有统计学意义(P均<0.05);观察组治疗4周、治疗12周胰岛β细胞功能指数高于对照组,差异有统计学意义(P均<0.05)。不良反应发生率组间比较,差异无统计学意义(χ^(2)=0.178,P=0.674)。结论 大柴胡汤加减结合常规西药治疗2型糖尿病的疗效较高,可降低临床症状积分,改善胰岛β细胞功能指标,且具有较高的安全性。

津力达颗粒辅助治疗对T2DM患者糖代谢指标及氧化应激反应的影响

目的:探讨津力达颗粒辅助治疗对2型糖尿病(T2DM)患者糖代谢指标及氧化应激反应的影响。方法:选取我院2022年1月—2023年4月收治的96例T2DM患者,按随机数字表法分为对照组与观察组,各48例。对照组予常规治疗,观察组基于常规治疗予津力达颗粒辅助治疗。对比2组糖代谢指标[空腹血糖水平(FBG)、餐后2 h血糖(2 h PBG)、糖化血红蛋白(Hb A1c)],胰岛细胞功能[胰岛β细胞功能(HOMA-β)、胰岛素抵抗指数(HOMA-IR)],氧化应激反应指标[丙二醛(MDA)、超氧化物歧化酶(SOD)]及不良反应。结果:治疗8周,观察组FBG、2 h PBG、Hb A1c、HOMA-IR、MDA水平较对照组低,HOMA-β、SOD水平较对照组高,差异具有统计学意义(P<0.05);观察组与对照组不良反应对比,差异无统计学意义(P>0.05)。结论:T2DM患者采用津力达颗粒辅助治疗可改善糖代谢与胰岛细胞功能,减轻氧化应激反应,且安全性好。

胰岛β细胞功能及同型半胱氨酸、尿微量白蛋白/肌酐比值对2型糖尿病患者心率变异性的影响研究

目的探讨2型糖尿病(T2DM)患者心率变异性(HRV)与胰岛β细胞功能及同型半胱氨酸(Hcy)、尿微量白蛋白/肌酐比值(ACR)的相关性。方法选择上海市第六人民医院收治的300例T2DM患者作为研究对象,男性156例,女性144例;年龄(55.54±8.90)岁,年龄范围为32~78岁。根据24 h正常窦性心搏RR间期标准差(SDNN)将患者分为HRV正常组(100 ms≤SDNN≤180 ms,n=163)及HRV下降组(SDNN<100 ms,n=137)。收集HRV正常组和HRV下降组患者的一般资料、生化指标及HRV指标,分析胰岛β细胞功能及Hcy、ACR与T2DM患者HRV下降的相关性,采用Logistic回归模型评估T2DM患者HRV下降的危险因素,绘制受试者工作曲线分析预测指标对T2DM患者HRV下降的预测价值。结果与HRV正常组比较,HRV下降组年龄较大,病程较长,空腹血糖(FPG)、糖化血红蛋白(HbA1c)、Hcy、空腹C肽(C_(0))、ACR水平较高,餐后2 h C肽(C_(2))、C_(2)/C_(0)水平较低,SDNN、5 min正常RR间期均值的标准差(SDANN)、相邻正常RR间期相差超过50 ms的心搏数占总窦性心搏数的百分比(pNN50)、相邻RR间期之差的均方根(rMSSD)、低频功率(LF)、高频功率(HF)水平较低,差异均有统计学意义(P<0.05)。经Pearson相关系数分析显示,C_(2)、C_(2)/C_(0)与HRV指标之间均呈显著性正相关(P<0.05),C_(0)、Hcy、ACR与HRV指标之间均呈显著性负相关(P<0.05)。经Logistic回归模型分析显示,病程较长、FPG升高、Hcy升高、C_(0)升高、C_(2)降低、C_(2)/C_(0)降低及ACR升高是T2DM患者HRV下降的独立危险因素(P<0.05)。病程、FPG、Hcy、C_(0)、C_(2)、C_(2)/C_(0)、ACR及各指标联合对预测T2DM患者HRV下降均具备一定价值,且联合预测价值更高。结论病程、FPG、Hcy、C_(0)、C_(2)、C_(2)/C_(0)及ACR是T2DM患者HRV下降的独立危险因素,均具备一定预测价值,且联合预测价值更高。

初诊肥胖2型糖尿病患者血清Betatrophin水平与胰岛β细胞功能的关系

目的探讨初诊肥胖2型糖尿病患者血清Betatrophin水平与胰岛β细胞功能的关系。方法方便选择2014年1月—2015年1月初诊肥胖2型糖尿病患者100例为研究对象(观察组),另选择同期该院体检健康者(NGT)者100名为对照观察(对照组)。测量人体指标,检测相关代谢血生化指标,采用酶联免疫吸附实验(ELISA)法测定空腹血清Betatrophin水平,采用直线相关分析研究betatrophin与胰岛β细胞功能、体测及代谢指标的相关关系。结果观察组血清Betatrophin水平(422.5±247.60)pg/m L明显高于对照组(316.3±293.30)pg/m L,差异有统计学意义(P<0.05);相关性分析提示Betatrophin与腰臀比、HOMA-IR、FPG、2 h PG、HbA1c、FINS、TG呈正相关(r=0.215、0.216、0.249、0.447、0.338、0.452、0.470,P<0.01),与HDL-C、HOMA-β成负相关(r=-0.256、-0.363,P<0.05),差异有统计学意义(P<0.05)。结论初诊肥胖2型糖尿病患者的血清betatrophin水平较NGT组明显升高,并且与胰岛β细胞功能密切相关,推测其参与了糖尿病的发生。